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Buttitta v. Allied Signal

April 5, 2010


On appeal from the Superior Court of New Jersey, Law Division, Bergen County, Docket No. L-9592-02.

Per curiam.


Argued January 4, 2010

Before Judges Axelrad, Fisher and Sapp-Peterson.

Mark Buttitta died of mesothelioma, a rare and fatal cancer caused by exposure to asbestos. His widow, plaintiff Susan M. Buttitta, as personal representative of the estate, brought this action against numerous defendants, alleging that Mark contracted mesothelioma when directly exposed to asbestos at a General Motors (GM) warehouse, where he worked during several summers in the early 1970's, and indirectly, from contact with his father, who worked for GM from 1952 through the 1970's.

After the pretrial disposition of the claims against most of the defendants, a trial against the remaining defendants --Borg-Warner Corporation, Asbestos Corporation Ltd. (ACL), C.L. Zimmerman Company (Zimmerman), and Honeywell International, Inc. and its predecessor, Bendix (collectively Honeywell/Bendix) --was conducted in February 2008. Zimmerman and Honeywell/Bendix settled during trial. The jury returned a verdict in plaintiff's favor finding that Borg-Warner and ACL had manufactured, sold, or distributed a product not reasonably safe for its intended use, that Mark was exposed to the product, and that such exposure was a substantial contributing cause of his development of mesothelioma. The jury awarded plaintiff $8,000,000 for pain and suffering, $2,000,000 for loss of consortium, $9,281,660 for loss of earnings, $2,030,544 for loss of services, and $3,000,000 for each of their three daughters for loss of parental care and guidance.

In their separate appeals, which we dispose of in this single opinion, Borg-Warner and ACL raise numerous issues.


Borg-Warner argues that the judge erred in his rulings on:

(a) causation; (b) the admission of plaintiff's expert testimony; (c) Borg-Warner's claims against settling defendants; and (d) its motion for a remittitur. After careful review, we find no error in any of the judge's rulings.

A. Causation

Borg-Warner contends that the trial judge erred in denying its motion for judgment, arguing that plaintiff failed to prove sufficient exposure to its asbestos-containing clutches to warrant a finding of "medical causation"; that is, that its product was a "substantial factor" in causing Mark's mesothelioma. Borg-Warner also argues that the jury's determination of "medical causation" was "tainted" by the judge's erroneous admission of the deposition of John Froning, the former manager of a GM production facility.

A motion for judgment may be made at the close of a plaintiff's case, Rule 4:37-2(b), at the close of all the evidence, Rule 4:40-1, and after the verdict, Rule 4:40-2(b). All three motions are governed by the same evidential standard: "'[I]f, accepting as true all the evidence which supports the position of the party defending against the motion and according him the benefit of all inferences which can reasonably and legitimately be deduced therefrom, reasonable minds could differ, the motion must be denied....'" Verdicchio v. Ricca, 179 N.J. 1, 30 (2004) (quoting Estate of Roach v. TRW, Inc., 164 N.J. 598, 612 (2000)). We apply the same standard in reviewing a trial judge's ruling on such a motion. Estate of Roach, supra, 164 N.J. at 612.

In examining whether Borg-Warner was entitled to judgment, we must consider the evidence offered in support of plaintiff's claim, including, first, the extent of Mark's exposure to asbestos-related products.


Borg-Warner manufactured automotive parts, including disc type clutches, which were sold as a three-piece set that included a pressure plate, clutch disc and bearing. The clutch facing consisted of a disc of friction material attached to a clutch pressure plate. It was undisputed that in the 1970's the friction material in Borg-Warner clutches was made of chrysotile asbestos, and that no warnings were contained on the product or its packaging.

A 1972 study conducted by Borg-Warner revealed that its clutch manufacturing operations generated levels of airborne asbestos fibers in excess of the governing OSHA standards.*fn2 The study found that a "significant amount of the total asbestos exposures is coming from the loose fibers that are on the clutch facings." It also found that its "clutch-facing inspector," who was operating in a generally clean area, "received an exposure that is higher than most other employees' exposures." The report recommended that all employees working with clutch facings wear respirators, and that the plant install a "rigid housekeeping program," including installation of a ventilation system and the prompt disposal of scrap and sweepings.

From the early 1960's to the early 1980's, Borg-Warner was one of the original equipment manufacturer (OEM) suppliers of clutch products to GM; that is, it supplied clutches for installation on the assembly line in new production vehicles. Borg-Warner later "disposed of its clutch operation" and destroyed its records relating to "its product sales to any General Motors facility in New Jersey."

However, Froning, the former manager of the clutch and manual transmission group at the GM power train division in Michigan, testified at depositions in an unrelated case,*fn3 which were read to the jury here, that from the early 1960's to the mid-1980's Borg was GM's "prime" supplier of clutches, providing "virtually 100 percent" of the clutches installed in GM passenger cars and light trucks. Froning admitted his testimony was limited to clutches used in "new production," or OEM products, and that he did not know if GM used "different suppliers for clutch facings used in the aftermarket."


Mark Buttitta was born in December 1952. He worked as a "parts picker" at the GM distribution warehouses in Edgewater and Englewood during the summers of 1971 to 1973, and during his winter breaks while matriculating at Colgate University. As a summer employee, Mark was also responsible for sweeping the warehouse floor at the end of the shift. Mark worked with his father, who had been employed by GM since the 1940's. During the summer of 1971, Mark also worked with Frank Buttitta, Jr. (Frank, Jr.), his brother.

In his de bene esse deposition, played for the jury at trial, Mark testified that as a "parts picker," he, along with fifty to seventy-five other employees, were responsible for filling orders for parts submitted to GM by automobile dealers. The picker would retrieve parts from open racks or bins located at various locations within the "very busy" warehouse and place them in a cart. Some parts were packaged in boxes and some were stored loose on shelves. If the parts were packaged in a box, the parts picker would open the box, check to make sure it contained the correct parts and the required quantity, and then either remove the part or reseal the box for transport to the shipping area. Brakes were packaged in boxes containing four units; to fill an order, a parts picker would often retrieve one set of brakes from a box.

Mark said that, on some days, he would pick as many as fifty brake shoes or pads and twenty-five clutch pads or assemblies. Frank Ripley (Ripley), who had worked with Frank, Jr. and Mark at the GM warehouse, confirmed that brakes and clutches, which then contained asbestos, were the most common products picked at the warehouse.

Mark, Frank, Jr., and Ripley described the warehouse as being very dusty, with thick layers of dust on the shelves, boxes, and automotive parts, which became airborne when disturbed. The air was "stagnant" and there was visible dust "in the air." The warehouse had no windows and ventilation was poor. Mark wore street clothes to work; masks and respirators were not provided. He often returned home from work "covered with dust"; Frank said he came home covered in a "gray kind of dirt"; Ripley said that after a day working in the warehouse "you'd blow your nose in a handkerchief and you know there would be dust." Mark did not see any warnings on the boxes.

Mark recalled seeing GM, AC, Delco, Bendix, and Remme products, but did not name Borg-Warner. However, Frank gave the following testimony:

Q: During the time that you were a parts picker at GM, do you recall the brand names... on any of the boxes or the brakes... ?

A: Certainly I want to say Bendix. I remember AC, Delco, I believe that, at least at that time, was owned by General Motors, so that was quite a frequent name on boxes there.

Q: Any others that you recall?


A: For brakes. Primarily Bendix, I believe.

Q: Are there other names of manu-facturers or brands... that you recall, but you don't know what specific products they were on?

A: I want to say Raybestos. I... mentioned AC Delco. I want to say Borg Warner too. [Emphasis added.]

Ripley also identified Borg-Warner as a supplier of clutches and brakes:

Q:... [D]o you recall the brand names associated with [clutches and brakes] that you saw at the warehouse?

A: Yes, I remember the brand names. General Motors... Delco... Bendix... Inlin.... What is it Born -- Borg Warner. [Emphasis added.]

Frank and Ripley both recalled that the clutches handled by GM part pickers were packaged in thin, square, flat boxes similar to a "pizza box," which matched the packaging of Borg-Warner's clutches as depicted in its marketing material.


In August 2001, Mark, who had been in "excellent health," developed soreness in his right rib area, and an x-ray revealed that fluid had built up in his lung. A few months later, he was diagnosed with mesothelioma, a rare and fatal cancer of the pleura caused by exposure to asbestos. Mark underwent a course of chemotherapy, but the disease continued to progress. In July 2002, he underwent extensive surgery to remove the tumor, which had spread from the pleura, into his lung, diaphragm, lymph nodes, and the lining surrounding his heart. He underwent another surgery for removal of his right lung, but in October 2002, developed bloating caused by fluid build-up. On December 16, 2002, Mark underwent a third surgery, during which it was discovered that his abdominal cavity had been "essentially replaced by the tumor." Mark died on December 21, 2002.

Ronald Gordon, the director of the electron microscopy laboratory at Mt. Sinai Medical Center, and plaintiff's expert in diagnostic pathology, opined that exposure to "short asbestos fibers," or fibers measuring less than 5 microns*fn4 can be a cause of mesothelioma, and that Mark developed mesothelioma as a result of his exposure to asbestos during his summer employment at GM.

Gordon testified that exposure to all forms of asbestos, including chrysotile, can cause mesothelioma.*fn5 Upon inhalation, some of the larger asbestos fibers, fibers measuring greater than five microns, become "caught up" in the respiratory mucus cells and are cleared when the cilia push the mucus up into the throat, where the fibers are either coughed out or swallowed. Asbestos fibers inhaled into the lungs are engulfed by macrophages, or white blood cells. The "great majority" of these fibers are relocated to the lymph nodes or to the pleura, the thin membrane lining the lung and the chest wall. Gordon opined that small asbestos fibers, or fibers measuring less than five microns, are more likely to penetrate deeper into the lung because the larger fibers are more efficiently removed by the mucous system.

Gordon testified that several organizations, including the Occupational Safety and Health Administration, the National Institute for Occupational Safety and Health (NIOSH), the World Health Organization (WHO), and the Environmental Protection Agency (EPA) have concluded that exposure to chrysotile asbestos is a "causative factor" in the development of mesothelioma. He said there is no safe threshold for exposure to asbestos and disagreed with a March 2003 panel report prepared by the Eastern Research Group for the Agency for Toxic Substances and Disease Registry (ATSDR), which concluded that "asbestos... shorter than 5 [microns] are unlikely to cause cancer in humans."

In determining the exposure in this case, Gordon examined a piece of Mark's lung tissue, which had been removed during a biopsy, and found 20,700 fibers of asbestos per gram of lung tissue, or approximately 6 million fibers in one lung. Ninety percent of the asbestos fibers measured between one and four microns in length. Gordon found four types of asbestos in the lung sample: chrysotile, crocidolite, tremolite, and amosite, at a ratio of more than twice as much chrysotile and tremolite as crocidolite and amosite. Tremolite, which is often found in veins of chrysotile rock and is thus a contaminant of chrysotile, is more durable than chrysotile and remains in the lungs longer. Gordon concluded that the presence of tremolite in Mark's lungs tended to show that at some earlier point there had been a "significantly higher amount of chrysotile," which had been absorbed by the body. However, Gordon admitted that the amount of chrysotile found in Mark's lung tissue was less than the mean concentration of asbestos found in the background fiber burden levels of people with no occupational exposure. He explained that many older people living in urban areas have some background level of asbestos fibers, usually chrysotile, in their lung tissue as a result of exposure to ambient doses of commercial asbestos. Gordon admitted that he had testified in an unrelated case that there was no scientific proof that background levels of asbestos in lung tissue caused disease, but he said the background levels of asbestos always measure "less than one micron in length." Conversely, occupational exposure generally results in larger concentrations of asbestos measuring greater than one micron in length. Gordon concluded that because ninety percent of the asbestos fibers found in Mark's lungs measured between one and four microns in length, the finding was consistent with occupational and not background exposure.

Gordon also examined a sample of Mark's lymph nodes and found over 64,000 asbestos fibers per gram of tissue, or more than three times the amount found in his lung tissue. Ninety percent of the fibers measured greater than one micron in length, and there was five times as much chrysotile and tremolite as crocidolite and amosite. Gordon said he would expect to find virtually no asbestos fibers in the lymph nodes of an individual exposed solely to background levels of asbestos. He concluded that the levels of asbestos found in Mark's lymph nodes were consistent with "significant" occupational exposure to asbestos. And, although no sample of Mark's pleura was obtained for testing, Gordon said the concentration of asbestos in Mark's lymph nodes was a "very good indicator of what's in the pleura."

Gordon concluded that the size and distribution of asbestos fibers found in Mark's lung and lymph node, was a "significant causative agent" in his development of mesothelioma. The size of the fibers found in the samples was "very consistent" with Mark's occupational history. He opined that Mark's exposure to asbestos during the summers he worked at GM provided him with the dose, dimension, and durability of chrysotile fibers sufficient to cause and contribute to his development of mesothelioma.

Similarly, Jacqueline Moline, a physician specializing in occupational and environmental medicine, opined that working with asbestos-containing friction products, including clutches, can cause mesothelioma, and that Mark's exposure to these products caused him to develop the disease. She concluded that the analysis of Mark's lungs and lymph nodes showed elevated levels of asbestos "consistent with occupational exposure."

Significantly, she explained there is a distinction between asbestosis and cancer of the lung, which develop from continuous exposure to substantial quantities of asbestos over a period of years, and mesothelioma, which is associated with the "smallest exposure" to asbestos and can develop from the cumulative effects of minimal and infrequent exposure. She testified that "people can work for very short periods of time [with asbestos] and then develop... mesothelioma years later," and that typically there is a thirty-year latency period from exposure to development of mesothelioma.

Chrysotile, as opposed to other types of asbestos, "appears to have a much greater ability to move from the lung into the pleural space." Moline maintained that asbestos fibers that measure less than 5 microns are not safe and can cause mesothelioma. She testified that several government agencies, including OSHA, NIOSH, EPA, and an international body, WHO, have concluded there is no known safe threshold level of exposure, although OSHA set a "permissible standard" or "PEL" of 0.1 asbestos fibers, measuring longer than 5 micrometers per cc. The fact there was visible dust present at the GM plant indicated workers had a "significant exposure" to asbestos.

Similarly, Richard Dodson, plaintiff's expert in cell biology, who specializes in asbestos-related diseases, opined that Mark's exposure to asbestos, both directly by handling clutches at the warehouse, and indirectly, through contact with his father, contributed to his development of mesothelioma. He stated there is no safe level of asbestos exposure, and that even small quantities of asbestos are sufficient to cause mesothelioma, all exposures contribute to the disease, and cumulative exposures result in less efficient clearance rates.

Moreover, according to Dodson, studies have shown that the smaller chrysotile fibers, less than 3 microns in length, were "the prevalent type of fiber" found in the pleura of mesothelioma patients. Dodson explained that smaller particles of asbestos tend to be inhaled deeper into the lungs and have less chance of being removed through the mucous system. And, he stated "[t]here usually are multiple types of asbestos in the lung tissue in patients with mesothelioma."

According to Dodson, brake and clutch dust contains asbestos that can be easily inhaled. He experimented by rinsing a number of used clutches with distilled water, and found respirable asbestos fibers in the runoff. Additionally, Dodson studied the lung tissue of a clutch refabricator who died of mesothelioma, finding chrysotile asbestos in the man's lung tissue; he concluded that working with clutches can result in "[a]ppreciable exposure to asbestos" at a rate "sufficiently high to result in disease."

Similarly, William Longo, plaintiff's expert in the identification and quantification of asbestos, opined that opening a box of brakes that contained asbestos would result in a "significant" asbestos exposure. Longo testified that asbestos dust is only visible at ranges of 100 to 150 million particles per cubic foot of air and, as a result, airborne asbestos within the prior OSHA standard of 5 fibers per cc, or five million particles per cubic foot, would be "absolutely invisible." He conducted an analysis of the asbestos released into the air after opening a box of unused Delco brakes and found millions of chrysotile asbestos fibers "laying on top of the surface of the brake shoe" and a high concentration of asbestos in the dust particles in the box.


Borg-Warner's argument in seeking reversal of the denial of its motion for judgment is based upon the legal standard to be applied in mesothelioma cases. In denying Borg-Warner's motion, the judge relied on Kurak v. A.P. Green Refactories Co., 298 N.J. Super. 304, 311 (App. Div.), certif. denied, 152 N.J. 10 (1997), and found that the "frequency, regularity and proximity" test established in Sholtis v. Am. Cyanamid Co., 238 N.J. Super. 8, 28-30 (App. Div. 1989), was not applicable to mesothelioma cases because the disease can develop with infrequent exposure to a relatively small amount of asbestos. In applying the "substantial factor" test, the judge concluded that a reasonable jury could find that: Borg-Warner clutches were at the GM facility; Mark was directly exposed when he "picked" clutches from the shelves; and such exposure was a "substantial factor" in his development of mesothelioma. We conclude, for the reasons that follow, that the judge applied the proper legal standard.

In a product-liability action, a plaintiff must prove that the product was defective when it left the defendant's control, and that the defect caused injury to a reasonably foreseeable user. Coffman v. Keene Corp., 133 N.J. 581, 593 (1993). "Causation is a fundamental requisite for establishing any product-liability action." Id. at 594. In a toxic-tort product-liability action, a plaintiff must prove both a defect and "medical causation." James v. Bessemer Processing Co., 155 N.J. 279, 299 (1998); Coffman, supra, 133 N.J. at 594. In an asbestos failure-to-warn case, "[p]roduct-defect causation means that the absence of a warning proximately caused the plaintiff's injury, and medical causation means that exposure to the defendant's asbestos proximately caused the injury." Becker v. Baron Bros., 138 N.J. 145, 152 (1994).

The issue here centers on "medical causation." To prove medical causation, a plaintiff must show that exposure was a substantial factor in causing or exacerbating the disease.

James, supra, 155 N.J. at 299; Sholtis, supra, 238 N.J. Super. at 30-31. However, "[i]n the toxic-tort field, the modern trend has been to relax or broaden the standard of determining medical causation." Vassallo v. Am. Coding & Marking Ink Co., 345 N.J. Super. 207, 214 (App. Div. 2001). Proof that a defendant's conduct caused a plaintiff's injuries is "more subtle and sophisticated" in toxic-tort cases. Landrigan v. Celotex Corp., 127 N.J. 404, 413 (1992). And, "the task of proving causation is invariably made more complex because of the long latency period of illnesses caused by carcinogens or other toxic chemicals." Ayers v. Jackson, 106 N.J. 557, 585 (1987).

In Sholtis, we adopted the "frequency, regularity and proximity" test to determine whether the plaintiffs had made a prima facie case of "medical causation." 238 N.J. Super. at 28-31. The plaintiffs, who had worked at the defendant's plant for over four decades, developed asbestosis allegedly as a result of occupational exposure to the asbestos-containing products of multiple defendants. Id. at 14. We held that in order to prove that a specific defendant's product was a "substantial factor" in causing or exacerbating the disease, the plaintiff must prove "an exposure of sufficient frequency, with a regularity of contact, and with the product in close proximity" to the plaintiff, id. at 28; we explained that the "frequency, regularity and proximity" test appears to us to be well-reasoned, properly focusing upon the cumulative effects of the exposure. It is a fair balance between the needs of plaintiffs (recognizing the difficulty of proving contact) and defendants (protecting against liability predicated on guesswork). Industry should not be saddled with such open-ended exposure based upon "a casual or minimum contact."... Yet the phraseology should not supply "catch words"; the underlying concept should not be lost.

Since proof of direct contact is almost always lacking, especially in bystander cases, courts must rely upon circumstantial proof of sufficiently intense exposure to ...

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