JOSEPH MICHAEL PIZZUTO v. CHALMETTE REFINING LLC CHALMETTE REFINING CO LLC PBF HOLDING COMPANY LLC AND LIBERTY INSURANCE CORPORATION (2026)

Defendants, Chalmette Refining, LLC and Liberty Insurance Company (sometimes collectively referred to as “Defendants”),¹ appeal from the November 7, 2022 causation judgment and the November 30, 2023 compensation judgment of the Office of Workers’ Compensation, District 6 (“OWC”). Defendants appeal the OWC causation judgment finding that plaintiff, Joseph Michael Pizzuto was exposed to benzene in the course and scope of his employment with Chalmette Refining, LLC (the “Refinery”), and that more likely than not his exposure caused his adenocarcinoma. Additionally, Defendants and Pizzuto both appeal the November 30, 2023 compensation judgment awarding compensation and related expenses and costs therefor. For the reasons that follow, we reverse the November 7, 2022 judgment and vacate the November 30, 2023 judgment.

FACTS AND PROCEDURAL HISTORY

On April 15, 2021, Pizzuto filed a disputed claim for compensation (Form 1008) and an attached supplemental disputed claim for compensation pleading with the OWC, asserting a claim for workers’ compensation benefits based on disability arising from an occupational disease as provided in the Louisiana Workers’ Compensation Law (the “LWCL”), La. R.S. 23:1020.1, et seq.² Pizzuto alleged that he contracted adenocarcinoma, a form of lung cancer, from exposure to benzene while employed by the Refinery in Chalmette. Pizzuto identified two occasions on which benzene spilled and/or was sprayed directly on him and also alleged daily exposure to fumes while he was present in the Sulfolane Unit, which extracted an undiluted form of benzene.³ Pizzuto alleged that he became disabled on or about January 4, 2021, after his diagnosis of adenocarcinoma in his lungs in late 2019. Pizzuto further alleged that he was entitled to permanent and total disability benefits under the LWCL.

The parties ultimately stipulated that a bifurcated trial of the issues of compensability (the primary focus of which was causation) from the issue of entitlement to benefits would best serve the interests of justice and judicial economy. Following a two-day trial on causation on July 26 and 27, 2022,⁴ the OWC signed a partial final judgment on November 7, 2022, finding that “Pizzuto carried his burden to demonstrate that he was exposed to benzene while in the course and scope of his employment with Chalmette Refining, LLC and that more likely than not that exposure caused his adenocarcinoma.” As such, the OWC found that “Pizzuto ․ proved his entitlement to workers’ compensation benefits pursuant to Louisiana Revised Statute[s] 23:1031(A).” After the compensation trial, which was conducted on May 11, 2023 and August 11, 2023, the OWC issued a judgment awarding certain workers’ compensation benefits and costs to Pizzuto on November 30, 2023.

Defendants suspensively appealed both the November 7, 2022 and the November 30, 2023 judgments.⁵ Additionally, Pizzuto devolutively appealed the November 30, 2023 judgment. On appeal, Defendants assign the following errors:

1. [The] OWC refused to evaluate the methodology of Plaintiff's general causation expert. Doing so, [the] OWC committed legal error in abdicating its gatekeeper function so that the expert's testimony must be reviewed de novo.

2. [The] OWC found that there is no consensus in the medical community about whether exposure to benzene causes lung cancer and that, at most, the medical community no longer rejects an association between benzene and lung cancer. [The] OWC committed legal error when it found Plaintiff entitled to workers’ compensation for contracting lung cancer as a result of alleged exposure to benzene because general causation is not supported by current science. Alternatively, the OWC's decision is manifestly erroneous.

3. Because of the dearth of scientific evidence to establish general causation, it follows that there is no evidence of what dose of benzene could conceivably cause lung cancer. Accepting [the] OWC's findings of fact, [the] OWC still erred in finding specific causation.

Pizzuto assigns the following errors:

1. The [OWC] erred in not including language that Appellant Pizzuto was currently permanently totally disabled on the date of the May 31, 2023, trial, and that the Appellant Pizzuto's entitlement to permanent total disability benefits continued into the future until a change in his disability status.

2. The [OWC] erred in not including language that Appellant Pizzuto required ongoing medical treatment on the date of the May 31, 2023, trial and that the Appellant Pizzuto was entitled to receive that medical treatment under the [LWCL] subject to the procedures set out.

3. The [OWC] erred in allowing a credit for short-term disability benefits against the past permanent total disability benefits awarded.

LAW AND DISCUSSION

Refinery Assignment of Error No. 1 – Evaluation of Expert Methodology

In its first assignment of error, Defendants argue that the OWC failed to properly screen the methodology of Pizzuto's expert, Dr. Ernest Chiodo, who was offered as an expert in internal medicine, occupational medicine, and toxicology as well as a certified industrial hygienist. Defendants argue that the OWC legally erred in striking its pretrial memorandum to the extent it was a Daubert challenge and in failing to conduct any Daubert analysis.⁶

Daubert involves admissibility of the expert's opinion and specifically concerns the validity of the methodology employed by the expert. See Robertson v. Doug Ashy Building Materials, Inc., 2014-0141 (La. App. 1st Cir. 12/23/14), 168 So.3d 556, 567, writ denied, 2015-0365 (La. 4/24/15), 169 So.3d 364; Freeman v. Fon's Pest Management, Inc., 2017-1846 (La. 2/9/18), 235 So.3d 1087, 1090 (per curiam). However, pursuant to the parties’ joint stipulation and the corresponding July 18, 2022 order signed by the OWC, the deposition of Dr. Chiodo in addition to the depositions of other expert and lay witnesses “shall be admitted into evidence” in lieu of live testimony at trial with each party reserving the right “to argue and contest the relevancy (except admissibility) and weight of the submitted testimonial evidence.”

The district court judge has great discretion in the manner in which proceedings are conducted before his court, and appellate courts will not intervene absent an abuse of that discretion. See Thomas v. Department of Wildlife & Fisheries, 2018-0869 (La. App. 1st Cir. 10/2/19), 289 So.3d 579, 598, writ denied, 2019-01767 (La. 1/14/20), 291 So.3d 687. Accordingly, we are unable to conclude that the OWC abused its discretion in failing to conduct a Daubert analysis under the circumstances herein or in striking Defendants’ pretrial memorandum.⁷

The Defendants’ first assignment of error is without merit.

Defendants’ Assignments of Error Nos. 2 and 3 – Finding of General and Specific Causation

In their remaining assignments of error, Defendants argue that the OWC erred in finding both general and specific causation, focusing their argument on the lack of consensus in the medical and scientific community about whether exposure to benzene causes lung cancer (general causation) and the failure of Pizzuto to show what dose of benzene could cause lung cancer (specific causation).⁸

Burden of Proof

At trial in the instant matter, Pizzuto bore the burden of proving that he contracted an occupational disease, such that he is entitled to receive benefits under the LWCL. La. R.S. 23:1031.1; see LeCompte v. St. Tammany Parish School Board, 2020-0333 (La. App. 1st Cir. 4/26/21), 324 So.3d 1066, 1068, writ denied, 2021-00744 (La. 10/5/21), 325 So.3d 358. An occupational disease is defined in the LWCL as “that disease or illness which is due to causes and conditions characteristic of and peculiar to the particular trade, occupation, process, or employment in which the employee is exposed to such disease.” La. R.S. 23:1031.1(B).

Importantly, an occupational disease is one in which there is a demonstrated causal link between the particular disease or illness and the occupation. Crear v. Darling Ingredients, Inc., 2024-0891 (La. App. 1st Cir. 5/23/25), 417 So.3d 804, 808 (citing Arrant v. Graphic Packaging International, Inc., 2013-2878, 2013-2981 (La. 5/5/15), 169 So.3d 296, 309) (emphasis added). The causal link between the employee's illness and work-related duties must be established by a reasonable probability.⁹ Crear, 417 So.3d at 808 (citing Williams v. Temple Inland, Inc., 2008-2153 (La. App. 1st Cir. 12/23/09), 30 So.3d 760, 762). Moreover, in order to support a finding of an occupational disease, expert testimony in the form of certified reports, depositions, or oral examination in open court is required. Crear, 417 So.3d at 808. If the evidence leaves probabilities equally balanced or shows only possibilities, the plaintiff's case must fail. Buxton v. Iowa Police Department, 2009-0520 (La. 10/20/09), 23 So.3d 275, 291 (citing Prim v. City of Shreveport, 297 So.2d 421, 422 (La. 1974)); Alvis v. Peninsula Gaming Partners, LLC, 2020-0161 (La. App. 1st Cir. 11/12/20), 316 So.3d 54, 58. Accordingly, Pizzuto was required to prove by a reasonable probability that lung cancer is an occupational disease, i.e., that there is a demonstrated causal link between lung cancer and his occupation as a Stillman (and the alleged exposure to a toxic substance – benzene). See Crear, 417 So.3d at 808; Arrant, 169 So.3d at 309.

Proof of causation in toxic tort cases has two components, general and specific. Costanza v. Florida Marine Transporters, LLC, 2024-0913 (La. App. 1st Cir. 4/17/25), 409 So.3d 1138, 1144, writ denied, 2025-00649 (La. 9/24/25), 417 So.3d 61, cert. denied, --- S.Ct. ---, 2026 WL 568290 (2026) (citing Bradford v. CITGO Petroleum Corp., 2017-296 (La. App. 3d Cir. 1/10/18), 237 So.3d 648, 659, writ denied, 2018-0272 (La. 5/11/18), 241 So.3d 314). General causation refers to whether a substance is capable of causing a particular injury or condition in the general population, while specific causation refers to whether a substance caused a particular individual's injury.¹⁰ Costanza, 409 So.3d at 1144 (citing Knight v. Kirby Inland Marine Inc., 482 F.3d 347, 351 (5th Cir. 2007)).

Standard of Review

In a workers’ compensation case, as in other civil cases, the appellate court's review of factual findings is governed by the manifest error or clearly wrong standard. Williams, 30 So.3d at 761. The OWC's finding regarding causation is a factual finding. Id. at 762. The two-part test for the appellate review of a factual finding is: (1) whether there is a reasonable factual basis in the record for the finding of the district court, and (2) whether the record further establishes that the finding is not manifestly erroneous. Id. at 761-62 (citing Mart v. Hill, 505 So.2d 1120, 1127 (La. 1987)).

If there is no reasonable factual basis in the record for the OWC's finding, no additional inquiry is necessary. However, if a reasonable factual basis exists, an appellate court may set aside an OWC's factual finding only if, after reviewing the record in its entirety, it determines the OWC's finding was clearly wrong. Williams, 30 So.3d at 762. If an appellate court concludes that the factual findings are clearly wrong, the mere fact that some record evidence appears which would furnish a reasonable factual basis for the contested findings does not require affirmance. Mart, 505 So.2d at 1127. If the findings are reasonable in light of the record reviewed in its entirety, an appellate court may not reverse even though convinced that had it been sitting as the trier of fact, it would have weighed the evidence differently. Williams, 30 So.3d at 762 (citing Rosell v. ESCO, 549 So.2d 840, 844 (La. 1989)). Where there are two permissible views of the evidence, the factfinder's choice between them cannot be manifestly erroneous or clearly wrong. Williams, 30 So.3d at 762 (citing Stobart v. State through Department of Transportation and Development, 617 So.2d 880, 882-83 (La. 1993)). Nonetheless, an appellate court has a duty to determine if the factfinder was justified in his conclusions. Mart, 505 So.2d at 1127.

The OWC's Reasons for Judgment

In its reasons for judgment, the OWC first concluded that Pizzuto established that handling of and exposure to the nearly pure benzene product at his place of work was peculiar to his particular occupation, process, or employment. The OWC next found specific causation, determining that the medical evidence and testimony demonstrated that Pizzuto's exposure to benzene was the most likely cause of his cancer. Lastly, addressing the issue of general causation, the OWC concluded as follows:

Although benzene exposure is more commonly linked to lymphoma and leukemia type cancers, some studies have shown a relationship between benzene exposure and lung cancer. In 2012, the [International Agency for Research on Cancer (“IARC”)] issued a monograph refuting any causal links between benzene exposure and lung cancer. However, in 2018, the IARC issued a monograph stating, “On the basis of new data available since the last review, the Working Group also found limited evidence that benzene causes chronic myeloid leukemia and lung cancer, and acute myeloid leukemia in children. The Work[ing] Group's review of the large body of mechanistic studies took into account the key characteristics of carcinogens.” Thus, contrary to employer's contentions, there does exist in medical science a relationship between benzene and lung cancer. This information is from the IARC, [which] the group employer acknowledges is the “gold standard authoritative reviews ․ that collect all of the studies and articles on point and synthesizes, analyzes, and evaluates them.”

While there is not a consensus in the medical community about whether benzene exposure at any level can cause lung cancer, the scientific community is no longer rejecting that a relationship between benzene and lung cancer does exist. Science is constantly changing and advancing. New data supporting the relationship between benzene and lung cancer is a recently developing area of science. The change in the IARC monograph findings directly demonstrates this evolution.

In its reasons regarding general causation, the OWC specifically references and solely relies upon the IARC and two of its Monographs on the Evaluation of Carcinogenic Risks to Humans (“Monographs”): a 2012 Monograph identified as “Chemical Agents and Related Compounds, Volume 100 F, A Review of Human Carcinogens” (“2012 Monograph”) and a 2018 Monograph identified as “Benzene, Volume 120 (“2018 Monograph”).” Notably, the OWC reasons only indicated that “there does exist in medical science a relationship between benzene and lung cancer” and did not conclude that there is a “causal relationship.” Moreover, the OWC acknowledged that there is no consensus in the medical community about whether benzene exposure at any level can cause lung cancer, but it stated that the “scientific community is no longer rejecting that a relationship between benzene and lung cancer does exist.” Notwithstanding, the judgment itself simply states that Pizzuto carried his burden to show “more likely than not that exposure [to benzene] caused his adenocarcinoma.”

General Causation: Is Benzene Capable of Causing Lung Cancer in the General Population?

The record contains exhibits as well as the testimony of multiple witnesses regarding Pizzuto's exposure to benzene during his employment.¹¹ While the OWC next examined specific causation and concluded that Pizzuto's exposure to benzene was the most likely cause of his lung cancer, the next step was to determine whether benzene causes adenocarcinoma, i.e., general causation. See Costanza, 409 So.3d at 1144 (citing Knight, 482 F3d at 351). Before an association or relative risk is used to make a statement about the probability of individual (specific) causation, the inferential judgment—that the association is truly causal rather than spurious—is required, as an agent cannot be considered to cause the illness of a specific person unless it is recognized as a cause of that disease in general. Michael D. Green, et al., “Reference Guide on Epidemiology” in Reference Manual on Scientific Evidence, Third Edition (2011) by the Federal Judicial Center (“Reference Manual”), 611.¹² Accordingly, we first address whether the OWC was manifestly erroneous in concluding that exposure to benzene causes adenocarcinoma by evaluating the evidence presented.

Before reviewing and analyzing the evidence presented regarding general causation, it is helpful to have a general understanding of epidemiology, which focuses on the question of general causation, rather than that of specific causation. See Norris v. Baxter Healthcare Corp., 397 F.3d 878, 882 (10th Cir. 2005) (noting epidemiology is the best evidence of general causation in toxic tort cases). Epidemiology is the field of public health and medicine that studies the incidence, distribution, and etiology of disease in human populations. The purpose of epidemiology is to better understand disease causation and to prevent disease in groups of individuals. Epidemiology assumes that disease is not distributed randomly in a group of individuals and that identifiable subgroups, including those exposed to certain agents, are at increased risk of contracting particular diseases. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 551. Epidemiology cannot prove causation; rather, causation is a judgment for epidemiologists and others interpreting the epidemiologic data. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 598.

Epidemiologic evidence identifies agents that are associated with an increased risk of disease in groups of individuals, quantifies the amount of excess disease that is associated with an agent, and provides a profile of the type of individual who is likely to contract a disease after being exposed to an agent. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 552. An association identified in an epidemiologic study may or may not be causal. Assessing whether an association is causal requires an understanding of the strengths and weaknesses of the study's design and implementation, as well as a judgment about how the study's findings fit with other scientific knowledge. All studies have “flaws” in the sense that they have limitations that add uncertainty about the proper interpretation of the results. Some flaws are inevitable given the limits of technology, resources, the ability and willingness of persons to participate in a study, and ethical constraints. In evaluating epidemiologic evidence, the key questions involve the extent to which a study's limitations compromise its findings and permit inferences about causation. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 552-53.

Importantly, an association is not equivalent to causation nor does it necessarily imply a causal effect. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 552-53 n.7. While association describes the relationship between two events that occur more frequently together than one would expect by chance, causation is used to describe the association between two events when one event is a necessary link in a chain of events that results in the effect. Alternative causal chains may exist that do not include the agent but that result in the same effect. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 552 n.7. For factual causation to exist, an agent must be a necessary link in a causal chain sufficient for the outcome. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 552-53 n.7 (citing Restatement (Third) of Torts: Liability for Physical Harm § 26 (2010)). Epidemiologic methods cannot deductively prove causation; however, epidemiologic evidence can justify an inference that an agent causes a disease. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 553 n.7.

Once an association has been found between exposure to an agent and development of a disease, researchers consider whether the association reflects a true cause-effect relationship.¹³ Green et al., “Reference Guide on Epidemiology” in Reference Manual, 597. In assessing causation, researchers first look for alternative explanations for the association, such as bias or confounding factors.¹⁴ Green et al., “Reference Guide on Epidemiology” in Reference Manual, 598. If alternative explanations are not present, researchers apply the Bradford Hill criteria to evaluate whether an agent could be a cause of a disease. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 599-600; Wagoner v. Exxon Mobil Corp., 813 F.Supp. 2d 771, 803 (E.D. La. 2011) (“[T]he Bradford Hill criteria has been widely acknowledged as providing an appropriate framework for assessing whether a causal relationship underlies a statistically significant association between an agent and a disease.”). The Bradford Hill factors are: (1) temporal relationship; (2) strength of the association; (3) dose-response relationship; (4) replication of findings; (5) biological plausibility; (6) consideration of alternative explanations; (7) cessation of exposure; (8) specificity of the association; and (9) consistency with other knowledge. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 600. These factors are not rigidly applied in a general causation analysis, but instead provide guidance for an expert “[d]rawing causal inferences after finding an association.” Green et al., “Reference Guide on Epidemiology” in Reference Manual, 600.

The Monographs

Through the Monographs, the IARC stated that it sought to identify the causes of human cancer with the objective of preparing and publishing in the form of Monographs critical reviews and evaluations of evidence on the carcinogenicity of a wide range of human exposures.¹⁵ The IARC further stated that the Monographs represent the first step in carcinogen risk assessment, which involves the examination of all relevant information to assess the strength of the available evidence that an agent could alter the age-specific incidence of cancer in humans. The international working groups of experts participating in both Monographs reviewed all pertinent epidemiological studies and cancer bioassays in experimental animals, with those judged as being inadequate or irrelevant to the evaluation sometimes cited but not summarized.

According to the 2012 and 2018 Monographs, there is sufficient evidence that benzene is carcinogenic to humans. Deleo v. Bayou Lafourche Fresh Water District, 2002-0513 (La. App. 1st Cir. 2/14/03), 846 So.2d 17, 18-19, writ denied, 2003-0695 (La. 5/16/03), 843 So.2d 1132 (“Benzene is a known carcinogen.”). The 2012 Monograph unequivocally stated, “Benzene causes acute myeloid leukaemia/acute non-lymphocytic leukaemia[,]” and also observed a positive association (sometimes referred to as “limited evidence” in the Monograph) between exposure to benzene and acute lymphocytic leukemia, multiple myeloma, and nonHodgkin's lymphoma. The 2018 Monograph's findings fully supported these particular conclusions of the 2012 Monograph.

As noted by the OWC, the 2012 Monograph found that the evidence from occupational cohort studies of an association between benzene exposure and lung cancer available at that time was judged to be “inadequate,” indicating that the available studies at the time were of insufficient quality, consistency, or statistical power to permit a conclusion regarding the presence or absence of a causal association between exposure and cancer or that no data on cancer in humans is available. However, in the 2018 Monograph, which was the IARC'S sixth evaluation of the carcinogenicity of benzene, the IARC found “limited evidence that benzene causes ․ lung cancer” on the basis of new data available. (Emphasis in original.) The 2018 Monograph defined “Limited evidence of carcinogenicity” as an observed positive association between exposure and cancer for which a causal interpretation is considered to be credible, but chance, bias, or confounding factors could not be ruled out with reasonable confidence. This is in comparison to “Sufficient evidence of carcinogenicity” in which a causal relationship is considered established between exposure to the agent and human cancer, i.e., a positive relationship has been observed between the exposure and cancer in studies in which chance, bias, and confounding factors could be ruled out with reasonable confidence.

In finding limited evidence of carcinogenicity, the 2018 Monograph specifically identified the following occupational cohort and general-population cohort and case-control studies, all of which had a confidence interval of 95%,¹⁶ and provided the corresponding summaries. Notably, inclusion of a study in the Monographs does not imply acceptance of the adequacy of the study design or of the analysis and interpretation of the results, and the limitations were clearly outlined at the end of the study description as were the reasons for not giving a particular study further consideration.

“Bond et al. (1986)” studied mortality among 956 workers from a chemicals production plant in Michigan exposed to benzene, and updated results for this cohort were reported in “Collins et al. (2015).” Among the 956 workers who had been employed for a month or longer during the years 1938-1978 and followed up through 1982, overall cancer of the lung was not increased. In the update of the cohort, it was reported that among 2,266 United States chemical manufacturing plant workers beginning employment during the years 1940-1982 and followed up through 2009, no excess risk for cancer of the lung was observed. The 2018 Monograph noted that the “Bond et al. (1986)” cohort study had additional exposure types that were addressed in the analysis by removing workers exposed to arsenic, asbestos, or high levels of vinyl chloride.

“Collins et al. (2003)” reported that among 4,417 chemical manufacturing hourly workers in Illinois who began employment during the years 1940-1977 and were followed up through 1997, a 60% excess risk of cancer of the lung was observed with cumulative exposure to benzene at more than 6 parts per million-years (“ppm-years”).¹⁷

“Sorahan et al. (2005)” reported that among 5,514 workers exposed to benzene in 233 factories in the United Kingdom during the years 1966-1967 or earlier and followed up for mortality during the years 1968-2002, a significant increase in mortality from cancer of the lung was observed. Noted limitations of this study were that some of the deaths coded as cancer of the lung may actually have been due to mesothelioma and some cancer cases may have been missed or misclassified.

“Wong (1987a, b)” reported on a study of 4,602 workers exposed to benzene and 3,074 unexposed workers in several chemical plants in the United States, with “Wong (1987a)” specifically reporting results for exposure characterized as intermittent or continuous. “Wong (1987b),” a companion paper, presented results in the same population by cumulative exposure category for select outcomes. “Wong (1987a, b)” reported a standardized mortality ratio of 1.12; however, no exposure-response relation was observed.

“Wong et al. (1993)” reported data for a cohort of gasoline distribution workers in the United States – 9,026 of whom were land-based and 9,109 workers who operated on marine vessels between 1946 and 1985 – whose mortality outcomes were followed until 1989. A standardized mortality ratio of 0.66 was observed among land-based workers and 1.07 among marine workers.

“Linet et al. (2015)” updated the data on cancer among Chinese workers exposed to benzene, which was studied previously in “Hayes et al. (1996).”¹⁸ The study involved 74,827 benzene-exposed and 35,504 unexposed Chinese workers in spray and brush painting (coatings), rubber, chemical, shoemaking, and other industries. Workers exposed to benzene demonstrated a significant excess of mortality from cancer of the lung, with the highest relative risk for mortality being from workers in the rubber and coating industries.¹⁹ Relative risks for death were significantly elevated and of the same magnitude in the early (1972-1987) and later (1988-1999) follow-up periods. Mortality from cancer of the lung was in excess in the cohort overall due to men but not women and was increased among workers with greater estimated cumulative exposure (a relative risk of 1.7 for those with greater or equal to 400 ppm-years exposure verses no exposure). Noted strengths of the study were its large size and a 28-year follow-up. Noted limitations of the study were that exposure was dichotomized into exposed and unexposed only, with no further classification, and there was no control for potential confounding factors such as smoking or other occupational exposures. However, it was observed that the associations were similar in men and women, with the prevalence of smoking being much lower among Chinese women.

“Koh et al. (2011)” involved a study of 8,866 male workers at seven petrochemical plants producing or using benzene. No excess risk in cancer of the lung mortality or incidence in the workers was observed. Noted limitations were the small number of cases, the presence of healthy worker effect, lack of control for smoking, and the short follow-up period.

“Koh et al. (2014)” reported on a study of 14,698 male workers who were members of a regional petrochemical plant maintenance workers union from 2002-2007 and who worked at plants producing or using benzene. The study did not find an excess in cancer of the lung mortality or incidence in the workers. While the study had good coverage of the target population, it was limited by the short follow-up period, no quantitative exposure assessment, and lack of available tobacco exposure history.

“Bove et al. (2014)” reported on cancer of the lung in a cohort study of 309,901 United States military personnel who began service from 1975 to 1985 (most of whom were younger than 55 years at the end of the follow-up) and who were exposed to contaminated drinking water, with no quantitative estimate of benzene or other agents being derived. There was an elevated hazard ratio (which was adjusted for sex, race, rank, and education, but not for smoking) for cancer of the lung among personnel exposed to drinking water contaminated by benzene and other solvents. The elevation was due entirely to those with higher cumulative exposures, and the standardized mortality ratio was 0.92.

Several other pertinent studies were identified that were available at the time of the previous review for the 2012 Monograph, to wit: “Tsai et al. (1983)” reporting a standardized mortality ratio of 0.52 in a study of refinery workers; “Greenland et al. (1994)” observing an odds ratio of 0.58 when directly comparing exposed transformer repair workers with the indirectly exposed or unexposed counterparts; and “Bulbulyan et al. (1999)” reporting a standardized mortality ratio of 0.7 among female bookbinders.

“Villeneuve et al. (2014)” reported on a case-control study of 445 incident cases of cancer of the lung, trachea, and bronchus and 948 hospital- and population-based controls in Toronto from 1997-2002. The study assessed ambient volatile organic compounds from outdoor air pollution, including benzene. Information was collected on confounding factors including tobacco use and exposure to cigarette smoke. An interquartile range increase in estimated time-weighted average benzene exposure across previous residences was associated with cancer of the lung only when using population-based controls. Associations were also positive when using exposure ten years prior to interview, or at the time of the interview but smaller in magnitude. The limitations of this study were low participation rate of population controls and lung cancer cases.

“Yuan et al. (2014)” reported on a nested case-control study of 82 cases of cancer of the lung and 83 controls among lifelong nonsmoking Chinese men, aged 45-64 years at enrollment in the Shanghi Cohort Study. Urinalysis was conducted and the report found that elevated S-phenylmercapturic acid (“SPMA”), a metabolite of benzene, was associated with an increased risk of squamous cell carcinoma of the lung. Noted limitations of the study included the small study size, and although SPMA is specific to benzene, SPMA was measured at a single point in time and is not a good proxy for occupational benzene exposure.

Accordingly, in the 2018 Monograph, the IARC observed a positive association between exposure to benzene and lung cancer for which a causal interpretation is considered to be credible, but chance, bias, or confounding factors could not be ruled out with reasonable confidence. As noted in the Reference Manual, “an association is not equivalent to causation.” Green et al., “Reference Guide on Epidemiology” in Reference Manual, 552 (emphasis in original). At best, the 2018 Monograph established that it is possible that benzene causes lung cancer.

Dr. Ernest Chiodo

Pizzuto presented the deposition testimony of Dr. Chiodo, who was tendered as an expert in internal medicine, occupational medicine, and toxicology and as a certified industrial hygienist.²⁰

In his expert report, Dr. Chiodo summarily concluded that “[e]vidence based medicine supports the assertion that to a reasonable degree of medical certainty (more likely than not) benzene exposure causes lung cancer[,]” citing two articles utilizing a 1996 Chinese cohort study (“Chinese study”) - Song-Nian, Yin, Hayes, Richard B., Linet, Martha S., et al. An Expanded Cohort Study of Cancer Among Benzene-exposed Workers in China. Environ Health Perspect. 1996:104(6): 1339-134 and Hayes, Richard B., Song-Nian, Yin, Dosemeci, Mustafa, et al. Mortality among Benzene-exposed Workers in China. Environ Health Perspect. 1996:104(6): 1349-1352 – and a third article presenting a condensed history of the benzene bioassay story – Huff, James. Benzene-induced Cancers: Abridged History and Occupational Health Impact. Int J Occup Environ Health. 2007:13(2):213-221.

Dr. Chiodo testified that the Chinese study and the corresponding Hayes and Yin articles corroborated his opinion.²¹ The Yin article noted a statistically significant excess for lung cancer, finding that workers exposed to benzene had a relative risk of 1.4. As explained in the Reference Manual, relative risk is the ratio of the risk of disease or death among people exposed to an agent to the risk among the unexposed.²² A relative risk of 1 would indicate no association between exposure and disease, according to the Reference Manual. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 627. While noting that mortality from lung cancer was significantly increased due to a significant excess among males, the Yin article concluded that “benzene is possibly also associated with excess risk of․ lung cancer among humans.”

The Hayes article first noted that benzene exposure has been related to an increased risk of acute nonlymphocytic leukemia and sometimes to other lymphohematopoietic malignancies in numerous occupational studies. The article observed that the 1981 iteration of the Chinese study observed significantly elevated standardized mortality ratios among exposed compared to nonexposed workers for leukemia, with a standardized mortality ratio of 5.74, and for lung cancer, with a standardized mortality ratio of 2.31. A standardized mortality ratio is the ratio of the incidence of death observed in the study population to the incidence of death that would be expected if the study population had the same incidence of death as some selected standard or known population. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 628.

The Hayes article acknowledged that benzene has been found to cause cance at multiple sites, suggesting that excesses of hematological and nonhematological tumors in humans could be causally related to exposure. The article then observed that lung cancer mortality showed an exposure-response pattern in the study, noting that benzene exposure had not previously been related to lung cancer. Specifically, the article included a table reflecting the following data for individuals with cancer deaths relating to the “[t]rachea, broncus, and lung”: 41 individuals with no exposure to benzene died, reflecting a relative risk of 1.0; 10 individuals with less than 10 ppm-years cumulative exposure to benzene, reflecting a relative risk of 1.2; 13 individuals with 10-39 ppm-years cumulative exposure to benzene, reflecting a relative risk of 1.0; 19 individuals with 40-99 ppm-years cumulative exposure to benzene, reflecting a relative risk of 1.4; 38 individuals with 100-400 ppm-years cumulative exposure to benzene, reflecting a relative risk of 1.4; and 41 individuals with over 400 ppm-years cumulative exposure to benzene, reflecting a relative risk of 1.7.

The Hayes article specifically acknowledged that “[s]ome benzene-exposed workers in this cohort were employed in occupations that have previously been associated with increased lung cancer risk[,]” which included painters and leather workers. In fact, the 2018 Monograph, referencing the updated data from the cohort in “Linet et al. (2015),” similarly noted the lack of control for potential confounding factors such as smoking and other occupational exposures. Moreover, the Hayes article stated that further studies were planned to determine if the association of benzene with lung cancer risk was due specifically to benzene or to other types of exposure, including tobacco use. The Hayes article ultimately concluded that mortality due to lung cancer increased in direct relation to cumulative benzene exposure among industrial workers in China but indicated that the results were preliminary and that further investigations were planned to characterize the scope of benzene as a carcinogen in the cohort.

Dr. Chiodo was asked about the language used in the Hayes article about the results being “preliminary” and that further studies were planned to determine if the association of benzene with lung cancer risk was due specifically to benzene or to other types of exposure. Dr. Chiodo responded as follows:

First off, the analogy with this article is not the words. See lawyers think about words. I'm a lawyer too. ․ but the article they're holding is the numbers, so words in a medical article are like dicta in a lawsuit.

The numbers are like the holding, so they may say we think this is preliminary, whatever words they want to use for whatever ․ reason. Maybe it's preliminary for what purpose. Well, preliminary because we're about to close down all these factories in China.

It's preliminary to that consideration. That could be that. ․ [T]hat might be why ․ they use the words, but the ․ finding is the increased risk, number of deaths in people with lung cancer. The standard mortality rate ․ for lung cancer in ․ workers exposed to benzene[ ] is [2.31] times greater than non-benzene exposed workers.[23]

That is the finding of the study. That is like the holding in a lawsuit where the words are like the dicta in a lawsuit. The dicta doesn't mean anything. ․ So the numbers are the holding, the words are dicta. Why they use the word preliminary? I don't know. I think it's very – the numbers are conclusive.

When asked about the limitations of the Chinese study, specifically the failure to account for the confounding factor of smoking/tobacco use, Dr. Chiodo referenced the Yin article, which described a relative risk of 1.4, and stated “I might suspect they did sit down there and consider smoking.” He then stated as follows:

They have ․ a large number of workers in the population. They're looking at other factory workers exposed to benzene. ․

There are factory workers not exposed to benzene. They tend to have the same socioeconomic level. They tend to smoke. So I think that․ the finding of the increased relative risk in the one study of [1.4] and of the standard mortality [ratio] of [2.31] corroborates my opinion.[24]

․

[T]hey tend to be having the same type of smoking habit in benzene - factory workers exposed to benzene and factory workers not exposed to benzene.

Dr. Chiodo admitted that if presented with a person with lung cancer who was a heavy smoker and also was exposed to benzene, he could not say that more likely than not lung cancer was caused by benzene because he would not be able to minimize the contribution of the smoking in comparison to the benzene exposure. When asked about the deaths attributable to lung cancer in the study and how he would know that any of the deaths included heavy smokers, Dr. Chiodo responded that if they were all heavy smokers, the authors probably would not have included it.

Notwithstanding Dr. Chiodo's testimony, both the Hayes article cited by Dr. Chiodo and the 2018 Monograph noted the lack of control for the confounding factor of smoking in the Chinese study. Moreover, the 2015 updated article on the Chinese study, Linet, Martha S., Song-Nian, Yin, Gilbert, Ethel S. et al. A Retrospective Cohort Study of Cause-Specific and Incidence of Hematopoietic Malignancies in Chinese Benzene-Exposed Workers Int. J. Cancer. 2015:137:2184-2197, specifically addressed the confounding issue of smoking, stating that neither the extended cohort follow-up study nor the 1996 study referenced in the Hayes article had the data needed to take account of potential confounders such as smoking. The Linet article further admitted that smoking differences between exposed and unexposed workers may have contributed to the elevated lung cancer risks observed by the authors, additionally noting that an observed pattern suggested confounding by smoking.

When asked about the Linet article's admission that smoking was not considered in the analysis, Dr. Chiodo stated:

Well, first off, I don't know that that's the case and –

․

-- if you want to sit down ․ and show me the wordage, I think what she's probably gonna say is we didn't specifically, because we're comparing people that are factory workers with people ․ [who] are not exposed to benzene with people ․ [who] are factory workers exposed to benzene ․ and each side tends to smoke a lot. That's probably what she says.

An examination of the statements made by the authors in the Linet article demonstrate that Dr. Chiodo's suppositions are not accurate.

Little testimony was given by Dr. Chiodo on the Huff article, which “presents a condensed history of the benzene bioassay story with mention of benzene-associated human cancers.” A bioassay is a test for measuring the toxicity of an agent by exposing laboratory animals to the agent and observing the effects. Bernard D. Goldstein, et al., “Reference Guide on Toxicology” in Reference Manual, 680. Dr. Chiodo stated that, “I cited [the Huff article] because I believe it supported my opinion at the time, even though I don't remember what's in the article.”

Dr. Chiodo was asked about the IARC and the Monographs. He testified that he didn't know “one way or the other” if the IARC working group came to the same conclusion that he did regarding whether benzene exposure causes lung cancer. He stated that the IARC working group would be looking at a level of statistical significance as opposed to the level required in a lawsuit (more likely than not). Dr. Chiodo further stated that if someone is concluding differently, they were using that wrong level of analysis than proper in this case.

Recognizing articles finding that benzene does not cause lung cancer, Dr. Chiodo testified that “peer reviewed medical articles are written at the level of a [95%] or greater probab[ility]. That is somebody might have done a study and they ․ did not find that the results of their study were statistically significant at a [95%] or greater probability.” Dr. Chiodo quoted the Reference Manual, stating that “[a] common error made by lawyers, judges, and academics is to equate the level of alpha with the legal burden of proof. Thus, one will often see a statement that using an alpha of [0.05] for statistical significance imposes a burden of proof on the plaintiff far higher than the civil burden of a preponderance of the evidence (i.e., greater than 50%).” Green et al., “Reference Guide on Epidemiology” in Reference Manual, 577 n.81. However, Dr. Chiodo testified that he provided peer reviewed literature he believed supported the assertion that benzene causes lung cancer, not only at the more likely than not level, but at a 95% or greater probability.”

As further explained in the Reference Manual, “statistically significant” does not convey the magnitude of the association found in the study or indicate how statistically stable that association is. A confidence interval shows the boundaries of the relative risk based on selected levels of alpha or statistical significance.²⁵ The confidence interval does not provide the range within which the true risk must lie. Rather, the confidence interval reveals the likely range of risk estimates consistent with random error. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 580. Calculation of a confidence interval permits a more refined assessment of appropriate inferences about the association found in an epidemiologic study. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 579. Generally, the lower the alpha chosen (and therefore the more stringent the exclusion of possible random error), the wider the confidence interval.²⁶ Green et al., “Reference Guide on Epidemiology” in Reference Manual, 580. Confidence intervals are simply a statistical device for analyzing error that may result from random sampling. Systematic errors, i.e., bias, in the design or data collection are not addressed by statistical methods, such as confidence intervals or statistical significance. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 585 n.106.

Moreover, even where one concludes that findings of a study are statistically stable and that biases have not created significant error, additional considerations remain.²⁷ As the Reference Manual repeatedly notes, an association does not necessarily mean a causal relationship exists. To make a judgment about causation, a knowledgeable expert must also consider the possibility of confounding factors. The expert must also evaluate several criteria to determine whether an inference of causation is appropriate. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 591. Notably, the 2018 Monograph relied upon cohorts and case studies with 95% confidence intervals, but it made specific mentions of the limitations of the studies when applicable, including confounding factors, in its finding of limited evidence of carcinogenicity regarding the association of benzene and lung cancer. Dr. Chiodo largely ignored or provided unfounded assumptions for confounding factors in the studies and articles he selected to support his opinion.

Dr. Matthew Schuette

Pizzuto also presented the testimony of his treating pulmonologist, Dr. Matthew Schuette. Primarily, Dr. Schuette testified as to specific causation. He observed that Pizzuto was not a smoker and had not reported any exposure to anything commonly associated with lung cancer. Dr. Schuette also testified that around 10% of lung cancers in general are idiopathic, meaning no known cause. However, Dr. Schuette believed that due to Pizzuto's lack of exposure to known causes of lung cancer, coupled with reports showing “a possible association between benzene and lung cancer,” it was “safe to say that more likely than not that the benzene was the cause of his lung cancer.” Dr. Schuette's opinion in this regard only addressed the issue of specific causation.

As to general causation, Dr. Shuette compared the relative risks of benzene exposure and leukemia and lymphoma to the relative risks of benzene exposure and lung cancer. He testified that the risks were clearly higher when looking at the leukemia and lymphoma, noting that the “numbers [were] not as good with lung cancer” but that there were “a number of studies where there is at least a suggestion[.]”²⁸ Dr. Schuette testified that he believed there was “enough evidence out there to suggest that there could be a relationship here.” Dr. Schuette agreed that it was “not accepted universally medically that benzene exposure is associated with contracting lung adenocarcinoma” and that there was a “legitimate debate” regarding that point.

Dr. Matthew D. McElveen

Pizzuto also presented the testimony of Dr. Matthew D. McElveen, his treating oncologist. According to Dr. McElveen, some lung cancers are considered idiopathic, with about 9-10% of cases having no known cause. He testified that while he was aware some studies inferred exposure to benzene is a possible cause of lung cancer, none of the studies he read stated that benzene causes lung cancer. Additionally, he testified that, based on current science, there was a possibility that benzene exposure causes lung cancer.

In view of the entirety of the record, particularly the above and forgoing evidence and testimony regarding general causation, we find the evidence only shows a possibility that benzene exposure causes lung cancer or, at best, that the probabilities are equally balanced. See Buxton, 23 So.3d at 291 (citing Prim, 297 So.2d at 422); Alvis, 316 So.3d at 58. As to general causation, Dr. Schutte stated that there “could be a relationship” between benzene exposure and lung cancer, acknowledging there was a “legitimate debate” on the issue. Dr. McElveen only testified that it was possible that benzene exposure causes lung cancer. Neither of these experts provided sufficient evidence for Pizzuto to carry his burden of proof.

Moreover, Dr. Chiodo's general causation testimony, which was not cited by the OWC in its reasons as to general causation,²⁹ was neither reasonable nor well-founded. See Watts v. Watts, 5 52 So.2d 73 8, 740 (La. App. 1st Cir. 1989); see also Head v. Head, 30,585 (La.App.2d Cir.05/22/98), 714 So.2d 231, 234. Dr. Chiodo testified that the Chinese study and the corresponding Hayes and Yin articles corroborated his opinion that “[e]vidence based medicine supports the assertion that to a reasonable degree of medical certainty (more likely than not) benzene exposure causes lung cancer.” However, as stated supra. Dr. Chiodo largely ignored the Chinese Study's failure to account for confounding factors in his opinion and testimony, which failure was expressly acknowledged in the Hayes and Linet articles. He did not consider the Monographs or the Linet article, which article provided updated data on the Chinese study previously reported in the Hayes article and which observed a pattern that suggested confounding by smoking. Additionally, when asked about the impact of the confounding factors, Dr. Chiodo provided unfounded assumptions in order to ignore the impact. We find that the OWC abused its discretion to the extent it gave any weight to the general causation testimony of Dr. Chiodo. See Williams, 30 So.3d at 762-63.

Without evidence of a demonstrated causal link between benzene exposure and lung cancer, Pizzuto did not establish that more probably than not his exposure to benzene caused his adenocarcinoma and that his adenocarcinoma was an occupational disease.³⁰ See Alvis, 316 So.3d at 58; Crear, 417 So.3d 808; also see Arrant, 169 So.3d at 309. In fact, the OWC's reasons for judgment and the judgment itself failed to conclude that there was a demonstrated causal link between exposure to benzene and lung cancer or that Pizzuto established the existence of a causal link between exposure to benzene and lung cancer by a reasonable probability. See Crear, 417 So.3d at 808 (citing Arrant, 169 So.3d at 309 and Williams, 30 So.3d at 762). Rather, the OWC acknowledged, “there is not a consensus in the medical community about whether benzene exposure at any level can cause lung cancer, the scientific community is no longer rejecting that a relationship between benzene and lung cancer does exist.”

We find that the evidence and testimony did not provide a reasonable factual basis for a finding of general causation, i.e., that more likely than not benzene exposure causes adenocarcinoma. Therefore, we find that the OWC's ruling that “more likely than not [Pizzuto's] exposure [to benzene] caused his adenocarcinoma[,]” implicitly finding that benzene exposure more likely than not causes adenocarcinoma, was clearly wrong. See Williams, 30 So.3d at 761-62; Mart, 505 So.2d at 1127. Accordingly, we find merit in Defendants’ second assignment of error and pretermit Defendants’ remaining assignment of error.

CONCLUSION

For the above and foregoing reasons, we reverse the November 7, 2022 judgment, and judgment is hereby rendered in favor of defendants, Chalmette Refining, LLC and Liberty Insurance Company, dismissing with prejudice all claims of plaintiff, Joseph Michael Pizzuto. We further vacate the November 30, 2023 judgment awarding workers’ compensation benefits and costs to plaintiff, Joseph Michael Pizzuto.³¹ All costs of this appeal are assessed to plaintiff, Joseph Michael Pizzuto.

NOVEMBER 7, 2022 JUDGMENT REVERSED AND RENDERED; NOVEMBER 30, 2023 JUDGMENT VACATED.

FOOTNOTES

1.   Defendant, PBF Holding Company, LLC, was dismissed on November 21, 2023, with prejudice. PBF Holding Company, LLC was not cast in judgment in either the November 7, 2022 or November 30, 2023 judgments.

2.   Specifically, La. R.S. 23:1031.1(A) provides an “employee who is disabled because of the contraction of an occupational disease as herein defined ․ shall be entitled to the compensation provided in this Chapter the same as if said employee received personal injury by accident arising out of and in the course of his employment.”

3.   Pizzuto was employed as a Stillman in the Sulfolane Unit for seven years preceding the filing of his claim. According to the Refinery's job description, a Stillman “performs or directs others to perform the work entailed in the safe, environmentally sound, continuous operation of the equipment and refinery operations within the assigned process unit(s) with a focus on maintaining efficient and reliable operations.”

4.   Live testimony from the following witnesses was presented at the July 2022 trial: Pizzuto, Wayne Lacombe (an industrial hygienist employed by the Refinery), and John Lenfant V (a nurse practitioner and supervisor at the Refinery's occupational health clinic). The parties submitted the depositions (and corresponding exhibits) in lieu of live testimony of the following witnesses: Weldon “Hugh” McCormick (a Refinery employee who worked as an operator and Stillman in the Sulfolane Unit); Melissa Trebucq Spencer (a Refinery employee who previously worked as operator in the Sulfolane Unit); Michael Menesses Sr. (a former Refinery employee who worked as an operator and Stillman in multiple units); and Clyde Powell Jr. (a former Refinery employee who worked as an operator and stillman in multiple units). Additionally, the parties submitted the depositions of the following medical experts in lieu of live testimony: Dr. Ernest Chiodo; Dr. Judd Shellito; Dr. Douglas Swift; Dr. Matthew Schuette (treating pulmonologist); and Dr. Matthew D. McElveen (treating oncologist).

5.   Defendants previously appealed the November 7, 2022 judgment; however, this court dismissed the appeal on the parties’ joint motion in light of the fact that La. Code Civ. P. art. 1915(A)(5) does not apply in workers’ compensation cases. Rhodes v. Lewis, 2001-1989 (La. 5/14/02), 817 So.2d 64, 67-68 (citing Smith v. UNR Home Products, 614 So.2d 54 (La. 1993)) (finding that workers’ compensation cases do not precisely involve “liability and damages” as referenced in La. Code Civ. P. art. 1915(A)(5), making Article 1915(A)(5) inapplicable to such cases).

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

7.   Any remaining arguments made by Defendants regarding the evaluation of Dr. Chiodo's methodology necessarily concern the relevance and weight of his testimony, which is within the broad discretion of the OWC. See Williams v. Temple Inland, Inc., 2008-2153 (La. App. 1st Cir. 12/23/09), 30 So.3d 760, 762-63 (effect and weight to be given expert testimony is within the broad discretion of the trial judge). See also Pierron v. Kimpton, 2024-313 (La. App. 5th Cir. 5/14/25), 415 So.3d 414, 429-30, writ denied, 2025-00756 (La. 10/1/25), 417 So.3d 569 (noting that the admissibility of evidence in a bench trial is different from the requirements of jury trials because a judge, unlike a jury, by virtue of the judge's training and knowledge of the law is fully capable of disregarding any impropriety).

8.   The testimony showed that Pizzuto was a non-smoker and had never smoked tobacco in any form. He had never been exposed to asbestos or radon gas in his private life. Pizzuto's treating oncologist, Dr. McElveen, opined that smoking, asbestos, and radon, which are known causes of lung cancer, were not the cause of Pizzuto's lung cancer.

9.   The Supreme Court in Jordan v. Travelers Insurance Company, 257 La. 995, 1008, 245 So.2d 151, 155 (1971), stated as follows:In describing burden of proof, the courts sometimes speak of proof to a ‘reasonable certainty’ or to a ‘legal certainty’; or of proof by evidence which is of ‘greater weight’ or ‘more convincing’ than that offered to the contrary; or (in the case of circumstantial evidence) of proof which excludes other reasonable hypotheses than the defendant's tort with ‘a fair amount of certainty’. Whatever the descriptive term used, however, proof by direct or circumstantial evidence is sufficient to constitute a preponderance, when, taking the evidence as a whole, such proof shows that the fact or causation sought to be proved is more probable than not.

10.   Evidence concerning specific causation in toxic tort cases is admissible only as a followup to admissible general-causation evidence. Costanza, 409 So.3d at 1144 (citing Knight v. Kirby Inland Marine Inc., 482 F.3d 347, 351 (5th Cir. 2007)). Thus, there is a two-step process in examining the admissibility of causation evidence in toxic tort cases. First, the district court must determine whether there is general causation. Second, if it concludes that there is admissible general-causation evidence, the district court must determine whether there is admissible specific-causation evidence. Id. However, in this case, all of the expert evidence regarding both general and specific causation was admitted by stipulation.

11.   There was evidence of the two occasions benzene was spilled and/or sprayed on Pizzuto. Pizzuto testified that he was exposed to benzene in the Sulfolane Unit and would smell benzene in the unit. He testified that he smelled benzene “on a regular basis, because we found some problems. Different leaks that we had that we could smell it though the years.” On cross-examination, Pizzuto clarified that it was often a “whiff” or a faint benzene smell that would last a few seconds and then it would be gone. However, there were times when it would last for twenty minutes. Pizzuto also testified that when it rained hard such that the unit was flooded or had “a torrential downpour” for thirty minutes, he could see a sheen of benzene floating on the water, which came from the ground and was sometimes caused by leaks in underground piping.

12.   Reference Manual on Scientific Evidence, Third Edition (2011) by the Federal Judicial Center (“Reference Manual”) was introduced as an exhibit at the trial on causation.

13.   When epidemiologists evaluate whether a cause-effect relationship exists between an agent and disease, they are using the term causation in a way similar to, but not identical to, the way that the familiar “but for” test is used in law for cause in fact. Epidemiologists use causation to mean that an increase in the incidence of disease among the exposed subjects would not have occurred had they not been exposed to the agent. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 597-98.

14.   A confounding factor is defined in the Reference Manual as “[v]ariables that are related to both exposure to a toxic agent and the outcome of the exposure. A confounding factor can obscure the relationship between the toxic agent and the adverse health outcome associated with that agent.” Bernard D. Goldstein, et al., “Reference Guide on Toxicology” in Reference Manual, 681.

15.   The 2012 and 2018 Monographs state as follows:In 1969, the [IARC] initiated a programme on the evaluation of the carcinogenic risk of chemicals to humans involving the production of critically evaluated monographs on individual chemicals. The programme was subsequently expanded to include evaluations of carcinogenic risks associated with exposures to complex mixtures, lifestyle factors and biological and physical agents, as well as those in specific occupations. The objective of the programme is to elaborate and publish in the form of monographs critical reviews of data on carcinogenicity for agents to which humans are known to be exposed and on specific exposure situations; to evaluate these data in terms of human risk with the help of international working groups of experts in carcinogenesis and related fields; and to indicate where additional research efforts are needed. The lists of IARC evaluations are regularly updated and are available on the Internet at http://monographs.iarc.fr/.

16.   The Reference Manual explains that in a cohort study, researchers define a study population without regard to the participants’ disease status. The cohort may be defined in the present and followed forward into the future or constructed retrospectively as of sometime in the past and followed over time toward the present. In either case, researchers classify the study participants into groups based on whether they were exposed to the agent of interest. In prospective studies, the exposed and unexposed groups are followed for a specified time period, and the proportions of individuals in each group who develop the disease of interest are compared. Green, et al., “Reference Guide on Epidemiology” in Reference Manual, 557.In case-control studies, the researcher begins with a group of individuals who have a disease (cases) and then selects a similar group of individuals who do not have the disease (controls), which should ideally come from the same source population as the cases. The researcher then compares the groups in terms of past exposures. If a certain exposure is associated with or caused the disease, a higher proportion of past exposure among the cases than among the controls would be expected. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 559.A confidence interval is a range of possible values calculated from the results of a study. If a 95% confidence interval is specified, the range encompasses the results one would expect 95% of the time if samples for new studies were repeatedly drawn from the same population. Thus, the width of the interval reflects random error. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 580.

17.   Parts per million is a unit used to express concentrations of chemicals in environmental media. Joseph V. Rodricks, “Reference Guide on Exposure Science” in Reference Manual, 541. According to the 2018 Monograph, exposure estimates are quantitative and usually expressed as averaged mean benzene intensity (ppm) or cumulative exposure (ppm-years). The 2018 Monograph further explained that the most common metrics of benzene exposure in industry-based studies are the presumption of occupational exposure by duration (years), average exposure intensity (ppm), or cumulative exposure, which is the intensity of exposure multiplied by the number of years exposed (ppm-years).

18.   “Linet et al. (2015)” superseded “Hayes et al. (1996)” and “Yin et al. (1996a)”. “Hayes et al. (1996)” and “Yin et al. (1996b)” previously reported data for this cohort.

19.   The corresponding article to “Linet et al. (2015),” which was admitted into evidence, further clarified that elevated incidence and mortality from lung cancer was consistently observed in painters (coatings industry), further noting that, in addition to benzene, painters may also be exposed to solvents, pigments, extenders, binders, additives, asbestos, and crystalline silica. Moreover, insulation and rubber workers may also be exposed to asbestos. Linet, Martha S., Song-Nian, Yin,Gilbert, Ethel S. et al. A Retrospective Cohort Study of Cause-Specific and Incidence of Hematopoietic Malignancies in Chinese Benzene-Exposed Workers Int. J. Cancer. 2015:137:2184-2197.

20.   Counsel for Defendants conceded that Dr. Chiodo was an expert in the three medical specialties and reserved rights on the remaining expert qualification.

21.   These are the same Chinese study and articles (“Hayes et al. (1996)” and “Yin et al. (1996b)”) referenced in the 2018 Monograph.

22.   The Reference Manual provides the following example:[I]f 10% of all people exposed to a chemical develop a disease, compared with 5% of people who are not exposed, the disease occurs twice as frequently among the exposed people. The relative risk is 10%/5% = 2.

23.   Notwithstanding Dr. Chiodo's testimony, the standardized mortality ratio of 2.31 does not reflect the updated and expanded study results reported in the 1996 Hayes article; rather, the 2.31 standardized mortality ratio was the noted result from the prior version of the Chinese study in 1981.

24.   See footnote 23, supra.

25.   To minimize false positives, epidemiologists use a convention that the p-value must fall below some selected level known as alpha or significance level for the results of a study to be statistically significant. Thus, an outcome is statistically significant when the observed p-value for the study falls below the preselected significance level. The most common significance level, or alpha, used in science is 0.05 (equivalently, a confidence level of 95%). A 0.05 value means that the probability is 5% of observing an association at least as large as that found in the study when in truth there is no association. Although 0.05 is often the significance level selected, other levels can and have been used. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 576-77, 580.

26.   At a given alpha, the width of the confidence interval is determined by sample size. All other things being equal, the larger the sample size, the narrower the confidence boundaries (indicating greater numerical stability). For a given risk estimate, a narrower confidence interval reflects a decreased likelihood that the association found in the study would occur by chance if the true association is 1.0. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 580-81.

27.   Chance, bias, and confounding factors can cause an association found in a study to be erroneous. Green et al., “Reference Guide on Epidemiology” in Reference Manual, 572.

28.   One of the studies that Dr. Schuette indicated “kind of suggested” some connection was a study from Iran, looking at benzene, toluene, and xylene concentrations in the air, and found that areas with higher concentrations had higher risks of lung cancer. However, the study or article was not attached as an exhibit to the deposition and was not otherwise identified further in the deposition.

29.   However, it is noted that the OWC relied upon the specific causation testimony of Dr Schutte, Dr. McElveen, and Dr. Chiodo in its finding that Pizzuto's “exposure to benzene was the most likely cause of his cancer.”

30.   We further note that our review reveals no reported Louisiana cases involving benzene exposure and lung cancer and no reported out-of-state or federal cases finding a causal link between benzene exposure and lung cancer.

31.   We necessarily pretermit Pizzuto's assignments of error regarding the November 30, 2023 judgment awarding certain workers’ compensation benefits and cost.

HESTER, J.