Full opinion text
MEMORANDUM OPINION AND ORDER ON MOTIONS; ORDER GRANTING DEFENDANT’S MOTION FOR SUMMARY JUDGMENT JUSTIN L. QUACKENBUSH, Senior District Judge. The court has had under advisement the following eleven motions. 1. Defendant’s Motion to Exclude Opinions of Dr. Catón Based on Disclosure Violations (Ct. Rec. 67); 2. Defendant’s Motion in Limine to Limit the Testimony of Plaintiffs’ Treating Physicians (Ct. Rec. 71); 3. Defendant’s Motion to Exclude the Testimony of Plaintiffs’ Expert Witness Frank Gardner (Ct. Rec. 75); 4. Defendant’s Motion to Exclude Dose Opinions of Expert Sawyer due to Disclosure Violations (Ct. Rec. 79); 5. Defendant’s Motion to Exclude Testimony of Plaintiffs’ Expert Witness William Sawyer (Ct. Rec. 83); 6. Defendant’s Motion to Exclude the Testimony of Plaintiffs’ Expert Witness Marco Kaltofen (Ct. Rec. 87); 7. Defendant’s Motion to Exclude Causation Opinions Based on Unreliable Epidemiological Evidence (Ct. Rec. 91) 8. Defendant’s Motion for Summary Judgment on General Causation (Ct. Rec. 95) 9. Defendant’s Motion for Summary Judgment on Specific Causation (Ct. Rec. 100); 10. Defendant’s Motion to Exclude Plaintiffs’ Expert John Catón, M.D. (Ct. Rec. 127); and 11. Plaintiffs expedited Motion to Supplement the Record (Ct. Rec. 160). I. INTRODUCTION Neil Henricksen (“Henricksen”), a former gasoline tanker truck driver, and his wife brought suit against the Defendant (among others), ConocoPhillips (Defendant or “Conoco”), alleging that Henricksen’s acute myelogenous leukemia (AML) was caused by his occupational exposure to benzene and benzene-containing products, including Defendant’s gasoline. Plaintiffs assert products liability claims for negligence, strict liability and breach of warranty- By motions to exclude/motions in limine Defendant seeks to have the court decide whether Plaintiffs can reliably establish a medical or scientific link between exposure to gasoline and AML and whether Plaintiffs’ admissible evidence can establish that Henricksen’s exposure to Defendant’s gasoline proximately caused his illness. Focusing both on Plaintiffs’ general causation and specific causation case, Defendant seeks to exclude the testimony and reports of Plaintiffs causation experts Marco Kaltofen, Ph.D., Frank Gardner, M.D., William Sawyer, Ph.D., and Peter Infante, Ph.D., as well as Henricksen’s treating physicians. In contesting the reliability of the Plaintiffs’ proposed evidence Defendants have submitted reports and testimony of their own expert witnesses, David Pyatt, Ph.D., Ethan Natelson, M.D., John Spencer (an industrial hygienist), and David H. Garabrant, M.D., MPH. Specifically, Defendant argues that Plaintiffs cannot establish that exposure to benzene as a component of gasoline increases the risk of developing AML. Defendant also asserts that Plaintiffs can not demonstrate, through reliable testimony and evidence that Henricksen’s occupational exposure to benzene in gasoline was sufficient to cause his AML. Defendant challenges the methodology employed by Plaintiffs’ experts and argues their opinions have no scientific basis, are not supported by the material facts of this case, are not supported by reliable studies, have not been tested, have not been subjected to peer review, and are inadmissible under the Federal Rules of Evidence and as explained by the United States Supreme Court in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993) and subsequent decisions of the federal courts. In addition to its Daubert motions, Defendant has moved to strike any testimony on the subject of causation by treating physician John Catón and the dose opinions of William Sawyer based upon Plaintiffs’ alleged failure to timely disclose these individuals as experts. Defendant’s motions for summary judgment argue that because the opinions of Plaintiffs’ experts are unreliable and therefore inadmissible, Plaintiffs can not demonstrate that gasoline caused Henricksen’s AML. In their opposition to the summary judgment motions, Plaintiffs attempt to demonstrate a genuine issue regarding causation by proffering the testimony of the experts and the scientific data that Defendant has challenged in its motions in limine. Therefore, whether Plaintiffs can defeat the summary judgment motions turns on the extent to which Defendant’s motions in limine are meritorious. The parties have set forth an extensive evidentiary record, which includes the reports of each expert, excerpts from depositions, and numerous publications. Defendant requested an evidentiary hearing and oral argument. The court granted this request. The parties, by stipulation (Ct. Rec. 231), agreed not to present any live witness testimony at the hearing and agreed to rely solely on the written record. Appearing at the hearing on behalf of the Plaintiffs was Jackson Schmidt. Appearing on behalf of the remaining Defendant were Christopher Weiss, Brett Young, Stephen Dillard, and Leslie Weatherhead. After careful consideration of the extensive briefing on the motions, the responses, the replies, the evidence submitted, the applicable law, and counsel’s argument, the court finds the disputed testimony fails scrutiny under Daubert. Thus for the reasons that follow, Defendants’ Motions For Summary Judgment are GRANTED. II. THE RECORD EVIDENCE Before turning to the legal analysis, the court summarizes the facts before it and the evidence presented with respect to these issues. In doing so the court will review the Plaintiffs’ experts proffers and the substance of their opinions. Plaintiff Neil Henricksen worked as a gasoline truck driver from 1973-2003. As part of his duties, Henricksen loaded petroleum fuels, including gasoline, refined and sold by, among others, the Defendant ConocoPhillips. He loaded fuels at terminals in and around Spokane, Washington, including at Defendant’s Spokane terminal. Apparently, during his tenure as a truck driver, Henricksen drove a top-loading truck that was filled through a hatch at the top of the tank. It is alleged he regularly spilled gasoline on his skin. Half of his time was spent loading diesel fuel as opposed to gasoline. Plaintiffs do not contend exposure to diesel fuel was a contributing factor here. Conoco’s Spokane terminal allegedly did not have a vapor recovery system to prevent exposure to gasoline fumes. Ct. Rec. 147, Ex. 6. It is alleged the terminal also had a roof and partial walls on two of the four sides, such that fumes did not as easily dissipate as would in “open” terminals. In August 2003, at age 61, Henricksen was diagnosed with a form of cancer, Acute Myelogenous Leukemia (AML). He received chemotherapy and his AML went into remission for two years. In 2005, his AML returned and he was again placed into a second treatment with chemotherapy. He received a bone marrow transplant from a sibling and at the time of the filing of the present motions, he was again in remission. 1. AML AML is one of the most common types of leukemia in adults in the U.S., with approximately 13,000 new cases diagnosed each year. Ct. Rec. 104, Ex. A [Gardner ] at 51:4-8. AML afflicts people of all ages and from all cultures, though the risk of AML increases with age. Unlike asbestosis caused by asbestos exposure, AML is not a disease that implicates its cause. While there are various known causes of the disease,- the majority of cases have no known cause. One way AML has been classified is according to presumed causation. Cases can either be termed idiopathic or de novo (primary, endogenous), meaning onset without external or environmental stimulus, or secondary (event-related, exogenous) events which could be related to exposure to chemotherapy or radiation interventions in addressing preexisting hematologic disorders, or exposure to environmental toxins, including benzene. Ct. Rec. 104, Ex. B [Natelson Aff.]. The majority (80-90%) of all adult AML cases are de novo or idiopathic, with no readily identifiable cause. Ct. Rec. 104, Ex. E [Pyatt Aff.] at 20; Natelson, ¶ 17. Studies of patients with AML have shown the underlying biology of these two categories of AML is usually different. Either cytogenetic or a distinct pattern of chromosomal aberrations have been considered characteristic findings in nearly ninety percent of all secondary AML, which includes AML caused by exposure to benzene as opposed to gasoline containing benzene. Id. In de novo AML cytogenetic abnormalities are observed only in approximately fifty percent of the time. Pyatt Aff., ¶ 12. There was no evidence of chromosomal abnormality in Mr. Henricksen’s case. In addition, secondary forms of AML are commonly preceded by myelodysplastic syndrome (MDS) and are more resistant to standard treatment than de novo AML. Id. Mr. Henricksen’s AML was not preceded by MDS and after standard chemotherapy, remained in remission for two years. In addition, there are different forms or variants of AML which are assigned designations (M0-M7) based on “morphological and cytogenetic similarities” within each subtype. Pyatt Aff., ¶ 12. The Ml variant of AML is a frequently observed subtype comprising 20% of all de novo AML cases. Mr. Henricksen’s subtype was Ml. In the 10-15 years immediately prior to his diagnosis in 2003, Henricksen was predominately transporting diesel fuel. Plaintiffs have focused on the period from 1976-1983/1984 when Henricksen worked at the Parkwater Terminal as the years he experienced the majority of exposure to gasoline. Defendants’ experts claim the scientific studies have shown that exposures occurring within 10-15 years of clinical onset contribute to risk of AML, but those in more distant past do not. Pyatt Aff., ¶ 13; Ct. Rec. 104, Ex. v. [Garabrant Aff.] at ¶ 8. Plaintiffs experts disagree. Given the presentation and clinical and laboratory features of Henricksen’s disease, according to Defendant’s experts, there is no scientific way to separate the AML affecting Henricksen from the de novo AML occurring in people with no particular exposure to chemicals. Pyatt Aff., ¶15; Natelson, ¶17. Taken collectively, on medical probability alone, Defendant’s experts conclude Henricksen’s AML is far more consistent and must be considered de novo rather than secondary due to occupational exposure to the benzene in gasoline. Id. 2. Gasoline Gasoline is a complex mixture of chemical substances (as many as 150 distinct compounds and other additives). It is undisputed that one component of gasoline is benzene. Conoco’s gasoline contained between 1 and 4.9% benzene. Ct. Rec. 147, Ex. 7 [Conoco MSDS sheets] at 1. The chemical composition of gasoline vapor differs from the chemical composition of gasoline liquid. Benzene vapor makes up a small fraction (0.5-0.7%) of total gasoline vapor. Benzene vapor concentration is usually measured as parts of benzene per million parts of air (ppm). Ct. Rec. 94, Ex. V [Garabrant Aff.] at ¶ 7. Thus if there was one molecule of benzene in one million molecules of air, the benzene concentration would be one part per million. Id. In order to measure a person’s cumulative exposure to benzene, the average concentration during a typical workday is multiplied by the duration in years and is expressed in parts per million-years, or ppm-years. Id. This is sometimes referred to as a “time-weighted average” or TWA. The parties agree that scientific studies provide clear evidence of a causal relationship between occupational exposure to benzene and benzene-containing solvents and the occurrence of AML. Benzene exists in the environment everywhere and humans are exposed to benzene on a daily basis. Ct. Rec. 151, Ex. B (Sawyer Rebuttal Report) at 23. Benzene exists in air, water, soil, and in our food. Low exposures to which every human being is subjected, is often, and alternatively, referred to as “background exposure” or “ambient exposure”. No one, including the Plaintiffs’ experts, proffers an opinion that this level of exposure creates an increased risk of the development of AML. Everyone, including the Plaintiffs’ experts, agrees that something greater is required. The argument in this Daubert challenge, in part, revolves around the question of how much greater quantity of exposure is necessary to permit the causal attribution of AML to a particular benzene exposure. Though there is no unanimous agreement as to the threshold, both the Defendants and Plaintiffs agree the medical-scientific literature supports the conclusion that cumulative benzene exposure at levels between 50 and 500 ppm-years, can result in AML. It is Plaintiffs’ expert’s contention however, that far lower levels (as low as 1.5 ppm/years) of long term exposure to benzene are linked with a significantly elevated risk of AML. Just as the toxicity of benzene has been evaluated and studied, so has the toxicity of gasoline. Both parties experts recognize that no authoritative source (organization or regulatory agency) has identified gasoline as cancer-causing. It has been named as a “probable carcinogen” because animal studies with fuel vapors have demonstrated a significant increase in kidney cancer among male rats and liver cancer in female mice. The U.S. Occupational Safety and Health Administration (OSHA) does not mandate any occupational exposure limit for workers exposed to gasoline, whereas OSHA has promulgated a 1 ppm workplace exposure limit for benzene. The American Conference of Governmental Industrial Hygienists (ACGIH) has a recommended, allowable, 8-hour work day exposure limit for gasoline of 300 ppm, whereas the current recommendation for exposure to benzene is .5 ppm. General Causation SJ, Ex. B., Rose at 108:13-15. The National Institute for Occupational Safety and Health’s (NIOSH) recommended exposure limit is 0.1 ppm for an 8-hour TWA and 1 ppm for short-term exposure (NIOSH 1992b). The Defendant’s experts contend the observed toxicity of gasoline is different from the observed toxicity following exposure to pure benzene. While bone marrow toxicity is almost universally found following high-dose benzene exposure in experimental animals, Defendant’s experts say no studies of any species, including humans, have reported bone marrow toxicity following even chronic exposure to high levels of unleaded gasoline. Pyatt, ¶ 11. Some toxicological experts theorize that so called “competitive inhibition” between benzene and the other compounds found in gasoline mitigate the potential carcinogenic properties of the small amounts of benzene present in gasoline. Pyatt, ¶ 12; Natelson, ¶ 18. Toxicologically, Defendant contends it is unsupportable that exposure to benzene as a component of gasoline plays a role in the development of AML. Pyatt, ¶ 11. Defendant’s experts contend there is no scientific or medical literature to support the proposition that there is a sufficient level of benzene, as a constituent ingredient of gasoline, to result in a risk of AML by virtue of exposure to gasoline. Plaintiffs’ expert epidemiologist, Peter Infante, on the other hand, states in his report that the “toxicity of gasoline to the bone marrow has mirrored the toxicity of benzene even though the literature related to gasoline has lagged that of benzene.” Ct. Rec. 149. 3. Plaintiffs’ Experts Henricksen was treated by physicians John Catón and Jeanie Nichols of Cancer Care Northwest and George Earle Georges and Andrew Kominsky, of Seattle Cancer Care Alliance. Dr. Catón was Mr. Henricksen’s primary treating physician who apparently told the Henricksens and also presently believes that his AML was likely caused by occupational exposure to gasoline. Plaintiffs argue in opposition to the Defendant’s motions that they have presented sufficient reliable and valid evidence of both general and specific causation to raise a triable issue. Plaintiffs evidence on causation includes the testimony of expert witnesses Peter Infante, an epidemiologist, Frank Gardner, a medical doctor, William Sawyer, a toxicologist, and Marco Kaltofen, a civil engineer. Plaintiffs contend that their expert evidence demonstrates that even at low levels, exposure to benzene in gasoline increases the risk of developing AML. Below is a brief description of each expert and his conclusion. William Sawyer, Ph.D., is a toxicologist board certified in forensic medicine, toxicology and pharmacology. He has authored on benzene poisoning. Sawyer calculates Henricksen’s annual benzene exposure in this case as 1.118 ppm and his cumulative dose as 8.9 ppm-years. In his opinion, he concludes that “to within a reasonable degree of toxicological certainty ... Mr. Henricksen was exposed to dangerously high levels of carcinogenic benzene ...” and that “to within a reasonable degree of toxicological certainty ... Mr. Henricksen’s chronic toxic exposure excursions ... to benzene while top loading primarily contributed to the development of his AML.” Marco Kaltofen is a registered professional engineer and environmental scientist who has performed environmental, workplace and product investigation. He was hired by Plaintiffs to calculate Henricksen’s estimated exposure to benzene. Kaltofen estimates Henricksen’s “unadjusted daily benzene exposure” as 0.38 ppm. He then adjusts this number based upon features of Henricksen’s work and the length of time he performed the work, resulting in a cumulative dose estimate of 1.6625 ppm-years. He then multiplies that number by 5 to accommodate the fact that Henricksen worked at a terminal with a roof to come up with a dose estimate of 8.3125 ppm-years. Frank Gardner, M.D. is a Clinical Professor of Medicine in the Division of Hematology-Oncology in Galveston, Texas. He has studied and published on the treatment of leukemia. Gardner opines that on a more probable basis than not, benzene exposure was “a major cause of Mr. Henricksen’s acute myelogenous leukemia.” Ct. Rec. 148, Ex. A. “Mr. Henricksen, from his prolonged exposure to benzene in gasoline, initiated mutagenic changes in the bone marrow leading to his leukemia.” He bases this conclusion solely upon Mr. Henricksen’s description of his occupation and his belief that chronic low exposure to benzene can cause AML. Peter Infante, Ph.D., is an epidemiologist and is the managing member and President of Peter F. Infante Consulting, L.L.C., an environmental and occupational health consulting firm. In 1977, he conducted the first study of benzene exposed workers in the production of Pliofilm at Goodyear plants. In this case, based upon his review of the scientific literature, he opines that 1) both occupational exposure to benzene and to gasoline, which contains an average 1-2% benzene, are associated with an elevated risk of developing AML and 2) “Mr. Henricksen’s 29 years of occupational exposure to gasoline was a substantial contributing factor and the most likely cause of his development of AML.” Ct. Rec. 149. III. LEGAL STANDARDS A. Daubert In the seminal case of Daubert v. Merrell Dow Pharmaceuticals, Inc. 509 U.S. 579, 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993), the Supreme Court cast trial judges in the role of “gatekeeper[s] in determining whether to admit or exclude expert evidence[ ]” in accordance with Rule 702. See Dukes v. Wal-Mart, Inc., 509 F.3d 1168,1179 (9th Cir.2007) (internal quotation marks omitted). The Daubert Court “held that Federal Rule of Evidence 702 commands the primary focus for courts evaluating the admissibility of expert testimony.” Cooper v. Brown, 510 F.3d 870, 942 (9th Cir.2007). That Rule provides in part that “[i]f scientific, technical, or other specialized knowledge will assist the trier of fact to understand the evidence or to determine a fact issue,” an expert “may testify thereto.” Fed.R.Evid. 702. Before a witness may come “before the jury cloaked with the mantle of an expert[]” under Rule 702, the Ninth Circuit has cautioned that “care must be taken to assure that a proffered witness truly qualifies as an expert, and that such testimony meets the requirements of [that] Rule[.]” Jinro America Inc. v. Secure Investments, Inc., 266 F.3d 993, 1004 (9th Cir.2001). Thus, as a threshold matter, in accordance with Rule 702 the court must determine whether the proffered witness is “qualified as an expert by knowledge, skill, experience, training, or education^]” Fed.R.Evid. 702; see also Daubert v. Merrell Dow Pharm., Inc., 43 F.3d 1311, 1315 (9th Cir.1995) (“Daubert II”) (whether proffered expert testimony is admissible “only arises if it is first established that the individual ] whose testimony is being proffered [is] [an] expert[] in a particular ... field[ ]”). Defendant does not challenge the expert qualifications of any of Plaintiffs’ experts, except the treating physicians. Once a court makes the “preliminary” determination under Fed.R.Evid. 104(a) that a witness qualifies as an expert, the focus shifts to that witness’s proffered testimony. Rule of Evidence 702 permits a witness to give expert testimony if “(1) the testimony is based upon sufficient facts or data, (2) the testimony is the product of reliable principles and methods, and (3) the witness has applied the principles and methods reliably to the facts of the case.” Fed.R.Evid. 702. As interpreted by the Daubert Court, there is a two-part inquiry under Rule 702 for determining the admissibility of proffered expert opinion testimony. Expert testimony must be “not only relevant, but reliable.” Daubert, 509 U.S. at 589, 113 S.Ct. 2786. This requires consideration of whether: (1) the reasoning or methodology underlying the testimony is scientifically valid (the reliability prong); and (2) whether that reasoning or methodology properly can be applied to the facts in issue (the relevancy prong). Daubert v. Merrell Dow Pharms., Inc., 509 U.S. 579, 592-93, 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993). Reliability Prong. In determining reliability, a court may consider a number of factors including: (1) whether the theory can be and has been tested; (2) whether it has been subjected to peer review; (3) the known or potential rate of error; and (4) whether the theory or methodology employed is generally accepted in the relevant scientific community. Id. at 593-94, 113 S.Ct. 2786. However, “Daubert’s list of specific factors neither necessarily nor exclusively applies to all experts or in every case.” Kumho Tire Co. v. Carmichael, 526 U.S. 137, 141, 119 S.Ct. 1167, 143 L.Ed.2d 238 (1999). “[F]ar from requiring trial judges to mechanically apply the Daubert factors ... judges are entitled to broad discretion when discharging their gatekeeping function.” United States v. Hankey, 203 F.3d 1160, 1168 (9th Cir.2000) (citing Kumho, 526 U.S. at 150-52, 119 S.Ct. 1167). The court need not admit an expert opinion that is connected to the underlying data “only by the ipse dixit of the expert.” Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146, 118 S.Ct. 512, 139 L.Ed.2d 508 (1997). It may exclude such testimony if it determines “that there is simply too great an analytical gap between the data and the opinion proffered.” Id. “The trial court’s gate-keeping function requires more than simply taking the expert’s word for it.” Daubert v. Merrell Dow Pharms., Inc., 43 F.3d 1311, 1319 (9th Cir.1995) (“Daubert II ”). In addition, “any step that renders [the expert’s] analysis unreliable ... renders the expert’s testimony inadmissible. This is true whether the step completely changes a reliable methodology or merely misapplies that methodology.” In re Silicone Gel Breast Implants Products Liability Litigation, 318 F.Supp.2d 879, 890 (D.C.Cal.2004). Something doesn’t become scientific knowledge just because it’s uttered by a scientist; nor can an expert’s self-serving assertion that his conclusions were derived by the scientific method be deemed conclusive. Daubert II, at 1315-16. “[T]he expert’s bald assurance of validity is not enough. Rather, the party presenting the expert must show that the expert’s findings are based on sound science, and this will require some objective, independent validation of the expert’s methodology.” Id. at 1316. Relevance Prong. The relevance prong under Daubert means that the evidence will assist the trier of fact to understand or determine a fact in issue. Daubert, 509 U.S. at 591-92, 113 S.Ct. 2786. “The gatekeeping inquiry must be ‘tied to the facts’ of a particular ‘case.’ ” Kumho, 526 U.S. at 150, 119 S.Ct. 1167 (quoting Daubert, 509 U.S. at 591, 113 S.Ct. 2786). “Encompassed in the determination of whether expert testimony is relevant is whether it is helpful to the jury, which is the ‘central concern’ of Rule 702.” Mukhtar v. California State University, Hayward, 299 F.3d 1053, 1063 n. 7 (9th Cir.2002) (citation omitted). Federal Rule of Evidence 702 states that “[i]f scientific, technical, or other specialized knowledge will assist the trier of fact to understand the evidence or to determine a fact in issue,” an expert “may testify thereto,” Fed.R.Evid. 702. Burden of Proof. “It is the proponent of the expert who has the burden of proving admissibility.” Lust v. Merrell Dow Pharmaceuticals, Inc., 89 F.3d 594, 598 (9th Cir.1996). Admissibility of the expert’s proposed testimony must be established by a preponderance of the evidence. See Daubert, 509 U.S. at 592 n. 10, 113 S.Ct. 2786 (citing Bourjaily v. United States, 483 U.S. 171, 175-76, 107 S.Ct. 2775, 97 L.Ed.2d 144 (1987)). The party presenting the expert must demonstrate that the expert’s findings are based on sound principles and that they are capable of independent validation. Daubert II, 43 F.3d at 1316. Defendant’s Daubert motions do not challenge the credentials of plaintiffs’ experts (other than the treating physicians). All of the experts utilized in this case have impeccable curriculum vitaes, and many have extensive experience testifying as experts. Accordingly, the only Daubert issue to decide is whether Plaintiffs’ experts have employed a reliable methodology in reaching the conclusions they propose to offer to the jury at trial. B. Summary Judgment Summary judgment is not “a disfavored procedural shortcut but rather [it is] an integral part of the Federal Rules as a whole, which are designed ‘to secure the just, speedy, and inexpensive determination of every action.’ ” Celotex Corp. v. Catrett, 477 U.S. 317, 327, 106 S.Ct. 2548, 91 L.Ed.2d 265 (1986) (quoting Fed. R.Civ.P. 1). It is appropriate “if the pleadings, depositions, answers to interrogatories, and admissions on file, together with the affidavits, if any, show that there is no genuine issue as to any material fact and that the moving party is entitled to a judgment as a matter of law.” Fed. R.CivJP. 56(c). In evaluating a motion for summary judgment, the court views the evidence and draws all reasonable inferences therefrom in the light most favorable to the nonmoving party. United States v. Diebold, Inc., 369 U.S. 654, 655, 82 S.Ct. 993, 8 L.Ed.2d 176 (1962). The movant’s burden is “discharged by showing ... that there is an absence of evidence to support the nonmoving party’s case.” Celotex, 477 U.S. at 325, 106 S.Ct. 2548. Only after the movant meets its initial burden does any obligation on the part of the nonmovant arise. Id. at 323, 106 S.Ct. 2548. Nevertheless, once the movant has met this initial burden, the opposing party must present evidence establishing a material issue of fact. Id. at 325, 106 S.Ct. 2548. The nonmoving party must go “beyond the pleadings” and present evidence designating “specific facts showing that there is a genuine issue for trial.” Id. at 324, 106 S.Ct. 2548. An issue of fact is “material” if it is essential to the proper disposition of the claim. Anderson v. Liberty Lobby, Inc., 477 U.S. 242, 248, 106 S.Ct. 2505, 91 L.Ed.2d 202 (1986). In essence, the inquiry is “whether the evidence presents a sufficient disagreement to require submission to a jury or whether it is so one-sided that one party must prevail as a matter of law.” Id. Further, a jury question does not exist because of the presence of a mere scintilla of evidence; rather, there must be significant probative evidence tending to support the complaint and conflict in substantial evidence to create a jury question. Fazio v. City & County of San Francisco, 125 F.3d 1328, 1331 (9th Cir.1997). IV. ANALYSIS A. Causation Because the Defendant has not challenged the qualifications of Plaintiffs’ experts, the court focuses on the substance of Plaintiffs’ proffered expert testimony. In particular, whether the methodology by which the experts have reached their conclusions is reliable and whether those conclusions will assist the trier of fact in resolving an issue of fact in this case. In resolving this issue “we must look to the governing substantive standard ...” Daubert v. Merrell Dow Pharms., 43 F.3d 1311, 1320 (9th Cir.1995). Courts in toxic tort cases often separate the causation inquiry into general causation and specific causation. To survive summary judgment on their allegations, Plaintiffs must show (on a more probable than not basis) that Henricksen was exposed to a product that is capable of causing a particular condition he complains of in the general population (general causation), and that his exposure did in fact result in those injuries (specific causation). Jaros v. E.I. DuPont (In re Hanford Nuclear Reservation Litig.), 292 F.3d 1124, 1133 (9th Cir.2002). In Hanford, the Ninth Circuit explained that the general causation inquiry was “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. Plaintiffs argue this case is not one where general causation is an issue because there is no dispute that benzene is capable of causing the illness Henricksen suffers from, and gasoline contains benzene. Since these facts are undisputed, Plaintiffs argue this case becomes a question only of dose. According to Defendant, however, gasoline and benzene are not the same, and as a matter of science, the chemical composition and toxicity is different from pure benzene. These competing characterizations of the issue raise the first question the court will decide in its analysis: what is the product at issue here-benzene or gasoline that contains benzene? Is there a difference and, if so, is the difference meaningful in the Daubert context? Defendant calls this a gasoline case. Plaintiffs call this a benzene case and say any other characterization is a “red herring”, a “cheap parlor trick” and a “misdirection” of the Defendant. The framing of the issue defines the Plaintiffs’ burden, so it is important. This is a product’s liability action and Defendant’s product is gasoline. It is undisputed that Henricksen’s exposure was to the mixture gasoline, not simply to the substance benzene. Benzene and gasoline, as evidenced by the unrebutted testimony of Defendant’s expert, are not one in the same product. Ct. Rec. 104, Ex. E [Pyatt Aff.] at 14-18. Gasoline is a mixture of chemicals, which contains as a small component, benzene. There are scientific studies devoted to the study of benzene (and benzene exposure from gasoline vapors) and a whole body of scientific studies devoted to the study of gasoline. In fact the common approach to the evaluation of the gasoline exposures is to measure the individual toxic compounds, including benzene. Because gasoline exposure is a source of benzene exposure, evaluations of both gasoline and its toxic component benzene are obviously relevant to the Plaintiffs’ case. At the same time, the court can not simply presume that the qualitative toxic and carcinogenic effects of benzene from any source are the same. If it is possible to extrapolate from studies of benzene or other benzene-containing products conclusions regarding gasoline, then it will be incumbent upon Plaintiffs to explain and demonstrate why the extrapolation is scientifically proper. This is even more true given the vast difference in threshold limit values for these substances; studies in the record such as Glass , indicating that “exposure to benzene concentrate resulted in a higher risk of leukemia than exposure to the same amount of benzene encountered in a more dilute form such as in gasoline”; and Defendant’s unrebutted expert evidence that the toxicity of gasoline has been tested and is “categorically different than the toxicity observed following exposure to pure benzene.” Pyatt, at ¶ 11; Ct. Rec. 104, Ex M [Jamall, I. and Willhite, C., Is Benzene Exposure from Gasoline Carcinogenic, 10 J. Environ. Monit.176 (2008) ]. The general causation question before the court is whether exposure to the benzene-component of gasoline is capable of causing AML. Specific causation is defined simply as “whether exposure to an agent was responsible for a given individual’s disease.” Federal Judicial Center, Reference Manual on Scientific Evidence 396 (2d ed. 2000). In determining whether an alleged chemical exposure caused a particular disease or illness, an expert must establish the following criteria: (1) the toxic substance at issue must have been demonstrated to cause in humans the disease or illness suffered by the plaintiff; (2) the individual must have been exposed to a sufficient amount of the substance in question to elicit the health effect in question; (3) the chronological relationship between exposure and effect must be biologically plausible; and (4) the likelihood that the chemical caused the disease or illness in an individual should be considered in the context of other known causes. See David L. Eaton, Scientific Judgment and Toxic Torts-A Primer in Toxicology for Judges and Lawyers, 12 J.L. & Pol’y 5, 38-40 (2003) (“Eaton”). Several appellate courts have held that an expert who seeks to opine on specific causation must pay careful attention to the dose-response relationship (that is, the relationship in which a change in amount, intensity, or duration of exposure to a chemical is associated with a change in risk of disease) and the amount of exposure the plaintiff allegedly suffered. See, e.g., McClain v. Metabolife Int’l, Inc., 401 F.3d 1233, 1241-42 (11th Cir.2005); Mitchell v. Gencorp, Inc., 165 F.3d 778, 781 (10th Cir.1999) (“It is well-established that a plaintiff in a toxic tort case must prove that he or she was exposed to and injured by a harmful substance manufactured by the defendant.... In order to carry this burden, a plaintiff must demonstrate ‘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 or she may recover.’ ”) (citation omitted); Wintz By and Through Wintz v. Northrop Corp., 110 F.3d 508, 513 (7th Cir.1997); Wright v. Willamette Indus., Inc., 91 F.3d 1105, 1106 (8th Cir.1996); Allen v. Pa. Eng’g Corp., 102 F.3d 194, 199 (5th Cir.1996) (“Scientific 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.”). However, as Plaintiffs point out, it is not always necessary for a plaintiff to quantify exposure levels precisely or use the dose-response relationship, provided that whatever methods an expert uses to establish causation are generally accepted in the scientific community. While precise or exact information concerning dosage or the dose-response relationship is not always required, the boundaries of allowable expert testimony are not so wide as to permit an expert to testify as to specific causation without having any measurements of a plaintiffs’ exposure to the allegedly harmful substance. Hardyman v. Norfolk & Western Ry. Co., 243 F.3d 255, 264 (6th Cir.2001). Plaintiffs’ experts have drawn conclusions about both the capacity of benzene (and benzene in gasoline) and its particular effect in Henricksen’s case. Defendant has attempted to draw sharp lines between the general and specific causation inquiries, filing separate summary judgment motions on each. The court notes, however, that while the division between general and specific causation is frequently helpful, the core issue that the jury will have to address in the case is whether Henricksen’s exposure to gasoline was a substantial cause of his AML. In the end, the Daubert question comes down to whether Plaintiffs’ experts’ conclusions can validly assist the jury in deciding this question. Certainly, Defendant’s concession that its product contains a known carcinogen—benzene—does not excuse Plaintiffs from having to show the benzene contained in Defendant’s gasoline is capable of causing the illness at issue. The court must begin by examining each of the experts’ conclusions to determine if the method the expert has used to reach that conclusion is reliable. Then the court must examine those conclusions that are sufficiently reliable to be admissible and determine if, taken collectively, they form a sufficient causal chain to aid the trier of fact in reaching the ultimate conclusion on causation: whether Henricksen’s exposure to gasoline was a substantial factor in his development of AML. To prove their case on general and specific causation, the categories of evidence relied upon by the parties’ experts includes animal studies, differential diagnosis, and epidemiological studies. Differential diagnosis is the process of elimination that physicians routinely use to identify the “most likely” cause of a particular individual’s illness. It is an acceptable source of data on specific causation. Hall v. Baxter Healthcare Corp., 947 F.Supp. 1387, 1413 (D.Or.1996). By examining the patient’s symptoms, medical history, diagnostic test results, etc., a doctor can eliminate alternative causes and reach a conclusion about the most likely cause of a particular patient’s condition. It is important to note, however, that differential diagnosis cannot demonstrate general causation, because it assumes, without proving, that all of the potential causes considered are capable of causing the condition at issue. “Indeed differential diagnosis assumes that general causation has been proven for the list of possible causes it eliminates[.]” Id. As for epidemiological studies, “The field of epidemiology addresses the incidence, distribution and etiology (causation) of disease in human populations by comparing individuals exposed to a particular agent to unexposed individuals to determine whether exposure increases the risk of disease.” In re Silicone Gel Breast Implants Products Liab. Lit., 318 F.Supp.2d 879, 892 (C.D.Cal.2004). Scientists use “relative risk” to identify an association between, for example, the ingestion of a drug and a disease. For example, if a study found that 10 out of 1000 women with breast implants were diagnosed with breast cancer and 5 out of 1000 women without implants (the “control” group) were diagnosed with breast cancer the relative risk of implants is 2.0, or twice as great as the risk of breast cancer widiout implants. This is so because the proportion of women in the implant group with breast cancer is 0.1 (10/1000) and the proportion of women in the non-implant group with breast cancer is 0.05 (5/1000). And 0.1 divided by 0.05 is 2.0. Id. A relative risk of 1.0 suggests that there is no association between the product and the disease, that is, the same numbers of people using the product are diagnosed with the disease as those not using the product. Similarly, a relative risk of less than 1.0 suggests that the product is actually “protective” of the disease: fewer people using the product contract the disease than those not taking the product. Id. at n. 5. In general, epidemiology studies are probative of general causation: a relative risk greater than 1.0 means the product has the capacity to cause the disease. “Where the study properly accounts for potential confounding factors and concludes that exposure to the agent is what increases the probability of contracting the disease, the study has demonstrated general causation-that exposure to the agent is capable of causing [the illness at issue] in the general population.” Id. at 893 (internal quotation marks and citation omitted). In the Ninth Circuit, such studies can also be probative of specific causation, but only if the study shows the relative risk is greater than 2.0, that is, the product more than doubles the risk of getting the disease. Daubert v. Merrell Dow Pharms., Inc., 43 F.3d 1311, 1315 (9th Cir.), cert. denied 516 U.S. 869, 116 S.Ct. 189, 133 L.Ed.2d 126 (1995) (“Daubert II”). When the relative risk is 2.0, the alleged cause is responsible for an equal number of cases of the disease as all other background causes present in the control group. Thus, a relative risk of 2.0 implies a 50% probability that the agent at issue was responsible for a particular individual’s disease. This means that a relative risk that is greater than 2.0 permits the conclusion that the agent was more likely than not responsible for a particular individual’s disease. B. Treating Physicians Defendant has moved this court to prohibit Henricksen’s treating physicians from testifying on the subject of causation because they were not timely disclosed as experts on this subject and did not prepare expert reports. John Catón, M.D. was one of Henricksen’s treating physicians. He is board certified in hematology, internal medicine, and oncology. Although Mrs. Henricksen testified during her deposition that during a doctor visit Dr. Catón indicated Mr. Henricksen’s AML was likely related to his occupational exposure to benzene contained in gasoline, Dr. Catón was disclosed only as a fact witness. Plaintiffs indicated he would testify “as to all aspects of the care and treatment of Mr. Henricksen, including diagnosis, treatments, prognosis, and the nature and course of the disease and its affects on human physiology.” Ct. Rec. 44 [Plaintiffs’ Final Trial Witness List]. Plaintiffs separately listed other expert witnesses who would address causation. In early January, 2008, defense counsel inquired in emails whether the treating physicians would address causation. Plaintiffs counsel responded “I don’t know. I have not hired them as experts and so I assume that they will say what they will.” Ct. Rec. 70 (Weiss Deck), Ex. 2 [Jan. 4, 2008 email]. None of Caton’s chart notes contain an entry opining on causation. Dr. Catón did not prepare an expert report, which would have been due February 1, 2008. Eight days before the discovery cutoff, on April 24, 2008, Plaintiffs revealed in an email to defense counsel that Dr. Catón would address causation. Dr. Catón was not deposed until after the discovery cutoff. Immediately prior to his deposition, Plaintiffs’ lawyer gave Dr. Catón highlighted materials including an epidemiological article and a Conoco Material Safety Data Sheet (MSDS). Dr. Catón testified at his deposition that 1) common sense told him that Henricksen’s AML was probably the result of having been exposed to benzene in the gasoline he hauled for decades; 2) that he had read in medical textbooks, including “Haskell” (which he claimed to have brought with him to the deposition) about the connection between gasoline and AML; and 3) the cause of Henricksen’s disease played no role in Henricksen’s diagnosis, prognosis or treatment. Weiss Deck, Ex. 9 [Catón Depos.] at 176:7-10. Defense counsel had no advance notice of Caton’s reliance upon “Haskell” as a source. After the deposition defense counsel located the text Haskell and it was discovered that the page at the deposition was not in that text and Haskell’s chapter on AML makes no reference to gasoline. Plaintiffs claim that no one talked to Dr. Catón until the end of the discovery period, and for that reason, no one knew what his testimony would be. Plaintiffs admit they did not “track[ ] down” Dr. Catón to ask him whether he held an opinion as to what caused Henricksen’s AML until the end of the discovery period. Catón informed Plaintiffs’ counsel at that time that it was caused by work around the benzene in the gasoline fumes, and that he had formed that opinion at the time of his diagnosis. Plaintiffs argue Dr. Catón is not subject to the reporting requirements of Fed. R.Civ.P. 26(a)(2)(B) because he isn’t considered a “retained expert” because he’s a treating physician, and causation is part of the ordinary care of a patient (and an observation Catón made at the time of his care). Courts generally allow expert testimony by treating physicians without need for a report, provided that the opinions do not extend beyond treatment. See Fielden v. CSX Transp. Inc., 482 F.3d 866, 870-71 (6th Cir.2007) (holding that a formal report is not required when determining causation is an integral part of treating a patient); see also Watson v. United States, 485 F.3d 1100, 1107 (10th Cir.2007). Nevertheless, even if a party elects to call a physician to testify solely to the treatment, the party must still, consistent with the court’s scheduling order, disclose that person as someone he or she intends to call as an expert. See Musser v. Gentiva Health Services, 356 F.3d 751, 757-58 (7th Cir.2004). “Disclosing a person as a witness and disclosing a person as an expert witness are two distinct acts.” Id. The court held that “[f]ormal disclosure of experts is not pointless. Knowing the identify of the opponent’s expert witnesses allows a party to properly prepare for trial. [The defendant] should not be made to assume that each witness disclosed by the [plaintiffs] could be an expert witness at trial.” Id. Dr. Caton’s opinion on causation in this case is a type of expert testimony which “results from a process of reasoning which can be mastered only by specialists in the field.” Fed.R.Evid. 701, advisory committee’s note, 2000 Amendments. Accordingly, Plaintiffs were required to have disclosed Catón as an expert witness under Rule 26(a)(2)(A). Rule 37(c)(1) “gives teeth to [this] requirement ],” Yeti by Molly, Ltd. v. Deckers Outdoor Corp., 259 F.3d 1101, 1106 (9th Cir.2001), by prescribing: “If a party fails to provide information or identify a witness as required by Rule 26(a) ... the party is not allowed to use that ... witness to supply evidence ... at a trial, unless the failure was substantially justified or is harmless.” Fed.R.Civ.P. 37(c) (1). The Advisory Committee Notes to the 1980 Amendment to Rule 37 state that this is an “automatic,” “self-executing sanction.” “[T]he burden is on the party facing sanctions to prove harmlessness.” Yeti by Molly, 259 F.3d at 1106. The Ninth Circuit analyzed this harmless element in Yeti by Molly “by looking at whether the failure to disclose the information prejudiced the opposing party.” Galentine v. Holland Am. Line-Westours, Inc., 333 F.Supp.2d 991, 993 (W.D.Wash.2004). The need to indicate any treating physician that may be called as an expert is necessary for the defense to adequately prepare, and the Defendant will not be made to assume that such witnesses could be experts. See Musser, supra. Plaintiffs have not sustained their burden of showing Defendant would not be harmed if the late disclosure is allowed. Allowing Dr. Catón to be disclosed as an expert witness at this stage — well beyond the discovery cutoff— of the proceeding is not harmless. For the reasons stated, Defendant’s Motion to Exclude Dr. Caton’s Proposed Causation Testimony (Ct. Rec. 67) is GRANTED. This ruling renders Defendant’s Daubert motion to exclude Dr. Caton’s opinions (Ct. Rec. 127) MOOT. However, even if the court were to disregard the disclosure violation, Dr. Caton’s general and specific causation testimony would be subject to exclusion under Daubert, because his opinion lacks any reliable support. Dr. Catón himself admits that he is not rendering a “scientific opinion” and that he did not consult any literature before opining that AML can be caused by gasoline exposure and that Henricksen’s AML most likely resulted from his occupational exposure. In addition to Dr. Catón, Henricksen was treated by Drs. Nichols, Georges, and Kominsky. The same reasons as justify the exclusion of Dr. Caton’s causation opinion, would justify prohibiting these physicians from offering expert testimony. They were not disclosed by Plaintiffs as expert witnesses on any subject and Defendant would be materially prejudiced at this point, should Plaintiffs attempt to solicit expert testimony from them at trial. Defendant’s motion to exclude any such testimony is unopposed as no response was filed by Plaintiffs. Accordingly, Defendant’s Motion in Limine to Limit the Testimony of Plaintiffs’ Treating Physicians (Ct. Rec. 71) is GRANTED. C. Frank Gardner Frank Gardner is a medical doctor from Galveston, Texas retained by the Plaintiffs for a causation opinion (both general and specific). Gardner rendered his report on November 7, 2007 wherein he opines Henricksen’s “prolonged exposure to benzene in gasoline, initiated mutagenic changes in the bone marrow leading to his leukemia.” Ct. Rec. 148 [Gardner Deck], Ex. A. Gardner’s methodology in reaching this conclusion is as Defendant describes: Henricksen has AML; Henricksen worked as a tanker truck driver loading and unloading gasoline; gasoline contains benzene; therefore Henricksen’s AML was caused by exposure to gasoline. Gardner admits that gasoline is not identified by any regulatory body as a human carcinogen. Plaintiffs admit that Gardner did not have a specific dose calculation before reaching his opinion and that he relied upon the “universal knowledge that gasoline contains benzene and benzene causes AML at very low doses.” Ct. Rec. 146 at 70. Defendant asserts Rule 702 bars Dr. Gardner’s testimony because his methodology for reaching his conclusions is flawed. Specifically, Defendant points out that (1) Gardner admits gasoline is not identified as a carcinogen; (2) Gardner fails to cite to any epidemiological study (or objective source) demonstrating that gasoline causes AML, he merely asserts his personal opinion; (3) Gardner fails to consider any other possible causes of Henricksen’s disease; (4) Gardner has no evidence of the dose of gasoline or benzene to which Henricksen was allegedly exposed and he did not attempt to ascertain actual exposure to either gasoline or benzene (Gardner Deposition at 59:17-20; 59:23-60; 49:5-9); and (5) Gardner relies upon incomplete or erroneous underlying facts including incorrectly assuming Henricksen’s job duties involved loading 90% gasoline, that he stood above the hatch and sometimes on the ground while loading his truck, and that he kept his truck running while unloading it. The Ninth Circuit requires general causation opinions to be supported by reliable epidemiological studies or if there are none, a reliable differential diagnosis through which, to a reasonable degree of medical certainty, all other possible causes of the victims’ condition can be eliminated, leaving only the toxic substance as the cause. Gardner’s opinion that exposure to benzene as a component of gasoline can cause AML is not supported by reliable studies and is instead based upon assumptions. In fact, Gardner testified in his deposition that he did not find it important or relevant to support his opinion by studies. Ct. Rec. 78, Ex. A (Gardner at 87:24-88:2). Gardner’s inability to point to any source which reliably supports his conclusion, renders his opinion merely personal opinion. The scientific record does not reflect that there is “universal” knowledge that benzene causes AML at very low doses, as Gardner concludes. Because of this lack of scientific support, the court can not conclude Gardner’s opinion is based upon scientifically valid principles, and therefore under Daubert, his general causation conclusion must be excluded. Gardener’s specific causation opinion also has severe problems. Though proof of Henricksen’s benzene exposure through specific quantitative measurement is not a requirement, exposure at some level must be shown before a link between benzene exposure and AML could be drawn. All of the experts in this case agree benzene-induced diseases are dose dependent, and Gardner testified in his deposition that duration and frequency of exposure are important factors to consider. Yet, in his report, Gardner did not attempt to quantify dose or even estimate Henricksen’s level of exposure to benzene. Implicitly, Gardner’s opinion presumes that exposure to benzene in gasoline can cause AML in any dose and that Henricksen’s exposure was sufficient. Gardner’s opinion is undermined by his failure to analyze or evaluate (his own or any other expert’s) information pertaining to dose or the actual level of Henricksen’s exposure. This renders his opinion on specific causation inherently unreliable. The court notes the shortcomings of Gardner’s testimony in this case are similar to those identified by the Castellow court in a case very similar to this one, in which Gardner’s opinion was excluded, Castellow v. Chevron USA, 97 F.Supp.2d 780, 795 (S.D.Tex.2000). Likewise, in order to result in an admissible conclusion, Gardner’s analysis should “reliably rule out reasonable alternative causes of [the alleged harm] or idiopathic causes.” Soldo v. Sandoz Pharmaceuticals Corp., 244 F.Supp.2d 434, 567 (W.D.Pa.2003). Admissible expert testimony need not rule out all alternative causes, but “where a defendant points to a plausible alternative cause and the doctor offers no explanation for why he or she has concluded that it was not the sole cause, that doctor’s methodology is unreliable.” Heller v. Shaw Indus., Inc., 167 F.3d 146, 156 (3d Cir.1999) (quoting In re Paoli Railroad Yard PCB Litig., 35 F.3d 717, 759 n. 27 (3d Cir.1994).) Here, Gardner (and all of Plaintiffs experts, for that matter) fail to exclude-much less address in their reports-the likelihood that Henricksen’s AML had no known cause. The affidavits of Pyatt and Natelson are unrebutted as to the fact that 80-90% of all cases of AML are idiopathic, having no known cause. Faced with similar situations, other courts have excluded experts’ differential diagnoses where they failed to adequately account for the likelihood that the disease was caused by an unknown factor. Doe v. Ortho-Clinical Diagnostics, Inc., 440 F.Supp.2d 465, 478 (M.D.N.C.2006), for example, excluded the testimony of plaintiffs’ expert because “he did not properly perform the differential diagnosis given his failure to consider within his analysis the high probability that an unknown genetic cause cannot be ruled out as the specific cause of Minor Child Doe’s autism.” Similarly, in Whiting v. Boston Edison Co., 891 F.Supp. 12 (D.Mass.1995), the court excluded expert testimony that radiation was the cause of plaintiffs acute lymphocytic leukemia. The court reasoned that “[d]ifferential diagnosis, as the technique is used in the medical profession, consists of the comparison of a patient’s symptoms to symptoms associated with a known set of diseases. The idea is to find the disease that matches the symptoms. If 90 percent of the causes of a disease are unknown, it is impossible to eliminate an unknown disease as the efficient cause of a patient’s illness.” Id. at 21 n. 41. It seems the only reason cited for distinguishing Henricksen’s disease from one of “no known cause” was the existence of a known risk factor, namely exposure to benzene. Standing alone, the presence of a known risk factor is not a sufficient basis for ruling out idiopathic origin in a particular case, particularly where most cases of the disease have no known cause. This is not to say that where most diagnoses of a disease are idiopathic it is impossible to prove specific causation. But in those cases, analysis beyond a differential diagnosis is required. Gardner could have compared the presentation of Henricksen’s symptoms with those in chemically induced AML cases. However, in this case, perhaps they didn’t because doing so would not have served Plaintiffs’ purposes. Henricksen’s presentation is very different from the typical case of chemically induced AML. None of the features characteristic or commonly seen in secondary AML have been associated with Henricksen’s case. Thus in addition to the reasons cited above, because Gardner’s methodology employed fails to adequately account for the possibility that Henricksen’s AML was idiopathic, the court finds that his conclusion that prolonged exposure to benzene in gasoline was the cause of his AML is unreliable and therefore inadmissible. D. William Sawyer 1. Disclosure Defendant has moved to strike the testimony of William Sawyer arguing Plaintiffs violated the rules of discovery in making his disclosure. William Sawyer was disclosed by Plaintiffs as a toxicology expert who would testify to the “toxic effects of benzene and gasoline, the mechanisms of injury, the medical literature, and general and specific causation in this case.” Ct. Rec. 44 [Final Witness List filed 12/14/2008]. On the same disclosure, Plaintiffs identified Marco Kaltofen as an expert on dose, because this was the specific area on which he would opine. On February 1, 2008, Plaintiffs disclosed Sawyer’s expert report in which he expressed opinions regarding dose. Sawyer was not deposed until March 13, 2008, at which time he was extensively questioned about his dose calculations. On April 21, 2008, eleven days before the discovery cutoff, Plaintiffs served a supplemental disclosure regarding Sawyer indicating they would have Sawyer testify to everything stated in his report and at his deposition. Defendant’s motion to strike argues that Sawyer’s disclosure as a dose expert was untimely and that fairness and judicial economy justify striking his dose opinion based upon its late disclosure. Defendant contends that it selected just one expert on dose, relying upon the presumption that Plaintiffs also only had one expert on dose. Defendant’s also contend Sawyer’s dose testimony is cumulative because Plaintiffs already have a dose expert — Kaltofen. The court finds that the Defendant should not have been “surprised” that any testimony related to toxicology could include opinions on dose, nor is it unusual to have two experts on dose. Plaintiffs timely disclosed Sawyer as an expert on both specific and general causation. Defendant was not prejudiced because it had already retained a dose expert who had time to review Sawyer’s initial disclosure relating to dose in preparing his expert report. Moreover, Sawyer was deposed prior to the deposition of their dose expert. Accordingly, Defendant’s Motion to Strike Dose Opinions of Sawyer due to Disclosure Violations (Ct. Rec. 79) is DENIED. 2. Daubert Defendant also moves the court to exclude the opinions of Williams Sawyer and preclude others from relying on his opinions, based upon Daubert. The court finds in Defendant’s favor that Plaintiffs have not demonstrated that Sawyer’s testimony is the product of reliable principles and methods, and that he has applied the principles and methods reliably to the facts of the case. At each step of his analysis, Sawyer bases his analysis upon speculation and/or erroneous data, and without adequate explanation, these steps render his methodology unreliable and misleading, and his opinions are therefore inadmissible. Sawyer’s opinion is that Henricksen was exposed to “dangerously high levels” of benzene which primarily contributed to his development of AML. Ct. Rec. 151, Ex. A. In essence, Sawyer’s methodology to calculate Henricksen’s dose was as follows. First, Sawyer estimated the amount of benzene Henricksen was likely exposed to on a daily basis. To do this he relied upon the .baseline benzene exposure value reached in a study (Kawai ) of 10 Japanese truck drivers, under unknown conditions, during a 14-minute loading activity. The calculation from the Japanese study he reli