“Insufficient evidence as a matter of law.” This language, contained in a brief one paragraph opinion in which New York’s highest court affirmed an appellate decision to set aside a jury verdict in favor of plaintiffs, describes the court’s rationale for determining that the plaintiff failed to prove her claims under the state’s jurisprudence. In Juni v. A.O. Smith Water Prods. Co., et al., Mary Juni pursued claims on behalf of her deceased husband, Arthur Juni, who was diagnosed with mesothelioma. Mr. Juni spent over 25 years working as a mechanic on automobiles manufactured by defendant Ford Motor Company, including work with brakes and clutches (“friction products”).

The plaintiff introduced evidence at trial that the chrysotile asbestos-containing automotive component parts utilized by Mr. Juni during the course of his automotive work was the cause of his mesothelioma. Ford, while not disputing the presence of chrysotile asbestos in its parts, submitted expert testimony that demonstrated the chrysotile asbestos contained in the friction products would have undergone a chemical transformation while subjected to high temperatures during the manufacture and use in vehicles, thus converting the asbestos into a benign substance called forsterite, which does not cause mesothelioma.

The jury found in favor of Mrs. Juni, but the trial court set aside the verdict against Ford, reasoning that the evidence was legally insufficient to support the verdict because plaintiff’s experts failed to refute testimony provided by Ford’s experts that chrysotile asbestos in friction products is converted to forsterite and rendered non-toxic.

The Appellate Division noted in its opinion that plaintiff’s expert, Dr. Jaqueline Moline, offered only that Mr. Juni’s cumulative exposures to asbestos caused his mesothelioma.  Dr. Moline admitted, however, that: (1) there were no measurements of any claimed exposures to Mr. Juni; (2) studies have shown that more than 99% of debris from brake wear did not contain asbestos; and (3) she was unsure whether the exposures claimed by Mr. Juni were to unchanged chrysotile asbestos fibers rather than forserite. Moreover, plaintiff’s expert Dr. Steven Markowitz testified only generally as to the propensity of chrysotile asbestos in friction products to cause mesothelioma if it becomes airborne and is inhaled. Dr. Markowitz conceded, however, that almost all of the published, epidemiological literature has shown no increased risk for mechanics who work on friction products. Moreover, like Dr. Moline, Dr. Markowitz conceded that only 1% of brake dust is comprised of asbestos, and that the high heat associated with brake drums converts most asbestos in brake linings into forsterite. Importantly, the Appellate Division concluded that the expert testimony offered by the plaintiff was “equivocal, at best,” and addressed only the increased risk and association between asbestos and mesothelioma, yet failed to quantify or provide any scientific basis for Mr. Juni’s alleged exposure to asbestos from Ford products, if any at all. The Appellate Division held that as neither plaintiff’s experts offered testimony specific to any dust created by Ford’s friction products to which Mr. Juni was allegedly exposed, the trial court properly vacated the verdict. In doing so, the Appellate Division reasoned that a causation opinion must be based on scientific testimony tied to a specific product rather than testimony regarding exposures related to categories of products.

The Court of Appeals affirmed the decision of the Appellate Division, holding that “the evidence was insufficient as a matter of law to establish that respondent Ford Motor Company’s conduct was a proximate cause of the decedent’s injuries pursuant to the standards set forth in Parker v. Mobil Oil Corp., 7 NY3d 434 (2006) and Cornell v. 360 W. 51st St. Realty, LLC, 22 NY3d 762 (2014).” The standard the Court referred to in Parker, a benzene case, and Cornell, a mold case, requires that a plaintiff in a toxic tort claim prove: (1) a plaintiff’s exposure to a toxin; (2) that the toxin is capable of causing the particular illness (general causation); and (3) that plaintiff was exposed to sufficient levels of the toxin to cause the illness (specific causation).

Justice Wilson’s concurring opinion elucidates the Court’s finding that plaintiff’s evidence was insufficient. For instance, Justice Wilson clarified that the verdict was properly set aside due to “a gap in proof as to the toxicity of the products at issue.” Justice Wilson noted that Ford’s expert provided evidence that the conversion of chrysotile asbestos to forsterite rendered conventional asbestos toxicology irrelevant. The concurring opinion makes clear that the court’s decision is not that Ford’s scientific opinions are correct, instead, the Court found the plaintiff failed to rebut Ford’s expert testimony.  In fact, Judge Wilson refers to testimony offered by one of plaintiff’s experts that “no one knows” whether the friction product dust to which Mr. Juni was exposed was toxic. Justice Wilson further noted that the Court’s reasoning is similar to the Court’s reasoning in Parker, where the plaintiff’s expert only testified as to the association between exposure to benzene, generally, rather than the question central to that case: whether exposure to gasoline that contained benzene as a component is associated with the disease at issue.

The opinion of the trial court to overturn the Juni verdict, which was upheld by the Appellate Division, and the Court of Appeals, underscores a growing emphasis on plaintiff’s burden to demonstrate causation. Indeed, the Court of Appeals decision in Juni has been used to support motions for summary judgment in other cases and by Courts that have allowed such motions. In Mantovi v. American Biltrite, Inc., et al., for instance, a defendant manufacturer described the burden of proof under Parker and Juni as follows: (1) as to general causation, the plaintiff must first show that chrysotile asbestos fibers released from floor tile are capable of causing disease, and (2) as to specific causation, the plaintiff must go further and demonstrate that the plaintiff was exposed to fibers released from the floor tiles manufactured by the defendant at levels sufficient to cause disease. Because the plaintiff’s expert relied upon no studies or reports concerning any association between floor tiles and mesothelioma, the Court held that he lacked the foundation of offer a general causation opinion, and the traditional “cumulative exposure” testimony was insufficient. Further, because plaintiff’s experts lacked any evidence from which they could compare the alleged exposure levels due to defendant’s products to other studies, any specific causation opinions of plaintiff’s expert was unfounded as well.

The Parker, Juni, and now Mantovi holdings represent a positive development for defendants impacted by speculative and generic evidence advanced by plaintiffs that do not address the product-specific defenses on which many companies defending asbestos personal injury matters rely. While studies correlating fiber release with development of asbestos-related disease exist for some categories of products, like insulation, many other products are not represented in the scientific literature. These holdings suggest that plaintiffs may be unable to establish general causation as to these lesser-studied products. The typical one-size-fits-all testimony from plaintiff’s experts that “asbestos causes disease” should no longer defeat summary judgment. Rather, NYCAL courts may begin demanding that plaintiff’s experts point to studies specifically associating drywall, friction products, circuit breakers, and other products, not just asbestos, with disease development. In short, the Juni decision has the potential to impact defenses advanced by a number of companies which face asbestos litigation in New York by enforcing plaintiffs’ burdens of proof.