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Jeannette Lewis, Administratrix of the Estate of Nicholas Lewis, Sr v. Airco

July 15, 2011

JEANNETTE LEWIS, ADMINISTRATRIX OF THE ESTATE OF NICHOLAS LEWIS, SR., AND JEANNETTE LEWIS, INDIVIDUALLY, PLAINTIFF-APPELLANT/CROSS-RESPONDENT,
v.
AIRCO, INC., AS SUCCESSOR IN INTEREST TO AIR PRODUCTS AND CHEMICALS, INC.; ALLSTATE INSURANCE COMPANY; HONEYWELL INTERNATIONAL, INC., F/K/A ALLIED SIGNAL, INC., INDIVIDUALLY AND AS SUCCESSOR IN INTEREST TO ALLIED CHEMICAL CORPORATION; THE AMERICAN CHEMISTRY COUNCIL, F/K/A/ THE CHEMICAL MANUFACTURERS ASSOCIATION AND THE MANUFACTURING CHEMISTS ASSOCIATION; BRIDGESTONE/FIRESTONE, INC., INDIVIDUALLY AND AS SUCCESSOR IN INTEREST TO THE FIRESTONE TIRE & RUBBER COMPANY AND FIRESTONE PLASTICS COMPANY, A DIVISION OF THE FIRESTONE TIRE & RUBBER CO.; CONDEA VISTA COMPANY, INDIVIDUALLY AND AS SUCCESSOR IN INTEREST TO CONOCO, INC., INDIVIDUALLY AND AS SUCCESSOR IN INTEREST TO THE CONTINENTAL OIL COMPANY AND THOMPSON-APEX COMPANY AND CONOCO CHEMICALS; THE DOW CHEMICAL COMPANY, INDIVIDUALLY AND AS SUCCESSOR TO UNION CARBIDE CORP.; ETHYL CORPORATION; GENCORP, INDIVIDUALLY AND AS SUCCESSOR IN INTEREST TO GENERAL TIRE AND RUBBER COMPANY; POLYONE CORPORATION, F/K/A/ THE GEON COMPANY; GEORGIA GULF CORPORATION, AS SUCCESSOR IN INTEREST TO GEORGIA PACIFIC CORPORATION; GOODYEAR TIRE AND RUBBER COMPANY; GULF OIL CORPORATION, INDIVIDUALLY AND AS SUCCESSOR IN INTEREST TO CHEVRON U.S.A., INC.; PHARMACIA CORPORATION F/K/A MONSANTO COMPANY;*FN1 NEW JERSEY MANUFACTURERS INSURANCE CO.; OCCIDENTAL CHEMICAL CORPORATION, INDIVIDUALLY AND AS SUCCESSOR IN INTEREST TO OCCIDENTAL ELECTROCHEMICALS CORPORATION AND HOOKER CHEMICAL CORPORATION AND DIAMOND SHAMROCK CHEMICALS COMPANY AND DIAMOND CHEMICALS COMPANY AND DIAMOND SHAMROCK CORPORATION AND DIAMOND ALKALI COMPANY; OCCIDENTAL ELECTROCHEMICALS CORPORATION; OLIN CORPORATION; PACTIV CORPORATION; PANTASOTE, INC.; RHONE-POULENC, INC., INDIVIDUALLY AND AS SUCCESSOR IN INTEREST TO STAUFFER CHEMICAL COMPANY; THE SOCIETY OF THE PLASTICS INDUSTRY, INC.; TENNECO AUTOMOTIVE, INC.; TENNECO, INC.; EPEC POLYMERS, INC., AS SUCCESSORS TO TENNECO OIL COMPANY; SENTRY INSURANCE COMPANY; SHINTECH, INC.; UNION CARBIDE CORPORATION; UNIROYAL, INC., INDIVIDUALLY AND AS SUCCESSOR IN INTEREST TO U.S. RUBBER COMPANY; WHITTAKER CORPORATION, INDIVIDUALLY AND AS SUCCESSOR TO GREAT AMERICAN CHEMICAL CORPORATION; LIBERTY MUTUAL CORP., AND ZENECA, INC., F/K/A ICI AMERICAS, INC., DEFENDANTS, AND GOODRICH CORPORATION, F/K/A B.F. GOODRICH COMPANY; PPG INDUSTRIES, INC.; SHELL OIL COMPANY, INDIVIDUALLY AND AS SUCCESSOR IN INTEREST TO SHELL CHEMICAL, INC. AND SHELL CHEMICAL COMPANY; AND HEXION SPECIALTY CHEMICALS, INC., F/K/A/ BORDEN CHEMICAL, INC., DEFENDANTS-RESPONDENTS/ CROSS-APPELLANTS.



On appeal from the Superior Court of New Jersey, Law Division, Essex County, Docket No. L-10503-02.

Per curiam.

NOT FOR PUBLICATION WITHOUT THE APPROVAL OF THE APPELLATE DIVISION

Argued October 6, 2010

Before Judges Fuentes, Gilroy and Ashrafi.

This is an occupational-exposure, toxic-tort products liability action. Plaintiff, Jeannette Lewis, as Administratrix of the Estate of Nicholas Lewis, Sr. (Lewis), and individually, appeals from the December 15, 2008 order that barred the trial testimony of two of her liability experts; and from the February 5, 2009 order that denied her first motion for reconsideration and granted defendants Goodrich Corporation (Goodrich), PPG Industries, Inc. (PPG), Shell Oil Company (Shell), and Hexion Specialty Chemicals, Inc. (Hexion) (collectively, the defendants) summary judgment. Plaintiff also appeals from the March 20, 2009 order that denied her second motion for reconsideration.

Goodrich, PPG, and Shell cross-appeal from: the November 8, 2007 order that denied their motions for summary judgment on plaintiff's inadequate warning and civil conspiracy claims; the May 29, 2008 order that denied their motions for reconsideration; the December 15, 2008 order that denied their motions seeking to bar the testimony of two of plaintiff's liability experts; and the February 5, 2009 order that denied their motions for reconsideration of the order that denied summary judgment on plaintiff's inadequate warning claims based on the state-of-the-art defense. In a separate cross-appeal, Hexion appeals from the same orders as the other three defendants. We reverse on the appeal, and affirm in part and reverse in part on the cross-appeals.

I.

Prior to his death on December 31, 2000, Lewis had worked at the Pantasote, Inc., manufacturing facility in Passaic from 1961 to 1989. At its facility, Pantasote manufactured polyvinyl chloride (PVC)*fn2 resins and products. Vinyl chloride monomer*fn3 (VCM) (also known in the industry as vinyl chloride), an established carcinogen, is used in the production of PVC. Although occupational exposure to VCM has been causally associated with angiosarcoma (ASL), an extremely rare form of liver cancer, Lewis' cause of death was not from ASL, but rather from hepatocellular carcinoma (HCC), the most common form of liver cancer. In June 2003, believing that her husband's death was caused by exposure to VCM at the Pantasote facility, plaintiff filed a third-amended complaint against numerous parties, including those that manufactured and/or supplied VCM to Pantasote. The third amended complaint alleged causes of action sounding in negligence, products liability failure-to-warn of the risks caused by exposure to VCM, and civil conspiracy to fraudulently conceal those risks from the public.

On December 8, 2006, defendants filed motions for summary judgment on the fraud, civil conspiracy, and inadequate warning claims. On November 8, 2007, the court entered an order supported by an oral decision of October 25, 2007, granting the motions on the fraud claim, but denying the motions on the civil conspiracy and inadequate warning claims.

Also on December 8, 2006, defendants filed motions to exclude the trial testimony of plaintiff's four experts: Dr. Peter Infante, an epidemiologist; Dr. Howard Kipen, an occupational physician; Dr. David Groth, a pathologist; and James Jones, an industrial hygienist. On December 3, 2008, following an extensive N.J.R.E. 104(a) hearing in January and May 2008, the court granted the motion as to Infante and Kipen, determining that their conclusions that VCM exposure caused HCC were not sufficiently reliable, but denied the motion as to Groth, and as to Jones in part. The court entered a memorializing order on December 15, 2008.

In December 2008, defendants filed a motion for summary judgment contending that plaintiff could not prove general and specific causation without Infante's and Kipen's testimony.

Plaintiff filed a cross-motion for reconsideration of the order barring not only those two experts from testifying at trial, but also from barring Jones' testimony in part. On February 5, 2009, the trial court entered an order supported by an oral decision of February 3, 2009 denying plaintiff's motion for reconsideration and granting defendants' motions for summary judgment dismissing the complaint. On February 20, 2009, plaintiff filed a second motion for reconsideration. The court denied the motion on March 20, 2009.*fn4

II.

A. Vinyl Chloride and the Pantasote Facility and the Manufacturing Process.

Under normal pressure, VCM is a colorless flammable gas that has a mild sweet odor detectable at concentrations between 2,000 and 3,000 parts per million (ppm). According to a 1992 United States Environmental Protection Agency (USEPA) publication, inhaled VCM has been shown to increase the risk of developing ASL. Acute short term exposure to high levels of VCM affects the central nervous system. Long-term exposure is linked to liver damage and acroosteolysis, a degenerative disease causing loss of bone tissue in the hands and sensitivity to cold.

A-3509-08T3

Pantasote manufactured PVC resins and products, including vinyl film and sheeting, plasticized compounds, and thermoformed products. In 1957, Pantasote manufactured PVC resins in plant 1, and in 1960 Pantasote expanded production to include the larger plant 2. Until 1984, the facility used about 145,000 pounds of VCM a day to produce approximately 160,000 pounds of PVC, operating twenty-four hours a day, seven days per week, with three rotating shifts of workers. Goodrich, PPG, and Shell supplied VCM to the plant; Hexion did not. Pantasote ceased production in 1984 and demolished the plants.

Former Pantasote employees described the Pantasote facility and the PVC manufacturing process, in relevant part, as follows. Liquefied VCM was shipped to the facility in 10,000 to 22,000 gallon rail tank cars and unloaded to underground storage tanks. VCM was then piped in a closed system, from the storage tanks to polymerization reactors where, under pressure, it was combined with deionized water and a suspending agent to produce a PVC slurry. The polymerization process took between eight to twelve hours to complete. The reactor building was ventilated by ceiling and side-mounted fans, which forced air through ducts to bag houses and separators, prior to venting into the atmosphere.

After the polymerization process was completed, the PVC slurry was first transferred to outside storage tanks and then to a centrifuge and a dryer. The resultant powdered blend of PVC was air-conveyed through a dust collector, a sifter, and then to a bagging machine. The bags of PVC resin were stored in an adjacent warehouse for shipment, or for manufacturing products at the plant.

In the compounding process, bags of PVC resin were mixed with various additives such as plasticizers, fillers, and stabilizers, to produce PVC compounds. PVC products were manufactured in a semi-closed process in the calendaring buildings, where the compounded product was rolled into thin sheets of plastic. The buildings were ventilated by ceiling and hood exhaust fans.

B. The Workers' Exposure.

Lewis worked at the Pantasote plant as a service operator, chemical operator, or yardman. Although the record indicates that these titles were interchangeably used throughout his employment, Lewis was in charge of unloading VCM from the rail tank cars into the underground storage tanks, regenerating the water and demineralization units in the reactor buildings, transporting bags of PVC resin by forklift to various places within the plant, and measuring levels of PVC resins in the storage silos.

Lewis' co-workers testified at depositions that VCM had been released into the ambient air in the workplace at levels high enough to have had a detectable odor, either from leaks or from the normal manufacturing process. Joseph Genardi, a co-worker who performed the same job as Lewis, testified that he smelled VCM, which he described as having a "sweet smell," when he unloaded the rail tank cars in the closed pump house. It generally took Genardi three and one-half to five hours to unload the cars. The unloading process involved removing plugs from the tank car valves, attaching lines to the valves, opening the valves, and adjusting the air pressure to force VCM into the underground storage tanks. According to Genardi, there were "always leaks" in the valves, and sometimes in the fittings and gaskets, and when the transfer was completed, the lines to the tank cars were disconnected and any remaining VCM in the line was released and then vented outside the pump house.

Further, Genardi said he always smelled VCM in the reactor rooms, where he and Lewis worked. During a typical shift, Genardi entered the reactor room in plant 1 every hour, and entered the reactor room in plant 2 twice each shift. He was exposed to VCM when the reactors were opened, when slurry was dumped into the sewers, and when the seals in the reactor rooms were broken and VCM had to be vented out into the atmosphere because otherwise, the whole reactor building would become "filled with vinyl chloride."

Genardi also smelled VCM in the warehouse when he transported the bags of PVC resin by forklift. About three times a week a bag of PVC powder broke, spilling its contents into the warehouse. He said he "would actually smell, not strong, very faintly you would smell vinyl chloride and the resin . . . . It's a smell you never forget."

Michael Rapavi, Lewis' foreman, testified at depositions that prior to 1975, he often smelled VCM in the reactor rooms, in the vicinity of the slurry tanks, in the warehouse, and toward the front area of the plant if the wind was blowing in that direction and if VCM was being vented out from one of the buildings. Lewis' son, Nicholas Lewis, Jr., who began working at the facility in 1976, testified that once while he was walking outside plant 1, he asked his father what that odor was, and his father responded that he "believed" it was VCM. Lewis, Jr., also smelled VCM by the unloading area near the railcars and outside the storage area.

C. Exposure Limits, Toxicity and Monitoring of VCM.

Although VCM was known to be highly flammable and had anesthetic effects when inhaled in high concentration, it was initially considered to be very low in toxicity. In 1947, the American Conference of Government Industrial Hygienists (ACGIH) recommended a maximum allowable concentration (MAC) of exposure to VCM of 500 ppm. MACs, subsequently renamed "threshold limit values" (TLV), are the maximum average concentrations of contaminants to which workers may be safely exposed in an eight-hour day. Also in 1947, an experiment, the Seeler study, revealed no signs of toxicity to animals fed a diet supplemented with PVC.

The "Chemical Safety Data Sheet SD-56" (SD-56), published in 1954 by the Manufacturing Chemists Association (MCA), of which Pantasote and defendants were members, reflected that assessment, and provided that "[a]side from the risk of fire and explosion, vinyl chloride presents no other very serious problem in general handling. The presently accepted upper limit of safety as a health hazard is 500 ppm."

However, in 1959, the industry learned that there were indications of VCM toxicity in ongoing laboratory animal experiments conducted by Dow Chemical scientists, T.R. Torkelson and V.K. Rowe. The Torkelson study exposed rats and other small animals to VCM levels ranging from 50 ppm to 500 ppm, levels that had been considered safe for human exposure, for seven hours a day over the course of seven months.

In a letter dated May 12, 1959, Rowe, commented on the ongoing Torkelson study, and informed the Director of Goodrich's Department of Industrial Hygiene and Toxicology that the 500 ppm threshold established by the ACGIH was based on a flawed animal study. Rowe wrote that "[w]e feel quite confident . . . that 500 ppm is going to produce rather appreciable injury when inhaled 7 hours a day, five days a week for an extended period." In another comment on the study in an interoffice correspondence dated November 24, 1959, a Union Carbide employee wrote that [a]n off-the-record phone call from V.K. Rowe gives me incomplete data on their current repeated inhalation study. Six months at 500, 200 and 100 [ppm] has not found a no-effect level. Even 100 [ppm] produced organ weight changes and gross pathology, with micropathology expected. [VCM] is more toxic than has been believed.

An experiment conducted and published in 1960 by E. Mastromatteo and others also found some congestion in the livers of laboratory animals exposed to high levels of VCM. And, the Torkelson study, published in 1961, concluded that VCM exposure had a "slight capacity" to cause liver damage in laboratory animals. The authors recommended that the TLV be lowered to 50 ppm, and Dow began applying this exposure value in some of its plants.

However, in a subsequent study published by D. Lester and others, the authors found only increased liver weights in rats exposed to VCM, changes they did not consider significantly pathologic. Thus, they concluded that a TLV of 500 ppm for VCM "seems to offer an adequate margin of safety for human exposure."

Faced with these differing results, in 1962, the ACGIH sided with Lester, and found that, although the available data concerning the toxicity of VCM was "conflicting, the preponderance indicates a compound of relatively low toxicity with which a threshold limit of 500 ppm is consistent."

In 1963, Goodrich began testing employees at its Louisville plant for liver function. In a letter dated June 7, 1965, Rex Wilson, a physician employed by Goodrich, stated that it had been his experience that VCM is a "hepatoxin when exposure is prolonged and high in amount."

In the mid-1960's, reports surfaced linking VCM exposure to acroosteolysis in humans. In Wilson's 1967 published report of thirty-one cases of acroosteolysis, twenty-seven of the workers were autoclave workers, that is, they cleaned polymer from PVC reactors. Goodrich reported observations of acroosteolysis in some of its PVC workers at an October 6, 1966 MCA meeting. Some industry members predicted that the TLV level for VCM would be reduced to 50 ppm.

As a result, Pantasote installed a hydraulic washing system in plant 2, which obviated the need for autoclave workers to enter the reactor vessel and clean the walls. It also installed additional exhaust fans to increase ventilation, and restricted access to the reactor areas and tank farms to only essential personnel in plants 1 and 2.

In August 1968, scientists employed by Dow Chemical Company presented a report at the Gordon Research Conference on Industrial Hygiene that suggested "long-term weighted exposures at or above 300 ppm could result in adverse functional changes." In 1970, the newly created Occupational Safety & Health Administration (OSHA) followed the established exposure limits and set federal standards for VCM of 500 ppm, the maximum average concentration of VCM to which a worker could be exposed in an eight-hour workday.

In that same year, P. L. Viola, an Italian researcher, presented his findings at a conference, reporting that rats developed cancerous tumors of the skin, lungs and bones after being exposed to 30,000 ppm of VCM four hours a day, five days a week, for twelve months. The results were subsequently published in 1971, with Viola stating that "[n]o implications to human pathology can be extrapolated from the experimental model reported in this paper."

The Viola study was extensively discussed by members of the VCM industry. On November 16, 1971, a Pantasote representative attended an MCA meeting during which the results of the Viola study were described. The association's members agreed to sponsor independent research regarding the carcinogenicity of VCM. The MCA also found that "[t]he seriousness of Dr. Viola's findings, if properly substantiated, can have potentially damaging results for the entire vinyl chloride industry."

In 1972, the MCA revised SD-56, warning that "[c]hronic overexposure [to vinyl chloride] may produce liver injury." It stated that "[r]ecent research studies from Italy indicate that repeated, long-term high level exposures of rats to [VCM] vapor can result in the development of malignant tumors. However, many years of industrial experience . . . have not demonstrated any carcinogenicity to humans." And, it stated that VCM "does not present a serious industrial health hazard provided workers are adequately supervised and observe the proper means of handling it." OSHA "has set a 500 ppm Ceiling Value on permitted employee exposures. Based upon animal and human observations, this level provides considerable margin of safety for industrial exposures." However, in 1970 ACGIH recommended that the TLV level for VCM exposure be reduced from 500 to 200 ppm.

In November 1972, several members of MCA, including defendants, executed a "Secrecy Agreement," securing release of data, and pledging not to reveal information outside the organization about a European animal study on the effects of VCM, which was being conducted by Cesare Maltoni at the University of Bologna. The MCA learned that Maltoni had found positive carcinogenic effect in rats at doses of 250 ppm of VCM, and one case of ASL.

At a meeting in February 1973, MCA members expressed the need to defocus their concern about carcinogenicity and VCM, and to refute the European research. In July of 1973, an MCA task force met with OSHA, but withheld information about the European studies and called into question the results of the Viola study.

On January 23, 1974, Goodrich issued a press release disclosing that three of its VCM-exposed workers at its Louisville plant had died of ASL; two died in 1973, and the third died in 1971. Four other deaths from ASL were reported at Goodrich's plant in Shawinigan, Quebec, with the earliest death occurring in 1968. As a result, in April 1974, OSHA issued a temporary emergency VCM exposure limit of 50 ppm, and effective April 1975, set a permissible exposure limit of 1 ppm as an eight-hour time-weighted average, and 5 ppm as a ceiling value averaged over a period exceeding fifteen minutes. 29 C.F.R. § 1910.1017 (2010). Areas exceeding that standard were designated as "regulated areas."

In conformance with those standards, Pantasote installed a monitoring system in plants 1 and 2, areas that had exceeded the OSHA standard. All other areas, including calendaring, compounding, and thermoforming, did not exceed the OSHA action level.

No sampling data for the period prior to 1974, other than as set forth by Pantasote in correspondence to the USEPA, was available for the facility. For example, in a memo to the USEPA, dated June 14, 1974, Pantasote reported that atmospheric levels of VCM at the plant perimeter, on the side where tank cars were unloaded and the reactor was located, ranged from .9 to 5.5 ppm. Pantasote used devices to collect PVC emissions, including a monomer recovery system, dust collectors, and vent bags on the storage silos. The systems collected approximately 8% of the total monomer used. It estimated that without the systems, 724 pounds of PVC per hour would be released into the atmosphere, and that the systems reduced emissions to about .36 pounds per hour.

On October 17, 1974, a representative from the National Institute for Occupational Safety and Health (NIOSH) visited the Pantasote facility and reported that the company had an active health, safety, and sampling program and [is] interested in cooperating with the NIOSH survey program. [It is] concerned that the vinyl chloride levels may be somewhat higher in their processing plant in that it is located between the two . . . [PVC] resin production plants. Information on vinyl chloride is transmitted to their employees through union-management meetings . . . and direct meetings [with] the resin plant employees. Sampling is conducted in the resin . . . and processing plants . . . . The sampling program is under constant change to comply with OSHA regulations. The . . . samples are analyzed in [its] laboratories at this site.

In interoffice correspondence dated March 23, 1976, Pantasote reported that there had been high exposure levels of VCM loose at all times since the plant opened in 1958, and that the company was doubtful that they could lower the exposure levels to comply with the federal standards.

By the mid-1970's, Pantasote conducted medical tests on its plant employees, including Lewis. Not only were signs posted in the plant warning that VCM was a "Cancer Suspect Agent," but also warnings were imprinted on the bags of PVC manufactured at the plant. Pantasote also provided some of its workers with respirators, although Lewis, Jr., testified that his father did not use one.

Industry-wide, occupational exposure to VCM decreased substantially after 1975. In 1981, the Pantasote plant reduced the content of VCM in the PVC resin, thereby further lowering VCM exposure.

D. Expert Evidence (Exposure and Warning).

James Jones, a certified industrial hygienist, was first contacted by plaintiff sometime after Lewis' death, and after demolition of Pantasote plants 1 and 2. Jones received a B.S. in chemical engineering and completed some graduate work. As an undergraduate, he worked at Goodrich's Louisville plant. Later, at the NIOSH, he directed the exposure assessment portion of its VCM study, and gathered data on employee exposures to VCM by visiting six or seven PVC production facilities. In 1974, he assisted the NIOSH director in preparing to testify before OSHA concerning establishing new exposure limits for VCM.

Jones opined that from 1961 to 1974, Lewis had been exposed to a significant quantity of VCM. He explained that no quantitative exposure sampling data existed prior to 1974, and that because Pantasote's manufacturing facility no longer existed he was not able to monitor the current exposure levels. Thus, he relied significantly upon VCM odor threshold levels to estimate Lewis' exposure. He used a 2,000 ppm odor threshold, as set forth in some scientific literature, although the USEPA had established a higher threshold of 3,000 ppm, and VCM manufacturers had shown thresholds ranging upwards between 1,200 to 3,800 ppm. He explained that whenever a worker smelled VCM, that worker would have then already been exposed to VCM levels above 2,000 ppm, which he said constituted a "substantial exposure."

Jones concluded, based on Lewis' job functions, the reports of pervasive odor of VCM at the facility, and Jones' experience in other PVC plants, that Lewis had been exposed to in excess of 40 to 50 ppm of VCM annually, or a cumulative minimum exposure, from 1961 to 1974, of 520 to 650 ppm. He opined in his report that Lewis' VCM exposure would have been variable, but . . . [Lewis] would have been regularly exposed to levels that were very high (probably in the thousands of ppm range) while unloading VCM tank cars and because of ambient VCM concentrations caused by the release of VCM from reactors and resin storage silos. He did not [wear] a respirator during this time [.] . . .

Lewis' [cumulative] VCM exposure would likely be in excess of 500 ppm-years [i.e., over the years he worked at Pantasote], primarily because of exposure before 1974.

Jones further testified that the exposure warnings given to the Pantasote workers prior to 1974, about the risk of developing liver damage from exposure to VCM were inadequate. By 1970, defendants were aware of animal studies linking VCM exposure to liver cancer, reports that workers in foreign PVC plants developed liver damage, and recommendations in the scientific literature that VCM exposure levels should be lowered to 50 ppm. Jones concluded in his report:

[I]n light of these multiple indications that VCM was harmful to workers at exposure levels as low as 50 ppm and the finding of cancer in VCM exposed animals, users of VCM should have begun monitoring and controlling exposures to VCM, and suppliers of VCM and the MCA should have lowered their exposure recommendations at least as early as 1961 and given adequate warning of the various health effects found in humans and animals. If this had been done, worker exposure levels at this plant would likely have been lowered much earlier than 1974, and the potential for harm, such as liver disease and cancer, to . . . Lewis, and other workers would also have been significantly reduced.

E. Lewis' Diagnosis.

In August 2000, Lewis, then seventy-five years old, physically active, with no history of hepatitis or alcohol abuse, was diagnosed with "metastatic disease to the liver and adrenals." During an examination conducted on November 2, 2000, Dr. Michael Maroules reported that Lewis had "widely disseminated cancer." A computerized tomography (CT) scan revealed that Lewis had a huge tumor in his liver, measuring in excess of 15 centimeters, multiple tumors in his lungs, and tumors in his adrenal glands. Lewis died on December 31, 2000.

It was undisputed that Lewis had not developed ASL. ASL is a sarcoma, or cancer of the connective tissue, which develops in the endothelial lining or sinusoidal cells, and is causally associated with exposure to VCM. HCC, accounting for approximately 80% of all primary liver cancers, is a carcinoma or cancer of the epithelial tissue, which develops in the hepatocytes or liver cells. The major risk factors for developing HCC are infection with the hepatitis-B and -C viruses, and the abuse of alcohol.

There was, however, some dispute as to whether Lewis had primary HCC, and whether the cancer had metastasized from, not to, his liver. Most malignant liver tumors metastasize to the liver from other areas of the body, but there are six types of cancers that originate in the liver, including HCC and ASL. Some records indicated that Lewis' tumor had metastasized to his liver. For example, a radiologist's report dated October 18, 2000, indicated that Lewis' CT scan findings were "consistent with metastatic disease." In Dr. Maroules' oncology report dated November 2, 2000, he stated that a "CT guided biopsy of the liver revealed malignancy, possibly endocrine." Maroules also noted in his report that the biopsy results were "consistent for endocrine source," but testified at depositions that he could not "definitely say what kind of cancer [Lewis] had." Moreover, Lewis' cause of death was listed on the death certificate as "[m]etastatic carcinoma to the liver, primary unknown."

However, other records supported a diagnosis of HCC. A November 7, 2000, pathology report revealed that the tests results "favor hepatocellular carcinoma." The hospital discharge summary, dated November 12, 2000, listed a final diagnosis of "[h]epatocellular carcinoma with metastasis." Another pathology report dated November 14, 2000, stated ...


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