Court Opinion

ID: 9872685
Source: CourtListenerOpinion
Date Created: 2023-09-26 21:11:49.61008+00
Date Added: 2024-06-11T13:47:35.533053
License: Public Domain

OPINION OF THE COURT
Saxe, J.
This appeal requires us to address whether a plaintiff who seeks damages for contracting mesothelioma based on exposure to a defendant’s asbestos-containing products must satisfy the standards expressed in Parker v Mobil Oil Corp. (7 NY3d 434 [2006]) and Cornell v 360 W. 51st St. Realty, LLC (22 NY3d 762 [2014]) by offering evidence that, if it does not provide an exact mathematical quantification of that exposure, at least provides some “scientific expression” (Parker at 449) of the level of exposure to toxins in defendant’s products that was sufficient to have caused the disease.
Plantiffs decedent, Arthur Juni, commenced this personal injury action due to his mesothelioma allegedly caused by claimed exposure to asbestos-containing products while he worked as an auto mechanic. Juni died on March 16, 2014, after which his widow, Mary Juni, who also has a loss of consortium claim, was substituted as administratrix for Juni’s estate. This appeal concerns only the trial of claims against defendant Ford Motor Company, based on Juni’s exposure to asbestos over the years he worked on the brakes, clutches, and manifold gaskets of Ford vehicles, during which work, plaintiff says, asbestos dust was released.
After a trial in which a jury returned a verdict in plaintiff’s favor, the trial court granted defendant Ford Motor Company’s motion to set aside the verdict (48 Misc 3d 460 [2015]; CPLR 4404 [a]). We affirm that determination.
As the trial court recognized, under CPLR 4404 (a) the court may set aside a verdict or judgment entered after trial, and direct that judgment be entered in favor of a party entitled to judgment as a matter of law, if the verdict was not supported by legally sufficient evidence, since under those circumstances there is “no valid line of reasoning and permissible inferences which could possibly lead rational [jurors] to the conclusion reached by the jury on the basis of the evidence presented at trial” (Cohen v Hallmark Cards, 45 NY2d 493, 499 [1978]).
As the trial court pointed out, plaintiff was obliged to prove not only that Juni’s mesothelioma was caused by exposure to asbestos, but that he was exposed to sufficient *236levels of the toxin from his work on brakes, clutches, or gaskets, sold or distributed by defendant, to have caused his illness. We agree with the trial court that the standards enunciated by Parker and Cornell are applicable here, that they are not altered by Lustenring v AC&S, Inc. (13 AD3d 69 [1st Dept 2004], lv denied 4 NY3d 708 [2005]) or other asbestos cases, and that plaintiff’s evidence failed to satisfy that standard.
The Court of Appeals recently succinctly reiterated the standard in Sean R. v BMW of N. Am., LLC (26 NY3d 801 [2016]):
“In toxic tort cases, an expert opinion on causation must set forth (1) a plaintiff’s exposure to a toxin, (2) that the toxin is capable of causing the particular injuries plaintiff suffered (general causation) and (3) that the plaintiff was exposed to sufficient levels of the toxin to cause such injuries (specific causation) (see Parker v Mobil Oil Corp., 7 NY3d 434, 448 [2006]). Although it is ‘not always necessary for a plaintiff to quantify exposure levels precisely’ (id.), we have never ‘dispensed with a plaintiff’s burden to establish sufficient exposure to a substance to cause the claimed adverse health effect’ (Cornell v 360 W. 51st St. Realty, LLC, 22 NY3d 762, 784 [2014]). ‘At a minimum, . . . there must be evidence from which the factfinder can conclude that the plaintiff was exposed to levels of th[e] agent that are known to cause the kind of harm that the plaintiff claims to have suffered’ (id., quoting Wright v Willamette Indus., Inc., 91 F3d 1105, 1107 [8th Cir 1996])” (26 NY3d at 808-809).
Therefore, the fact that asbestos, or chrysotile, has been linked to mesothelioma, is not enough for a determination of liability against a particular defendant; a causation expert must still establish that the plaintiff was exposed to sufficient levels of the toxin from the defendant’s products to have caused his disease (see Sean R., 26 NY3d at 809). Even if it is not possible to quantify a plaintiff’s exposure, causation from exposure to toxins in a defendant’s product must be established through some scientific method, such as mathematical modeling based on a plaintiff’s work history, or comparing the plaintiff’s exposure with that of subjects of reported studies (Parker at 449).
The evidence presented by plaintiff here was insufficient because it failed to establish that the decedent’s mesothelioma *237was a result of his exposure to a sufficient quantity of asbestos in friction products sold or distributed by defendant Ford Motor Company. Plaintiff’s experts effectively testified only in terms of an increased risk and association between asbestos and mesothelioma (see Cornell, 22 NY3d at 783-784), but failed to either quantify the decedent’s exposure levels or otherwise provide any scientific expression of his exposure level with respect to Ford’s products (see Sean R., 26 NY3d at 809; Parker, 7 NY3d at 449).
While both of plaintiff’s experts asserted that the asbestos in Ford’s friction products was a cause of Juni’s mesothelioma, the concessions made by both of plaintiff’s experts so undermined their assertions of causation as to render those assertions groundless or unsupported. Dr. Jacqueline Moline, plaintiff’s expert in internal medicine and occupational and environmental science, asserted that Juni’s “cumulative exposures to asbestos caused his mesothelioma,” referring to “the sum total of [his] exposure to asbestos . . . over [his] lifetime,” but she admitted that “there were no measurements of what Mr. Juni was exposed to,” noting that “[h]e was exposed in different locations where historically there have been mixed exposures,” and that “[a]ll of his occupational exposures were substantial factors” contributing to his disease. Further, Dr. Moline’s testimony that the visibility of the dust itself indicates the magnitude of the exposure “at levels that are . . . capable of causing disease” was undermined when on cross-examination she conceded that studies have shown that more than 99% of the debris from brake wear is not comprised of asbestos fibers. In addition, Dr. Moline acknowledged that most chrysotile fibers in brake pads undergo a transformation during the braking process, and she did not know whether the fibers from the brake debris to which Juni was exposed were still active.
Plaintiff’s other expert witness, Dr. Steven Markowitz, an internist, occupational medicine specialist, and epidemiologist, provided opinions that, after cross-examination, were similarly lacking in support on the issue of causation by Ford products. While he asserted that “chrysotile in friction products, if it becomes airborne and inhaled, can cause malignant mesothe-lioma” he acknowledged that 21 of 22 epidemiological studies that addressed asbestos exposure to mechanics working on friction products found no increased risk of mesothelioma. He also acknowledged that chrysotile has a curly and flexible *238structure, with shorter fibers, dissolves in the lungs, to an extent, and can clear the lungs through macrophages and translocation, and that when asbestos fibers in braking equipment are mixed with certain resins during manufacturing, “they would not be respirable.” Further, Dr. Markowitz conceded that the high heat generated within the brake drums when the brakes are applied converts most of the asbestos in the brake lining to another mineral known as forsterite, and that studies have shown that only 1% of the dust blown out from brake drums is comprised of asbestos.
The trial court was at pains to point out that unlike here, in other litigation Dr. Markowitz has offered a scientific basis for claims that visible dust emanating from a particular defendant’s asbestos-containing product contained enough asbestos dust to be hazardous, citing Caruolo v John Crane, Inc. (226 F3d 46 [2d Cir 2000]), in which Markowitz cited studies that measured the amount of asbestos fibers released by the products there at issue, and showed that the amount was hazardous. In contrast, no such supportive reports were offered at this trial. Rather, the reports or studies of mesothelioma in garage mechanics or those who work with friction products in a vehicle repair setting showed only an association between the work and mesothelioma.
Our dissenting colleague suggests that the proof in asbestos cases need not be analyzed using the same criteria as those we use to analyze exposure in other toxic tort cases, namely, the quantification or other “scientific expression of . . . exposure” required by Parker. The dissent also suggests that applying the same criteria would set an insurmountable standard for asbestos claims. However, there is no valid distinction to be made between the difficulty of establishing exposure to, say, benzene in gasoline and exposure to asbestos. In each type of matter, a foundation must be made to support an expert’s conclusion regarding causation.
Moreover, our decisions in Lustenring v AC&S, Inc. (13 AD3d 69 [2004], supra) and other asbestos cases (see e.g. Penn v Amchem Prods., 85 AD3d 475, 476 [1st Dept 2011]; Matter of New York Asbestos Litig., 28 AD3d 255, 256 [1st Dept 2006]) do not justify allowing a judgment in an asbestos case to stand based solely on a bare conclusion that because the plaintiff worked with the defendant’s asbestos-containing products, those products were a contributing cause of the plaintiff’s mesothe-lioma. The rulings in each of those cases are based on their *239discrete facts. Where the courts relied on evidence linking visible dust to the use of the particular defendant’s product, expert testimony established that the extent and quantity of the dust to which the plaintiffs had been exposed contained enough asbestos to cause the mesothelioma. In none of those case was the mere presence of visible dust considered sufficient alone to prove causation. For instance, in Lustenring, the evidence established that “both plaintiffs worked all day for long periods in clouds of dust,” which the expert testimony stated “necessarily contain[ed] enough asbestos to cause mesothelioma” (13 AD3d at 70). Here, in contrast to the expert testimony in Penn v Amchem Prods. (85 AD3d at 476), the testimony of plaintiff’s expert as to the contents of the dust to which the decedent was exposed was equivocal at best, and was insufficient to prove that the dust to which Juni was exposed contained any asbestos, or enough to cause his mesothelioma.
The trial court also correctly declined to adopt plaintiff’s theory of cumulative exposure to support the verdict. Neither of plaintiff’s experts stated a basis for their assertion that even a single exposure to asbestos can be treated as contributing to causing an asbestos-related disease. Moreover, reliance on the theory of cumulative exposure, at least in the manner proposed by plaintiff, is irreconcilable with the rule requiring at least some quantification or means of assessing the amount, duration, and frequency of exposure to determine whether exposure was sufficient to be found a contributing cause of the disease (see Parker, 7 NY3d at 449).
The dissent references a “consensus from the medical and scientific communities that even low doses of asbestos exposure, above that in the ambient environment, are sufficient to cause mesothelioma.” We do not agree that the existence of any such consensus entitles a particular plaintiff to be awarded judgment against a particular defendant by merely establishing some exposure to a product containing any amount of asbestos. Rather, the standards set by Parker and Cornell require that a plaintiff claiming that a defendant is liable for causing his or her mesothelioma must still establish some scientific basis for a finding of causation attributable to the particular defendant’s product. Here, the experts’ broad conclusions on causation lacked a sufficient foundation, and were therefore legally insufficient to establish that Juni’s exposure to asbestos from brakes, clutches, or gaskets sold or distributed by defendant constituted a significant contributing factor in causing Juni’s *240mesothelioma. There is therefore no valid line of reasoning or permissible inference which could have led the jury to reach its result.
Accordingly the judgment of the Supreme Court, New York County (Barbara Jaffe, J.), entered June 3, 2015, in favor of defendant Ford Motor Company, should be affirmed, without costs. The appeal from the order of the same court and Justice, entered April 13, 2015, should be dismissed, without costs, as subsumed in the appeal from the judgment.