PLAINTIFF’S CONSOLIDATED RESPONSE IN OPPOSITION TO DEFENDANTS GENCORP INC. F/K/A THE GENERAL TIRE & RUBBER COMPANY AND GENERAL TIRE & RUBBER COMPANY’S MOTIONS FOR SUMMARY JUDGMENT
Plaintiff Charles Ray Laningham (“Mr. Laningham”) files this consolidated response opposing Defendants Gencorp Inc. f/k/a The General Tire & Rubber Company and General Tire & Rubber Company’s (“Defendants”) No Evidence Motion for Summary Judgment and Defendants’ Motion for Summary Judgment Based on Lack of Medical Causation, and would respectfully show the Court as follows:
In this toxic tort case, Mr. Laningham has brought claims arising out his occupational exposure to benzene at Defendants’ General Tire Facility in Waco, Texas. During the course of his employment as a tire builder at the Waco tire facility from 1968-87, Mr. Laningham was exposed to benzene and benzene-containing products and solvents while performing work-related tasks such as washing rubber. In 2002, Mr. Laningham was diagnosed with non-Hodgkin’s lymphoma (NHL), and he died in 2005. Mr. Laningham has alleged that his non-Hodgkin’s lymphoma was caused by his excessive exposure to benzene while working at the General Tire Facility.
Defendants have brought no-evidence motions regarding two components of the causation element of Mr. Laningham’s case: whether benzene exposure can cause NHL, i.e., general causation, and whether non-Hodgkin’s lymphoma was a contributing cause of Mr. Laningham’s death. Defendants are not challenging Mr. Laningham’s ability to prove specific causation, i.e., whether benzene exposure caused Mr. Laningham to develop NHL in this case.
As an initial matter, Mr. Laningham objects to Defendants’ motions as premature. Defendants have already made a no-evidence motion for summary judgment on causation, a motion that was continued in October because Defendants have not produced documents that Mr. Laningham’s experts need for their specific causation opinions, including employee levels of exposure to benzene, air monitoring, and benzene health and safety data. Defendants are now trying to avoid the effect of that continuance by carving out particular components of the causation element. Defendants’ motions should be continued so that Mr. Laningham’s causation evidence may be considered as a whole, after Defendant have produced sufficient discovery data on specific causation.
If the Court decides to reach the merits at this time, Defendants’ motions should be denied because Mr. Laningham has ample evidence that raises a genuine issue of material fact on causation. Mr. Laningham’s expert epidemiologist, Dr. Peter Infante, testifies via the attached affidavit that reliable epidemiological literature supports his opinion that an association exists between benzene exposure and an elevated risk of NHL. See Affidavit of Peter Infante In Support of Plaintiff’s Response to Defendant’s Motion for Summary Judgment, December 6, 2006, (“Infante Affidavit”), attached as Exhibit 1, at ¶ 8. Moreover, Mr. Laningham offers the affidavit testimony of his expert oncologist, Dr. Frank Gardner, who has concluded that NHL suppressed Mr. Laningham’s immune system and thereby contributed to his death. See Affidavit of Frank H. Gardner, M.D., December 7, 2006, (“Gardner Affidavit”), attached as Exhibit 2, at ¶¶ 2, 4. Mr. Laningham will show that Dr. Infante’s and Dr. Gardner’s opinions on causation meet the Havner and Robinson criteria for reliability and admissibility. Defendants’ no evidence motions should be denied as Mr. Laningham has raised a genuine issue of material fact.
Defendants’ No-Evidence Motions Are Premature Because Discovery Is Not Complete and All Evidence of Causation Should Be Considered As A Whole.
Defendants’ motion is premature because Defendants are attempting to improperly subdivide the causation element for summary judgment purposes. Defendants have moved for a no-evidence summary judgment pursuant to Rule 166a(i), Texas Rules of Civil Procedure, which provides that “[a]fter adequate time for discovery, a party without presenting summary judgment evidence may move for summary judgment on the ground that there is no evidence of one or more essential elements of the claim or defense on which an adverse party would have the burden of proof at trial.” Tex. R. Civ. P. 166a(i) (emphasis added). The moving party is required to state the elements for which there is no evidence. See Flameout Design & Fabrication, Inc. v. Pennzoil Caspian Corp., 994 S.W.2d 830, 834 (Tex.App.–Houston [1st Dist.] 1999, no pet.).
Causation is “one element” of Mr. Laningham’s tort claim, which for analytical purposes is sometimes broken down into the components of general causation and specific causation. Texas courts have recognized that “[a]lthough causation is made up of several evidentiary components, causation itself is a single essential element of tort liability.” In re Mohawk Rubber Co., 982 S.W.2d 494, 497 (Tex. App. – Texarkana 1998, orig. proceeding) As the recent draft of the Restatement (Third) of Torts explained,
[C]ourts often address ‘exposure,’ ‘general causation,’ and ‘specific causation.’ Nevertheless, these items are not ‘elements’ of a Mr. Laningham’s cause of action, and in some cases may not require separate proof. So long as the Mr. Laningham introduces admissible and sufficient evidence of factual causation the burden of production is satisfied. . . . These categories function as devices to organize a court’s analysis, not as formal elements of the cause of action.
Restatement (Third) § 28 cmt. c (emphasis added).
Defendants are improperly treating general causation and cause of death as elements in their own right, when these are simply evidentiary components or organizational devices for the causation element. Defendants have already unsuccessfully attempted to move for summary judgment on causation as a whole, but that motion was continued at hearing held on October 16, 2006, because Defendants have not yet provided sufficient discovery documents for Mr. Laningham’s experts to develop specific causation opinions. Defendants should not be permitted to withhold evidence of specific causation and at the same time assert that Mr. Laningham has no evidence for the causation element of his claim.
The Texas Supreme Court has instructed that scientific evidence supporting causation should be considered in its entirety when determinations are made about the reliability of such evidence. In Merrell Dow Pharmaceuticals v. Havner, 953 S.W.2d 706 (Tex. 1997), it was held that the plaintiff has the burden to present evidence of causation that, “as a whole, ‘rises to a level that would enable reasonable and fair-minded people to differ in their conclusions.’” Id. at 711, quoting Burroughs Wellcome Co. V. Crye, 907 S.W.2d 497, 499 (Tex. 1995). The Texas Supreme Court offered the following guidelines for determining whether a plaintiff has met this burden:
[W]e emphasize that courts must make a determination of reliability from all the evidence. Courts should allow a party, plaintiff or defendant, to present the best available evidence, assuming it passes muster under Robinson, and only then should a court determine from a totality of the evidence, considering all factors affecting the reliability of particular studies, whether there is legally sufficient evidence to support a judgment.
Id. at 720 (emphasis added). Because this is a toxic tort case, there is no doubt that Defendants will later seek summary judgment on specific causation. Consistent with Havner, Mr. Laningham’s causation evidence should be considered as a whole instead of on the piecemeal basis that Defendants are attempting.
Defendants’ summary judgment motions should be continued until they have produced the outstanding discovery that Mr. Laningham needs to prove specific causation. The Texas Rules of Civil Procedure provide for the continuance of a summary judgment proceeding when the party opposing the motion has not had sufficient time for discovery. Rule 166a provides that when a party shows “he cannot for reasons stated present by affidavit facts essential to justify his opposition, the court may refuse the application for judgment or may order a continuance to permit affidavits to be obtained or depositions to be taken or discovery to be had or may make such other order as is just. Tex. R. Civ. Pro. 166a(g); Joe v. Two Thirty Nine Joint Venture, 145 S.W.3d 150, 161 (Tex. 2004). A party may seek additional time for discovery before a summary judgment hearing either by an affidavit explaining the need for further discovery or by a verified motion for continuance. See Tenneco, Inc. v. Enter. Prod. Co., 925 S.W.2d 640, 647 (Tex. 1996); El Dorado Motors, Inc. v. Koch, 168 S.W.3d 360, 369 (Tex. App. – Dallas 2005, no pet.).
As set forth in more detail in the attached affidavit, see Exhibit 3, Plaintiff has in good faith attempted to negotiate with Defendants for the production of the remaining documents needed for the specific causation component, and progress has been made. See also Letter to Eric G. Reeves from Kirk Claunch, November 27, 2006, attached to this affidavit as Exhibit 4. Once the specific exposure data is produced, Mr. Laningham can provide it to his experts and they can use it to estimate his cumulative benzene exposure and form opinions regarding specific causation. Consideration of this no-evidence motion should be continued until Mr. Laningham is able to provide the Court with evidence regarding all relevant components of causation.
Defendants Have Not Met Their Burden on Summary Judgment.
A no-evidence motion for summary judgment should not be granted if the respondent brings forth “more than a scintilla of probative evidence to raise a genuine issue of material fact.” Forbes, Inc. v. Granada Biosciences, Inc., 124 S.W.3d 167, 172 (Tex. 2003). More than a scintilla of evidence exists if the evidence “as a whole, ‘rises to a level that would enable reasonable and fair-minded people to differ in their conclusions.’” Havner, 953 S.W.2d at 711; Burroughs Wellcome, 907 S.W.2d at 499; Transp. Ins. Co. v. Moriel, 879 S.W.2d 10, 25 (Tex. 1994). In order “[t]o defeat a motion made under [Rule 166a(i)], the non-movant is not required to marshal its proof; its response need only point out evidence that raises a fact issue on the challenged elements.” Tex R. Civ. P. 166a(i), Comment to 1997 Change. As long as Mr. Laningham raises a fact issue, he is not required to prove he would prevail at a trial on the merits. See Greene v. Thiet, 846 S.W.2d 26, 33 (Tex. App. – San Antonio 1992, writ denied); Cloys v. Turbin, 608 S.W.2d 697, 700 (Tex. App. – Dallas 1980, no writ).
The general requirements of summary judgment practice govern the consideration of a no-evidence motion. See Flameout Design, 994 S.W.2d 830 at 834. When reviewing a motion for summary judgment the court should view the evidence in the light most favorable to the non-movant, disregarding all contrary evidence and inferences. See id.; Morgan v. Anthony, 27 S.W.3d 928, 930 (Tex. 2000); Randall’s Food Mkts., Inc. v. Johnson, 891 S.W.2d 640, 644 (Tex. 1995); Keszler v. Mem’l Med. Ctr. of E. Tex., 105 S.W.3d 122, 125 (Tex. App.—Corpus Christi 2003, no pet.).
The Evidence Raises Genuine Issues of Material Fact Regarding General Causation.
On the general causation component, Mr. Laningham offers the testimony of his expert epidemiologist, Dr. Peter Infante. In order for an expert’s testimony to be admissible under Rule 702, Texas Rules of Evidence, the expert must be qualified and the testimony must be relevant and based on a reliable foundation. See E.I. du Pont de Nemours & Co. v. Robinson, 923 S.W.2d 549, 556 (Tex. 1995).
- Mr. Laningham’s Expert Epidemiologist Dr. Peter Infante Is Qualified To Testify Regarding The Association Between Benzene Exposure And NHL.
Mr. Laningham’s expert epidemiologist, Dr. Peter Infante, is eminently qualified to testify regarding the hazards of benzene exposure. Dr. Infante is an epidemiologist who has specialized in occupational health and safety issues for more than thirty years. See Infante C.V. (Exhibit 5). 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.; Infante Affidavit at ¶ 3 (Exhibit 1). 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 Infante C.V. 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. See Infante Affidavit at ¶ 7.x.
- Reliable, Published Epidemiological Literature Supports Dr. Infante’s Expert Opinion That Benzene Exposure Causes NHL.
The question of “general causation” involves whether “a substance is capable of causing a particular injury or condition in the general population.” Havner, 953 S.W.2d at 714. Dr. Infante’s opinion on general causation is that an association exists between benzene exposure and an elevated risk of NHL. See Infante Affidavit at ¶ 8 (Exhibit 1). This opinion is based on numerous epidemiological studies that have documented an association between benzene exposure and an elevated risk of NHL. See id.
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. 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.
Dr. Infante has 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 NHL resulting from benzene exposure. See Infante Affidavit at ¶ 8. The relevant benzene studies are as follows:
|Study||Statistically Significant Findings Re NHL|
|Richard B. Hayes, et al., Benzene and Dose-Related Incidence of Hematologic Neoplasms in China, 89 Journal of the National Cancer Institute 14, 1067-68 (1997), attached as Exhibit 6.||Found that workers with 10 or more years of benzene exposure had a relative risk of developing non-Hodgkin’s lymphoma of 4.2 (95% CI = 1.1-15.9) and that workers with an average benzene exposure of more than 25 parts per million (ppm) had a relative risk of NHL of 4.7 (95% CI =1.2-18.1).|
|Song-Nian Yin, et al., A Cohort Study of Cancer Among Benzene-Exposed Workers in China: Overall Results, 29 Am. J. Indus. Med. 227, 232 Table IV (1996), attached as Exhibit 7.||Found a relative risk of 3.0 (C.I. 1.0-13.0) of NHL among benzene exposed workers in China.|
|See Pascale Fabbro-Peray, et al., Environmental Risk-Factors for Non-Hodgkin’s lymphoma: a population-based case-control study in Languedoc-Roussillon, France, 12 Cancer Causes and Control 201, 205-06, 208 (2001), attached as Exhibit 8.||Found a 2.0 odds ratio (95% CI = 1.1-3.9) for benzene exposure and NHL; also found association of more than 810 days of benzene exposure and non-Hodgkin’s lymphoma, with an odds ratio of 4.6 (95% CI = 1.1-19.2).|
|Ralph I. Nilsson et al., Leukaemia, lymphoma and multiple myeloma in seamen on tankers, 55(8) Occup. Env. Med. 517, 2 (1998), attached as Exhibit 9.||Found an odds ratio of 3.3 (95% CI =1.1-10.6), of NHL among men exposed to benzene while working on chemical and product tankers.|
|Lucia Miligi, et al., Occupational Exposure to Solvents and the Risk of Lymphomas, 17 Epidemiology 552 (2006), attached as Exhibit 10.||Found that workers exposed to all three aromatic hydrocarbons benzene, toluene and xylene, had an odds ratio of 2.1 (1.1-4.3) for NHL.|
|M. Hours, et al., Occupational exposures and haematologic malignancies: A case-control study in Lyon (France), 43 Rev. Epidem. et Sante Publ. 231 (1995), attached as Exhibit 11.||Found elevated odds ratios for NHL among workers exposed to mineral oils (odds ratio 14.86; C.I. 2.76-80.0), alkali compounds (odds ratio 2.90; C.I. 1.09-7.68) and inks (odds ratio 2.47; C.I. 1.09-5.17).|
One of the first epidemiological studies to show a statistically significant association between occupational exposure to benzene and NHL is Richard B. Hayes, et al., Benzene and Dose-Related Incidence of Hematologic Neoplasms in China, 89 Journal of the National Cancer Institute 14 (1997) (Exhibit 6). This large cohort study was conducted by the highly respected National Cancer Institute (NCI), part of the National Institutes of Health and the federal government’s principal agency for cancer research, in cooperation with the Chinese Academy of Preventative Medicine. The NCI study looked at a group of 74,828 benzene-exposed workers in a variety of factories in China to evaluate the relationship between occupational benzene exposure and the risk of developing specific hematologic neoplasms, including non-Hodgkin’s lymphoma. Id. at 1066. The unexposed comparison group consisted of 35,805 industrial workers in many of the same factories who were assigned to units where benzene was not used, which allowed the authors to control for factors such as environment, socioeconomic status, and available health care. See Deposition of Peter Infante, April 14, 2006 (Vol. 1) and May 4, 2006 (Vol. 2), Case Nos. A030272-CC/A030272GC, Stubbs v. Radiator Specialty Co./Wilkinson v. Radiator Specialty Co., District Court of Orange County, Texas, 128th Judicial Dist., attached as Exhibit 13, at Vol. 1, 375:12-21, 386:11-22. The study looked at the relative risk of non-Hodgkin’s lymphoma, which is the ratio of incidence rates of the disease in the benzene-exposed group to the incidence rates in the unexposed group. See Hayes, supra, at 1066 (Exhibit 6).The authors concluded that workers with 10 or more years of benzene exposure had a relative risk of developing non-Hodgkin’s lymphoma of 4.2 (95% CI = 1.1-15.9). Id. at 1067. Further, the risk for non-Hodgkin’s lymphoma increased with the duration of exposure and was strongest among workers who had distant exposure (more than 10 years). Id. at 1068. Another statistically significant finding was that workers with an average benzene exposure of more than 25 parts per million (ppm) had a relative risk of NHL of 4.7 (95% CI =1.2-18.1). Id. at 1068, Table 2.
While not every single data point in the NCI study was statistically significant, the study is important because it demonstrates a positive dose-response trend for benzene exposure and NHL. See Infante Depo. at Vol. 1, 244:10-15, 247:9-15; Vol. 2 at 60:17-21, 62:15-63:4, 65:20-66:3 (Exhibit 13). In other words, as explained in detail by Dr. Infante, the NCI study found an increase in the relative risk of developing non-Hodgkin’s lymphoma with an increase in the amount of exposure to benzene in the workplace. Id. The positive dose-response trend for non-Hodgkin’s lymphoma was seen in all four benzene exposure analyses done in the study – average exposure measured in ppm, constant exposure in ppm, duration in years, and cumulative exposure in ppm-years. See Hayes, supra, at 1068 (Exhibit 6); Infante Depo. at Vol. 2, 67:2-9 (Exhibit 13). In the field of epidemiology, a positive dose-response analysis is an impressive finding because all the errors in the exposure assessment are designed to bias the findings toward the null hypothesis of no association. See Infante Depo. at Vol. 2, 62:21-63:7 (Exhibit 13).
Another important article regarding this same China study is Song-Nian Yin, et al., A Cohort Study of Cancer Among Benzene-Exposed Workers in China: Overall Results, 29 Am. J. Indus. Med. 227, 232 Table IV (1996) (Exhibit 7). The study examined a very large cohort of Chinese workers exposed between 1972 and 1987 in 12 different Chinese cities. See id. at 227. The findings included an elevated risk of NHL among benzene-exposed workers, with a relative risk of 3.0 (C.I. 1.0-13.0). See id. at 232, Table IV.
Subsequent epidemiological studies have confirmed the NCI study finding of an association between benzene exposure and NHL. See Pascale Fabbro-Peray, et al., Environmental Risk-Factors for Non-Hodgkin’s lymphoma: a population-based case-control study in Languedoc-Roussillon, France, 12 Cancer Causes and Control 201 (2001) (Exhibit 8). The Fabbro-Peray case control study looked at a wide variety of occupational and environmental risk factors for non-Hodgkin’s lymphoma among more than four hundred persons diagnosed with the disease in a single county in France from 1992 to 1995. A control group was randomly selected from the voter registration rolls in the same county. Id. at 202. According to the authors,
The results showed a consistent, moderate to strong association between benzene exposure and NHL. Indeed, benzene showed a qualitative association with NHL. This was strengthened by the increasing effect with duration of exposure, a younger age at onset, a longer duration since first exposure, and a longer cumulative number of days of exposure, the latter used as a surrogate for the dose of exposure. The latter result shows that the association is stronger for high exposure than for low exposure.
Id. at 209. Specifically, the Fabbro-Peray study reported a 2.0 odds ratio (95% CI = 1.1-3.9), even after adjusting for sociodemographic confounding factors such as age, gender, urban setting and educational level. Id. at 205-06. Importantly, this statistically significant finding of a doubled risk had a consistent dose-response effect. Id. at 205. The study’s findings also included a statistically significant association between more than 810 days of benzene exposure and non-Hodgkin’s lymphoma, with an odds ratio of 4.6 (95% CI = 1.1-19.2). Id. at 208. The authors concluded that the “relatively strong association between history of benzene exposure and NHL observed in our study is potentially consistent with the recent findings of Hayes, et al. . . . .” Id. at 209.
Another study relied on by Dr. Infante is Ralph I. Nilsson et al., Leukaemia, lymphoma and multiple myeloma in seamen on tankers, Occup. Env. Med. 55(8): 517-521 (1998) (Exhibit 9). This study looked at the incidence of lymphatic and haematopoietic malignancies among deck crew workers exposed to cargo vapors on chemical, petroleum product, and crude oil tankers. Id. at 517. The study found a statistically significant odds ratio of 3.3 (95% CI =1.1-10.6), of non-Hodgkin’s lymphoma among men working on chemical and product tankers in the 1970’s and 1980’s, and that the risk increased with exposure time. Id. at 2, Table 1. This significant risk was possibly attributable to the workers’ benzene exposure while cleaning, loading and unloading tanks containing gasoline and other light refinery products, and was in contrast to the non-significant risk of non-Hodgkin’s lymphoma seen in crude oil tanker workers whose jobs did not involve exposure to benzene. Id. at 3-4.
Several other studies additionally support Dr. Infante’s opinion. A 2006 case-control study among workers in several regions in Italy found that workers exposed to all three aromatic hydrocarbons benzene, toluene and xylene, had a statistically significantly increased risk of NHL with an odds ratio of 2.1 (C.I. 1.1-4.3). See Lucia Miligi, et al., Occupational Exposure to Solvents and the Risk of Lymphomas, 17 Epidemiology 552, 552 (2006) (Exhibit 10). Similarly, a hospital based case-control study in Lyon, France observed significantly elevated odds ratios for NHL among workers exposed to benzene in mineral oils (odds ratio 14.86; C.I. 2.76-80.0), alkali compounds (odds ratio 2.90; C.I. 1.09-7.68) and inks (odds ratio 2.47; C.I. 1.09-5.17). See M. Hours, et al., Occupational exposures and haematologic malignancies: A case-control study in Lyon (France), 43 Rev. Epidem. et Sante Publ. 231 (1995) (Exhibit 11). Finally, a study reported in The Lancet found a significant excess of deaths caused by major lymphomas in men employed in occupations where benzene was used. See N.J. Vianna & A. Polan, Lymphomas and Occupational Benzene Exposure, 1 The Lancet 1394 (1979) (Exhibit 12).
The above studies demonstrate that the association between benzene exposure and NHL is observed consistently across different groups exposed to benzene in a variety of settings. Taken as a whole, these studies show an elevated risk of developing non-Hodgkin’s lymphoma in industrial plants, in tanker ships at sea, and across occupations and socioeconomic classes in France, Italy and China. Mr. Laningham’s causation evidence therefore satisfies Havner’s observation that “it is important that any conclusions about causation be reached only after an association is observed in studies among different groups and that the association continues to hold when the effects of other variables are taken into account.” Havner, 953 S.W.2d at 727.
In sum, there is a substantial body of epidemiological literature supporting Dr. Infante’s general causation opinion that benzene exposure is associated with an elevated risk of NHL. These studies satisfy the Havner criteria for reliability and admissibility of scientific evidence of causation. Mr. Laningham has therefore created a genuine issue of material fact on general causation, precluding summary judgment.
The Evidence Raises Genuine Issues of Material Fact Concerning NHL As Substantial Contributing Factor to Mr. Laningham’s Death.
Contrary to Defendants’ assertion, the evidence shows that Mr. Laningham’s NHL contributed to his death. It has long been established that more than one event or agent can combine to cause a single indivisible injury. See Havner v. E-Z Mart Stores, Inc., 825 S.W.2d 456, 459 (Tex. 1992) (“The act or omission need not be the sole cause.”); Wilson v. Brister, 982 S.W.2d 42, 44 (Tex. App. – Houston [1st Dist.] 1998, pet. denied) (“More than one action may be the proximate cause of the same injury.”); Texas Dept. of Transp. v. Olson, 980 S.W.2d 890, 893 (Tex. App. – Fort Worth 1998, no pet.) (“[T]here can be more than one proximate cause of an event.”). When multiple causes contribute to an injury, “[t]he plaintiff need not exclude all possibilities; it is sufficient to prove that the greater probability is that the defendant’s conduct, alone or in contribution with others, was the cause of the harm.” Berly v. D & L Sec. Servs. and Investigations, Inc., 876 S.W.2d 179, 182 (Tex. App. – Dallas 1994, writ denied). There may be more than one proximate cause of an injury, and all persons who contributed to the injury are liable. See Travis v. City of Mesquite, 830 S.W.2d 94, 98 (Tex. 1992); El Chico Corp. v. Poole, 732 S.W.2d 306, 313 (Tex. 1987); Boorhem-Fields, Inc. v. Burlington N. R.R. Co., 884 S.W.2d 530, 536 (Tex. App. – Texarkana 1994, no writ).
In the toxic tort context, the factual issue to be decided by the jury is whether exposure was a “substantial factor” in bringing about a plaintiff’s injuries. Borel v. Fibreboard Paper Products Corp., 493 F.2d 1076, 1094 (5th Cir. 1974). In order to defeat a motion for summary judgment, Mr. Laningham is “not required to prove [he] would prevail at a trial on the merits; [he] need only produce evidence sufficient to raise an issue of fact with respect to  causation.” Greene v. Thiet, 846 S.W.2d 26, 33 (Tex. App. – San Antonio 1992, writ denied).
Based on a review of Mr. Laningham’s available medical records, Plaintiff’s expert Dr. Gardner concluded that there is no evidence to indicate that Mr. Laningham’s NHL had been cured at the time of his death. See Gardner Affidavit at ¶ 7 (Exhibit 2). In Dr. Gardner’s opinion, Mr. Laningham’s death was not only related to his lung cancer, but also to the altered immune response from his large B-cell lymphoma, or NHL. See id. at ¶ 2. Dr. Gardner determined that the death certificate for Mr. Laningham, which only listed lung cancer as his cause of death, improperly disregarded his NHL and its contribution to his illness. See id. at ¶ 4.
Dr. Gardner is extremely well-qualified to testify regarding the contribution of NHL to Mr. Laningham’s death. 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 14). For several decades he has had an active laboratory program related to studies of bone marrow function and platelet physiology funding primarily by the United States Public Health Services. See Gardner Affidavit at 2 (Exhibit 2). He has published dozens of peer-reviewed articles in the field of hematology-oncology over the last fifty years. See id.; Gardner C.V.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.
The summary judgment evidence establishes that NHL was a substantial contributing factor to Mr. Laningham’s death. This evidence creates a genuine issue of material fact and precludes summary judgment on causation.
For the foregoing reasons, Plaintiff respectfully requests that the hearing on Defendants’ no-evidence motions be continued until Defendants produce all requested documents relevant to the causation element of Plaintiff’s claim. In the alternative, Plaintiff requests that Defendants’ motions be denied on the merits, as Plaintiff’s evidence raises a genuine issue of material fact on causation.
- ↑ Defendant has filed two no-evidence motions on causation that Mr. Laningham is addressing in this consolidated response. Defendants’ Motion for Summary Judgment Based on Lack of Medical Causation challenges Mr. Laningham’s evidence on general causation only. Defendants’ No Evidence Motion for Summary Judgment raises both general causation and the cause of death issue.
- ↑ Havner and its progeny have made clear that a showing of a relative risk of 2.0 is prima facie evidence of causation, but it is not a litmus test. See id. at 718; see also Minnesota Mining and Mfg. Co. v. Atterbury, 978 S.W.2d 183, 198 (Tex. App. – Texarkana 1998, pet. denied) (interpreting Havner as making “no requirement in a toxic tort case that a party must have reliable epidemiological evidence of a relative risk of 2.0 or greater).
- ↑ A cohort study is a type of epidemiological study that prospectively identifies groups and observes them over time to see if one group is more likely to develop disease. Havner, 953 S.W.2d at 721.
- ↑ A case control study retrospectively identifies individuals with a disease, and a suitable control group without the disease, and then examines postulated causes of the disease. Havner, 953 S.W.2d at 721.
- ↑ As the Havner case explained, An ‘odds ratio’ can be calculated for a case-control study . . . The odds ratio compares the odds of having the disease when exposed  versus when not exposed. If the ratio is 2.67, the odds are that a person exposed  is 2.67 times more likely to develop the disease under study . . . The numeric value of an odds ratio is at least equal to the relative risk . . . .” 953 S.W.2d at 721.