Plaintiff Donna Cashiola, individually and as a representative of the estate of Donald Page, and Plaintiffs Vivian Page and Randy Page, individually, (“Plaintiffs”) file this response to Defendant Exxon’s (“Defendant”) Motion to Strike Plaintiffs’ Expert Testimony on Causation, and would respectfully show the Court as follows:

Table Of Contents

Factual Background

In this toxic tort case, Plaintiffs have brought claims arising out of the death of Donald Page as a result of his occupational exposure to benzene at Defendant’s Exxon Baytown facility. In his positions at Exxon from the 1950’s to the 1980’s, Mr. Page was exposed to benzene through his skin and through inhalation while maintaining and repairing equipment, cleaning tools with solvents, collecting chemical samples, and cleaning up spills. Based on the particular occupational activities that repeatedly brought Mr. Page into contact with benzene, Plaintiffs’ expert industrial hygienist, Stephen Petty, calculated that Mr. Page’s combined dermal and inhalation exposure to benzene was 55 parts per million years (“ppm-years”) over the course of his career. See Petty Report, September 8, 2006, 31, Table 12, attached to Defendant’s Motion as Exhibit G.

In 2003, Mr. Page was diagnosed with acute myelogenous leukemia (AML) and he died two months later. Based on Mr. Page’s cumulative exposure to benzene, and the well-documented association between AML and benzene exposure in the epidemiological literature, Plaintiffs’ expert epidemiologist Dr. Peter Infante, and expert oncologist Dr. Frank Gardner, have both concluded that exposure to benzene was a cause of Mr. Page’s AML. As Dr. Infante explained, “[m]y specific causation opinion is that Mr. Page’s exposure to benzene while he was employed at the Exxon Baytown facility was a substantial contributing factor to his development of AML.” Deposition of Dr. Peter Infante, September 13, 2006, 223, excerpts attached as Exhibit 1. Dr. Gardner has also concluded that “it was the [benzene-containing] solvents in the coal slurries” that Mr. Page worked with at Exxon that caused him to get his disease. See Deposition of Frank Herbert Gardner, M.D., September 25, 2006, 105, 150, excerpts attached as Exhibit 2. Although Defendant now challenges those opinions as unreliable, Plaintiffs will show that Dr. Infante’s and Dr. Gardner’s opinions on general and specific causation meet the Havner and Robinson criteria for reliability and admissibility.

It is Universally Accepted in the Scientific Community that Benzene Exposure is a Cause of AML.

The question of “general causation” involves whether “a substance is capable of causing a particular injury or condition in the general population.” Merrell Dow Pharm., Inc. v. Havner, 953 S.W.2d 706, 714 (Tex. 1997). Exxon seeks to create confusion on this point by suggesting that benzene is not linked to leukemia. In fact, it is undisputed among serious scientists that benzene causes AML in human beings. See, e.g., Andrews & Snyder, Toxic Effects of Solvents and Vapors, in Casarett and Doull’s Toxicology 681, 685 (Mary O. Amdur et al. eds. 4th ed. 1991), attached as Exhibit 3; Aksoy, Malignancies Due to Occupational Exposure to Benzene, Am. J. Indus. Med. 7:395-402 (1985), attached as Exhibit 4, (“There is no doubt about the leukemogenic effect of benzene in man.”). As the Occupational Health and Safety Administration (OSHA) has concluded, “OSHA believes that [epidemiological] studies clearly demonstrate an association between benzene exposure and increased risk of leukemia. The Agency does not believe this conclusion is now seriously challenged.” OSHA Rule on Occupational Exposure to Benzene, 52 Fed. Reg. 34460, 34497 (September 11, 1987), excerpts attached as Exhibit 5. Moreover, in Mobil Oil Corp. v. Ellender, 968 S.W.2d 917 (Tex. 1998), the Supreme Court of Texas observed that the causal relationship between benzene exposure and leukemia had been established for more than half a century. See id. at 922.

Plaintiffs’ Experts’ Specific Causation Opinions Are Supported by A Body of Published Epidemiological Literature.

Statistically significant epidemiological studies have found that AML is caused by benzene exposure at or below 55 ppm-years.

According to Havner, the foundational data underlying an expert’s opinion must be reliable in order for the expert’s opinion to be reliable and admissible. See 953 S.W.2d at 714. Epidemiological studies are considered reliable evidence of causation if the results show at least a doubling of the risk of disease in the population exposed to the chemical at issue when compared to the unexposed population. See id. at 717. There is a doubling of the risk if the relative risk is greater than 2.0.[1] See id. at 721. For the relative risk of at least 2.0 to be considered “statistically significant,” the confidence interval (CI) should not include 1.0. See id. at 723.

Plaintiffs’ causation experts have relied on epidemiological studies that meet the Havner criteria of a doubling of the risk and statistical significance. These epidemiological studies provide evidence of a statistically significant greater than twofold risk of AML resulting from benzene exposure even less than the minimal exposure estimate of 55 ppm-years for Mr. Page. As a whole, four separate studies show that cumulative benzene exposure ranging from 2 ppm-years to 38.5 ppm-years results in statistically significant elevated risks of AML. See Ami S. Patel et al., Risk of Cancer as a Result of Community Exposure to Gasoline Vapors, 59(10) Arch. Env. Health 497, 501 (2004), attached as Exhibit 6; Tranguch Cancer Incidence Study; Updated Through 2002, Bureau of Epidemiology, Pennsylvania Dept. of Health, December 2003, at 5, attached as Exhibit 7; Deborah C. Glass et al., Leukemia Risk Associated With Low-Level Benzene Exposure, 14(5) Epidem. 569 (2003), attached as Exhibit 8; Pascal Guenel et al., Leukemia in Relation to Occupational Exposures to Benzene and Other Agents: A Case-Control Study Nested in a Cohort of Gas and Electricity Utility Workers, 42 Am. J. Indus. Med. 87 (2002), attached as Exhibit 9; G.G. Bond et al., An Update of Mortality Among Chemical Workers Exposed to Benzene, 43 British J. Indus. Med. 685, 690 (1986), attached as Exhibit 10. The risk of AML increased by at least fourfold in each of those studies. In addition, the Hayes study provides evidence that cumulative benzene exposure ranging from 40-99 ppm-years is equated with a relative risk of AML of 4.3 (CI 1.1 – 16.0). See Richard B. Hayes et al., Benzene and Dose-Related Incidence of Hematologic Neoplasms in China, 89 Journal of the National Cancer Institute 14 (1997), attached as Exhibit 11.

One of the studies relied on by Plaintiffs’ experts was published by G.G. Bond, et al., in 1986. See Bond et al., supra (Exhibit 10). That study “provides direct evidence of leukemia as a result of low-level benzene exposure.” Peter Infante, Benzene and Leukemia: The 0.1 ppm ACGIH Proposed Threshold Limit Value for Benzene, 7(4) Appl. Occup. Env. Hyg. 253, 257 (1992), attached as Exhibit 12. The Bond study found “a significant excess of mortality from myelogenous leukemia.” Bond et al., supra,at 690 (Exhibit 10). The average cumulative benzene exposure received by the cohort was only 38.5 ppm-years and the relative risk for AML was 4.44 (p=0.011). See Infante, supra, at 257 (Exhibit 12). Furthermore, of the five individuals with AML in that study, all but one had cumulative exposure below 55 ppm-years. See Bond et al., supra, at 688, Table 5 (Exhibit 10); Infante, supra, at 257, Table III (Exhibit 12). Case 1 had 54 ppm-years, case 2 had 1.5 ppm-years, case 3 had 25.4 ppm-years, and case 5 had 28.0 ppm-years. See Infante, supra, at 257, Table III. This finding is consistent with that in the Glass study, where the authors concluded that “[n]o evidence was found of a threshold [benzene] cumulative exposure below which there was no risk [of leukemia].” Glass et al., supra, at 569 (Exhibit 8).

The Bond study, and the other relevant studies, are presented below:

StudyBenzene Exposure Level in cumulative ppm-yearsStatistical Significance for AML[2]
Bond (Exhibit 10) 38.5 ppm-years RR[3] of 4.44 (CI 1.2 – 11.3).
Patel (Exhibit 6); Tranguch Cancer Incidence Study (Exhibit 7) Maximum 2 ppm-years; average .03 ppm-years Risk ratio[4] of 5.56 for AML and 4.4 (CI 1.09 – 10.24) for all leukemia.
Glass (Exhibit 8 ) Greater than 8 ppm-years Odds ratio[5] of 7.17 (CI 1.27 – 40.4).
Guenel (Exhibit 9) 16.8 ppm-years or greater Odds ratio of 4.6 (CI 1.2 – 17.4) for acute leukemias.
Hayes (Exhibit 11) 40-99 ppm-years RR of 4.3 (CI 1.1 – 16.0) for AML alone and RR of 6.0 (CI 1.8 – 20.6) for AML/MDS.

In addition to the epidemiological studies demonstrating significant associations between AML and cumulative benzene exposure at or below 40 ppm-years, there are a number of studies which demonstrate that benzene exposure levels of only 1 ppm cause toxic effects on blood cells. According to a 2004 study that looked at 250 workers exposed to benzene, “white blood cell and platelet counts were significantly lower than in 140 controls, even for exposure below 1 ppm in air.” Qing Lan et al., Hematotoxicity in Workers Exposed to Low Levels of Benzene, 306 Science 1774, 1774 (2004), attached as Exhibit 13. The authors concluded that their data “provide evidence that benzene causes hematologic effects at or below 1 ppm, particularly among susceptible subpopulations.” Id. at 1776. Another study similarly found that white blood cells and red blood cells were significantly lower in workers exposed to benzene at or below .5 ppm compared with an unexposed group, leading the authors to conclude that “chronic exposure to benzene at low ppm levels for prolonged periods may result in hematological suppression in humans.” Qingshan Qu et al., Hematological Changes Among Chinese Workers With a Broad Range of Benzene Exposures, 42 Am. J. Indus. Med. 275, 282 (2002), attached as Exhibit 14; see also Elizabeth Ward et al., Risk of Low Red or White Blood Cell Count Related to Estimated Benzene Exposure in A Rubberworker Cohort (1940-1975), 29 Am. J. Indus. Med. 247, 247 (1996), attached as Exhibit 15, (concluding that “there was no evidence for a threshold for the hematologic effects of benzene exposure, suggesting that even exposure to relatively low levels of benzene (e.g., <5 ppm) may result in hematologic suppression”). These studies demonstrate that even extremely low levels of benzene can cause toxicity to blood cells that proliferate when individuals develop leukemia.

Defendant has selectively quoted numbers from the EPA’s benzene risk assessment to present a distorted view to this Court of the benzene dose required for development of AML. Defendant has plucked the 90 ppm-year figure from the EPA report with no context or explanation. See Carcinogenic Effects of Benzene: An Update, U.S. EPA, (“EPA Report”) attached to Defendant’s Motion as Exhibit H. However, this same EPA report concludes, based on the shape of the dose-response curve, that the “Agency is fairly confident that exposure to benzene increases the risk of leukemia at the level of 40 ppm-years of cumulative exposure.” See EPA Report at 39 (Exhibit H to Defendant’s Motion).

Moreover, a deeper look at EPA’s data reveals that there is a doubling of the leukemia risk at a cumulative exposure much, much lower than 90 ppm-years. The EPA Report endorses a linear model in which the inhalation risk at 1 ppm ranges from 7.1 x 10-3 to 2.5 x 10-2. See id. at ii, 34. In other words, at 1ppm we will see leukemia deaths ranging from an extra 7.1 per 1,000 to 25 per 1,000. In addition, according to the EPA 1998 benzene risk assessment, a lifetime benzene exposure level is 76 ppm-years (1ppm year over an average life expectancy of 76 years). See id. at 32. It is possible to calculate the cumulative dose required for a twofold risk of leukemia using EPA’s own linear numbers of excess leukemia deaths of between 7.1 and 25.0 per 1,000 persons at a cumulative benzene dose of 76 ppm-years. Using EPA’s own numbers, a cumulative lifetime benzene dose of 21.6 ppm-years would double the risk of developing leukemia.[6]

OSHA has similarly assessed the risk of leukemia in relation to cumulative benzene exposure. Data from this risk assessment indicate a greater than twofold risk of leukemia from less cumulative benzene exposure than Mr. Page’s. OSHA went through an extremely thorough rulemaking process before issuing the current occupational benzene exposure limit of 1 ppm on an eight-hour time-weighted average. See OSHA Benzene Rule, 52 Fed. Reg. at 34460 (Exhibit 5). In establishing the 1 ppm limit, OSHA was convinced by the epidemiological literature of “a leukemogenic risk from low level benzene exposure.” Id. at 34474. OSHA’s quantitative risk assessment for benzene shows an extra 10 leukemia deaths per 1,000 workers at a cumulative benzene exposure level of 45 ppm-years. See id. at 34497. This results in a relative risk of 2.43 (CI 1.41 – 3.89)[7]. These numbers can also be used to calculate a twofold risk of leukemia at a cumulative exposure level of 37 ppm-years.[8]

Despite Defendant’s attempt to convince this Court otherwise, it is unquestionable that the epidemiological literature, as well as the benzene risk assessments of EPA (1998) and OSHA (1987), support Plaintiffs’ experts’ opinions that a twofold risk of AML is associated with benzene exposures at or below a cumulative dose amount of 45 ppm-years. Mr. Page’s cumulative exposure of 55 ppm-years therefore exceeds an amount of benzene exposure demonstrated in the literature to be associated with a greater than twofold risk for the development of AML.

Statistically significant epidemiological studies demonstrate latency periods for AML similar to the latency experienced by Mr. Page.

With regard to the latency issue, Defendants have both the facts and the epidemiology wrong. First, Plaintiffs dispute that there was a 56-year latency period between Mr. Page’s exposure to benzene and his benzene-related disease. Contrary to Defendant’s assertion that Mr. Page was initially exposed to benzene in 1947, Plaintiffs do not claim that Mr. Page had any benzene exposure prior to 1951.[9] In fact, the benzene exposure calculations performed by Plaintiffs’ industrial hygienist, Stephen Petty, begin with the dates 1951-55. See Petty Report, 31, Table 12 (Exhibit G to Defendant’s Motion).

In addition, although Mr. Page was diagnosed with AML in 2003, prior to that Mr.

Page’s doctors diagnosed him in 2000 with a condition called thrombocytopenia. See Gardner Depo. at 42 (Exhibit 2). Thrombocytopenia is a blood abnormality marked by a low platelet count. See id. at 149. Thrombocytopenia is known to be caused by benzene exposure. See id. at 37-38, 53; Infante Depo at 106 (Exhibit 1). In the opinion of Plaintiffs’ experts, Mr. Page’s thrombocytopenia was likely caused by his occupational exposure to benzene. See Gardner Depo. at 53 (Exhibit 2); Infante Depo. at 107 (Exhibit 1).

Thrombocyotopenia is also significant because it is a symptom of myelodysplasia (MDS). See Gardner Depo. at 37-38 (Exhibit 2). MDS is part of the same disease process as AML and is recognized as a precursor to AML. See Infante Depo. at 194-95 (Exhibit 1). Indeed, Mr. Page had myelodysplasia before he developed AML. See Gardner Depo. at 41 (Exhibit 2). The similarity and connection between MDS and AML therefore make the epidemiological literature on MDS extremely relevant when considering benzene exposure and AML.

When the correct facts are considered, Mr. Page had a maximum latency period of 49 years. This period is calculated from his 1951 initial exposure date to his diagnosis of thrombocytopenia in 2000. However, it is likely that Mr. Page’s actual latency period was considerably shorter than 49 years because he probably had thrombocytopenia for months or years before his diagnosis. Plaintiffs’ expert Dr. Gardner thinks that the latency period should be cut off before Mr. Page’s 2000 thrombocytopenia diagnosis because, as he testified,

[W]e don’t have any data . . . there’s no measurements [prior to 2000] . . . [M]ost people, by the time you diagnose myelodysplasia, we have no measurement as to the exact time that initiated. So, I presume he had it for a number of years before then. Most patients do, if they don’t have a lot of abnormalities of the chromosomes, it’s a somewhat slower pattern. So, I don’t know when it started.

Gardner Depo at 54 (Exhibit 2). Given Dr. Gardner’s expert medical opinion that Mr. Page probably had thrombocytopenia and myelodysplasia for a number of years before his 2000 diagnosis, it is reasonable to conclude that his latency period was closer to a range of 45-49 years.

Contrary to Defendant’s claims, the epidemiological literature identifies latency periods comparable to Mr. Page’s. A review of the relevant literature demonstrates a number of cases involving latency periods in the 40-50 year range and involving subjects who, like Mr. Page, died after the age of 70 (Mr. Page died at age 78).

StudyLatency Periods Greater than 40 Years
1992 Letter to OSHA and NIOSH from C.E. Ross, Medical Director of Shell, regarding the Final Report of Wood River Manufacturing Complex Epidemiology Study, “A Follow-Up Study of Mortality and Cancer Incidence Among Workers at the Wood River Manufacturing Complex,” by Drs. Delzell, Cole and Honda, at 3, attached as Exhibit 17. The Wood River study found a sixfold risk of the disorders myelofibrosis and myelodysplasia among retirees at least 70 years old that started working at Shell’s Wood River petrochemical plant in or before 1945. Since blue collar workers normally begin their work in their twenties, it is likely that there was at least a 40-year latency period among Shell’s petrochemical workers who developed blood disorders that are part of the same disease process as AML.
1983 Letters to OSHA and NIOSH from Shell regarding leukemia and benzene exposure, attachments III and IV, attached as Exhibit 18. This Shell study found a statistically significant fourfold risk of AML from benzene exposure. See Letter at 2, 4. The lists of the mortality cases at Shell’s Wood River and Shell’s Deer Park petrochemical refineries demonstrates at least 5 instances of latency periods greater than 40 years for individuals that died of AML or AML subtypes (myeloid leukemias):

Wood River (Attachment III)

– Case No. 4: 46-year latency

– Case No. 5: 41-year latency

– Case No. 7: 54-year latency

Deer Park (Attachment IV)

– Case No. 5: 44-year latency

– Case No. 8: 45-year latency

Sally R. Cowles et al., Medical Surveillance for Leukemia at a Petrochemical Manufacturing Complex: Four-Year Summary, 33 J. Occup. Med. 808, Tables 4 & 5 (1991), attached as Exhibit 19. There was a statistically significant risk of 4.6 (CI 1.26 – 11.77) for MDS among petrochemical workers at one Shell facility, including two individuals who were diagnosed after the age of 80 and one who was diagnosed at age 68.
Yasushi Honda et al., An Updated Study of Mortality among Workers at a Petroleum Manufacturing Plant, 37 J. Occup. Env. Med. 194, 197 (1995), attached as Exhibit 20. This study found that all workers who died of MDS started working in or before 1945 and died in the 1980s, giving them latency periods of at least 40 years.
S.N. Yin, et al., A Retrospective Cohort Study of Leukemia and Other Cancers in Benzene Workers, 82 Env. Health Persp. 207, 211 – Table 5 (1989), attached as Exhibit 21. This study found a significantly elevated standardized mortality ratio of 5.74 for leukemia among male benzene-exposed workers in China, including one case involving a latency period of approximately 50 years (case no. 5 in Table 5).

While most of Plaintiffs’ latency studies are published, Defendant tries to discount the importance of the Shell studies because they do not appear in a peer-reviewed journal. However, the context in which the data in these studies was collected and presented gives them significant indicia of reliability. The Shell studies are conducted by the petrochemical industry itself, which is presumably most familiar with its employees and its operations and which would likely be conservative in studying benzene-induced diseases among its workers. Moreover, Shell presented this information to a federal regulatory agency, OSHA, in the context of OSHA’s rulemaking to develop a benzene standard. The epidemiological data submitted by Shell was reviewed by the national experts at both OSHA and the National Institute for Occupational Safety and Health (NIOSH). Havner instructs that publication is only one factor to be considered in evaluating the reliability of expert studies and that publication is not a prerequisite for scientific reliability. See 953 S.W.2d at 714, 727. The epidemiological data that Shell reported to OSHA and NIOSH is certainly reliable in other important ways.

As the above epidemiological information indicates, Mr. Page’s latency period of up to 49 years is consistent with the experience of other benzene-exposed workers according to Shell’s internal data as well as a number of published studies. While a 49-year latency period is at the top of the latency range for benzene-induced AML, it is certainly not remarkable or unexpected. The latency period is not a fixed interval, but “will of course vary, depending on the nature of the exposure and disease, as well as on individual responses to exposure.” See Harvey Checkoway, Neil E. Pearce, & Douglas J. Crawford-Brown, Research Methods in Occupational Epidemiology 152 (1989). Mr. Page’s latency period is within the range established by relevant and published epidemiological literature, which supports Plaintiffs’ experts’ opinions that Mr. Page’s AML was caused by his exposure to benzene at Exxon’s oil refinery.

Plaintiffs’ Experts’ Causation Opinions Are Reliable.

There can be no serious question that the testimony of Plaintiffs’ causation experts is reliable under Rule 702 pursuant to the factors set forth in the Robinson case.[10] See E.I. du Pont de Nemours & Co. v. Robinson, 923 S.W.2d 549, 557 (Tex. 1995). The Robinson factors are used to determine “whether the underlying theories and techniques of the proffered evidence are scientifically reliable,” and therefore admissible under Rule 702. Id. Plaintiffs’ experts’ use of epidemiology to reach their causation opinions has long been recognized by Texas law as an acceptable and reliable methodology. As the Texas Supreme Court held in Havner, in toxic tort cases epidemiological studies meeting certain criteria can be offered as part of the evidence supporting general and specific causation. See Havner, 953 S.W.2d at 717. Epidemiological evidence is so important in toxic tort cases because direct human experimentation cannot ethically be done regarding the causal links between particular chemicals and diseases. See id. at 715. Therefore, “when the incidence of a disease or injury is sufficiently elevated due to exposure to a substance, someone who was exposed to that substance and exhibits the disease or injury can raise a fact question on causation.” Id.

As outlined above in Sections III.A and III.B, the opinions of Plaintiffs’ causation experts are grounded in numerous published epidemiological studies supporting their conclusions that Mr. Page’s AML was caused by his cumulative benzene exposure of 55 ppm-years and that the latency of his disease is consistent with the range of latency described in the relevant literature. These studies have been peer-reviewed and accepted by the epidemiological and medical communities. See Robinson, 923 S.W.2d at 557.

Defendants claim that Plaintiffs’ experts are required to testify regarding the minimum benzene exposure level for the development of AML. That is not the law as set forth by the Texas Supreme Court. According to Havner, a fact issue may be raised on specific causation by showing that the injured party is similar to those in the epidemiological studies relied on by the experts, including “that the exposure or dose levels were comparable to or greater than those in the studies.” 953 S.W.2d at 720. Plaintiffs have clearly demonstrated that numerous epidemiological studies have found an association between AML and benzene exposure at a cumulative dose even lower than Mr. Page’s dose of 55 ppm-years. Nothing more is required.

In an attempt to discredit Plaintiffs’ experts, Defendant makes the extraordinary claim that Drs. Infante and Gardner “use their theories almost exclusively for judicial purposes.” Motion at 14. A review of both doctors’ Curriculum Vitaes demonstrates that they have been practicing, teaching and publishing on leukemia and/or benzene exposure for most of their distinguished careers. See Curriculum Vitae of Dr. Peter Infante, attached as Exhibit 22; Curriculum Vitae of Dr. Frank Gardner, attached as Exhibit 23. Dr. Gardner has practiced medicine in the field of hematology and oncology for more than fifty years, specializing in the treatment of leukemia and other blood cancers and disorders, including those caused by chemical exposure. See Gardner C.V. (Exhibit 23). He has published dozens of peer-reviewed articles in the field of hematology-oncology over the last fifty years. See id. He has taught medicine throughout his career and is currently working as a clinical professor of medicine in the division of hematology-oncology at the University of Texas Medical Branch in Galveston, Texas. See id.

Dr. Infante is an epidemiologist who has specialized in occupational health and safety issues for more than thirty years. See Infante C.V. (Exhibit 22). Among his other qualifications, he served for almost twenty years as the Director of the Office of Standards Review in the Health Standards Program of the Occupational Health and Safety Administration, which is responsible for the regulation of toxic substances in the workplace. See id. In that position he oversaw the implementation of OSHA’s current benzene exposure standard of 1 ppm. Prior to that he was the Director of the Office of Carcinogen Identification and Classification for OSHA’s Health Standards Program. See id. Dr. Infante is a leader in the field of epidemiological research on the association between benzene exposure and leukemia, including AML, and has published landmark studies on this subject in peer-reviewed journals. See id. The OSHA temporary emergency standard on benzene was initiated based on Dr. Infante’s 1977 study of pliofilm workers exposed to benzene. In addition, he has received a special commendation from the United States Public Health Service for his contribution toward the understanding of the toxicity of benzene to humans.

While Defendants claim that Dr. Infante’s and Dr. Gardner’s opinions in this case are unreliable because their testimony has been previously excluded in other cases, the cases cited by Defendants have absolutely nothing to do with Plaintiffs’ case. The only case cited regarding Dr. Infante’s testimony, Chambers v. Exxon Corp., 81 F. Supp. 2d 661 (M.D. La. 2000), involved causation of a different disease, chronic myelogenous leukemia (CML). Dr. Infante has in fact been allowed to testify regarding the causation link between benzene and AML, the disease that is at issue in Plaintiffs’ case. See Coleman v. Ashland Chemical Co., No. 89-0387-AH-M, 1992 U.S. Dist. LEXIS 12122, *26 (S.D. Ala. July 30, 1992) (accepting Dr. Infante’s specific causation testimony that the plaintiff’s level of exposure to benzene was scientifically significant to his development of AML).

The cases regarding Dr. Gardner’s testimony are similarly inapposite to this case. The case of Missouri Pacific Railroad Co. v. Navarro, 90 S.W.3d 747 (Tex. App.– San Antonio 2002, no pet.) is not even a benzene case. While the case of Frias v. Atlantic Richfield, 104 S.W.3d 925 (Tex. App.–Houston [14th Dist.] 2003, pet. denied) was a benzene case, it involved causation of a completely different disease, aplastic anemia. Finally, the case of Castellow v. Chevron USA, 97 F. Supp. 2d 780 (S.D. Tex. 2000) is not comparable to Plaintiffs’ case because in that matter there was an absence of reliable information regarding the quantity of the plaintiff’s exposure. Here, of course, Dr. Gardner’s opinion is based on Plaintiffs’ expert Mr. Petty’s detailed exposure estimate of 55 ppm-years. See Gardner Depo. at 128 (Exhibit 2).


The general and specific causation opinions of Dr. Infante and Dr. Gardner are supported by a substantial body of epidemiological literature that meets the Havner criteria of a doubling of the risk and statistical significance. The epidemiological studies relied on by Plaintiffs’ experts demonstrate an association between AML and benzene exposure at a cumulative dose lower than Mr. Page’s 55 ppm-years. The epidemiological literature also demonstrates that Mr. Page’s latency period of approximately 49 years is within the range documented by relevant benzene studies. Dr. Infante and Dr. Gardner’s opinions are therefore reliable and admissible under both Havner and Robinson and their expert testimony on causation should be permitted in this case.

  1. The Supreme Court also noted, however, that “[w]e do not hold [] that a relative risk of more than 2.0 is a litmus test . . . .” Id. at 718.
  2. Some studies refer to AML as “acute nonlymphocytic leukemia” (ANLL).
  3. The Bond study states its findings as Standardized Mortality Ratio (SMR) of 444. See Infante, supra, at 257, Table III. An SMR is another way of expressing the strength of association between exposure to a chemical and the development of disease. The SMR “compares the ratio of the observed number of deaths from a specific cause in the study population to the number of deaths from this cause that would be expected in the general or standard population.” OSHA Benzene Rule, 52 Fed. Reg. at 34469 (Exhibit 5). “An SMR of 100 is the normal value if an excess is not observed. An SMR of 200 represents a 100% excess risk over normal.” Id. at 34462. An SMR divided by 100 is equivalent to a relative risk (RR) measurement. See id. at 34493. For example, if the SMR is 200, the relative risk would be 2.0. See id. at 34469. Therefore, because the Bond study found a SMR of 444, that results in a relative risk of 4.44.
  4. The risk ratio calculated in the Patel Pennsylvania studies is a Standardized Incidence Ratio (SIR), which is the same as an SMR except it refers to incidence of disease as opposed to mortality from disease. In this study the SIR was calculated by comparing the number of new cancer cases in the study area to the numbers that would have been expected based on the statewide cancer incidence rates. Tranguch Cancer Incidence Study at 3 (Exhibit 7).
  5. An odds ratio expresses an estimate of developing the disease for those exposed to a chemical versus those not exposed. OSHA considers odds ratios (OR) and relative risks (RR) to be equivalent measures of risk. See OSHA Benzene Rule, 52 Fed. Reg. at 34493 (Exhibit 5).
  6. This calculation involves several steps. First, the relative risk related to the 7.1 per 1,000 must be calculated. The formula for calculating relative risk is the probability of death from leukemia among a benzene-exposed population divided by the probability of death from leukemia among the U.S. general population. The background probability of death from leukemia for adults in the United States is .00707, or 7 per 1,000. See Mary C. White, Peter F. Infante, & Kenneth C. Chu, A Quantitative Estimate of Leukemia Mortality Associated with Occupational Exposure to Benzene, 2 Risk Analysis 195, 200 (1982), attached as Exhibit 16. The number of deaths observed per thousand would be 7.1 (extra) + 7 (expected) = 14.1. Therefore, 14.1 divided by 7 results in a relative risk of 2.01. The same calculation must be made for the extra 25 leukemia deaths per 1,000. Using the same expected number of 7 per 1,000, the observed number is 25 + 7 = 32. Then, 32 divided by 7 results in a relative risk of 4.6. Next, the upper limit of 25 (which has a 4.6 RR) is divided by the lower limit of 7.1 (which has a 2.01 RR) to determine that 25 is 3.52 times greater than 7.1. In order to determine the cumulative dose at which there is a twofold risk, 76 ppm-years is divided by 3.52 since the dose response is linear. The result is 21.6 ppm-years.
  7. The relative risk calculation is observed deaths divided by expected deaths. Expected deaths, as explained in footnote 5, is 7 per 1,000. Observed deaths is 10 + 7 = 17 per 1,000. When 17 is divided by 7, that results in a relative risk of 2.43.
  8. If there is a 2.43 RR at 45 ppm-years, there is a 2.0 RR at 37 ppm-years since the relationship of benzene exposure and risk of leukemia is linear at low exposure levels.
  9. Defendants claim that Plaintiffs’ discovery responses include an initial exposure date of 1947. The citation they provide does not support this assertion. Although Mr. Page began working at Exxon in 1947, Plaintiffs have never claimed that Mr. Page had any contact with benzene before 1951.
  10. “These factors include, but are not limited to: (1) the extent to which the theory has been or can be tested; (2) the extent to which the technique relies upon the subjective interpretation of the expert []; (3) whether the theory has been subjected to peer review and/or publication; (4) the technique’s potential rate of error; (5) whether the underlying theory or technique has been generally accepted as valid by the relevant scientific community; and (6) the non-judicial uses which have been made of the theory or technique.” Robinson, 923 S.W.2d at 557 (internal citations omitted).