In the matter of Rosati v Brigham Park Co-Op. Apartments, SEC No. 2, Inc.

Full title: John ROSATI, Plaintiff, v. BRIGHAM PARK CO–OPERATIVE APARTMENTS, SEC NO.2…

Court: Supreme Court, Kings County, New York.

Date published: Jul 17, 2012

36 Misc. 3d 1214 (N.Y. Sup. Ct. 2012)

2012 N.Y. Slip Op. 51315

961 N.Y.S.2d 361

Opinion

No. 15229/08.

2012-07-17

John ROSATI, Plaintiff, v. BRIGHAM PARK CO–OPERATIVE APARTMENTS, SEC NO.2, INC. and Wentworth Property Management, Inc., Defendants.

Natascia Ayers, Esq. of Jaroslawicz and Jaros LLC, for Plaintiff John Rosati. Arthur P. Xanthos, Esq. of Gartner & Bloom, P.C., for Defendants Brigham Park Co–Operative Apartments, SEC No.2, Inc. and Wentworth Property Management, Inc.

JACK M. BATTAGLIA

Natascia Ayers, Esq. of Jaroslawicz and Jaros LLC, for Plaintiff John Rosati. Arthur P. Xanthos, Esq. of Gartner & Bloom, P.C., for Defendants Brigham Park Co–Operative Apartments, SEC No.2, Inc. and Wentworth Property Management, Inc.
JACK M. BATTAGLIA, J.

In his Verified Complaint, plaintiff John Rosati alleges that he “purchased” and resided in apartment # 4A in a building located at 2270 Plumb 1st Street, Brooklyn, owned by defendant Brigham Park Co–Operative Apartments, Sec # 2, Inc. and managed by defendant Wentworth Property Management, Inc., and that “due to the defendants' recklessness, carelessness and negligence, mold was caused to form in [his] apartment, as a result of which [he] suffered severe and permanent personal injuries, as well as extensive property damage.” ( See Verified Complaint ¶¶ 8–10.)

Defendants moved for an order “[g]ranting a hearing pursuant to Frye v. United States, 293 F. 1013 (DC Cir1923), and thereafter dismissing plaintiff's bodily injury claims on the basis that he cannot show causation between any purported mold condition and his alleged illnesses.” (Notice of Motion for Frye Hearing dated April 1, 2011.) The motion first appeared on the calendar in the Jury Coordinating Part on May 3, 2011, and was adjourned eight times until October 31, 2011, on the determination of the justice presiding that the motion should be decided by the justice presiding over the action at trial. The action and motion were transferred to this Court on October 31, 2011.

“The long-recognized rule of Frye v. United States ... is that expert testimony based on scientific principles or procedures is admissible but only after a principle or procedure has gained general acceptance' in its specified field.” (People v. Wesley, 83 N.Y.2d 417, 422 [1994] [quoting Frye v. United States, 293 F 1013, 1014 (DC Cir1923) ].) “[T]he particular procedure need not be unanimously indorsed' by the scientific community but must be generally acceptable as reliable'.” ( Id. at 423 [quoting People v. Middleton, 54 N.Y.2d 42, 49 (1981) ] [footnote omitted].)

“Once Frye has been satisfied, the question is whether the accepted techniques were employed by the experts in this case'.” ( Id. at 429 [quoting People v. Middleton, 54 N.Y.2d at 50].) “The focus moves from the general reliability concerns of Frye to the specific reliability of the procedures followed to generate the evidence proferred and whether they established a foundation for the reception of the evidence at trial.” ( Id.) “The trial court determines, as a preliminary matter of law, whether an adequate foundation for the admissibility of this particular evidence has been established.” ( Id.)

“[N]ovel scientific evidence may be admitted without any hearing at all by the trial court” ( id. at 426), such as where the “reliability of the procedures has been ... accepted by all of the appellate courts that have addressed the issue” ( see People v.. Middleton, 54 N.Y.2d 42, 49–50 [1981];see also People v. LeGrand, 8 NY3d 449, 458 [2007].) The party seeking a Frye hearing has the initial burden of showing that there is “a question as to whether [an] expert's methodologies or deductions are based upon principles that are sufficiently established to have gained general acceptance as reliable.” ( See People v. Oddone, 89 AD3d 868, 869–70 [2d Dept 2011]; see also Ellis v. Eng, 70 AD3d 887, 891–92 [2d Dept 2010].) The moving party must show, in effect, that the proferred evidence is sufficiently “novel” to implicate Frye concerns. ( See Lipschitz v. Stein, 65 AD3d 573, 575–76 [2d Dept 2009]; Leffler v. Feld, 51 AD3d 410, 410 [1st Dept 2008]; Marsh v. Smyth, 12 AD3d 307, 308 [1st Dept 2004] [Saxe, J ., concurring].)

Where a Frye hearing is proper, the party proferring the “novel” evidence has the burden of establishing “general acceptance.” ( See Matter of Bausch & Lomb Contact Lens Solution Prod. Liab. Litig., 87 AD3d 913, 913 [1st Dept 2011]; Lewin v. County of Suffolk, 18 AD3d 621, 622 [2d Dept 2005].) “[T]he types of materials relevant to a determination of general acceptability” include “court opinions, texts, laboratory standards or scholarly articles,” as well as the testimony of expert witnesses.” ( See People v. Wesley, 83 N.Y.2d at 437] [footnote omitted] [Kaye, J., concurring].)

“The Frye test typically considers the admissibility of new scientific tests, techniques, or processes,” and “has also been applied to determine the admissibility of expert testimony based on new social and behavioral theories” ( see Ratner v. McNeil–PPC, Inc., 91 AD3d 63, 72 [2d Dept 2011].) Most pertinent here, “New York courts have also applied the Frye test to assess the reliability of an expert's theory of causation in a particular case.” (Lugo v. New York City Health & Hosps. Corp., 89 AD3d 42, 57 [2d Dept 2011].)

Broadly stated, the issue in this case is whether exposure to indoor mold causes illness. Specifically, although Plaintiff's several bills of particulars allege approximately 50 illnesses or symptoms, for present purposes the question is the relationship of exposure to indoor mold and chronic upper respiratory inflamation, bacterial infection, cough, obstructive sleep apnea, mold growing in nose, sinusitis, rhinitis/rhinosinusitus, abscesses in neck/throat, nosebleeds, asthma attacks, and nasal polypsosis.

When Defendants' motion for a Frye hearing was presented to this Court for determination, the most pertinent authority was the First Department's decision in Fraser v. 301–52 Townhouse Corp. (57 AD3d 416 [1st Dept 2008].) The plaintiff there had asserted causes of action against his cooperative building for “personal injuries (specifically, respiratory problems, rash and fatigue) allegedly caused by dampness in the building and the mold infestations that allegedly resulted from such dampness.” ( See id. at 416–17.) The lower court had held a Frye hearing, granted the defendants' motion to preclude the plaintiffs from offering certain expert evidence at trial, and then dismissed the plaintiffs' causes of action based on personal injury. A three-justice majority affirmed, concluding that the plaintiffs' experts had not established “the general acceptance of their view that indoor dampness and mold is capable of causing plaintiffs' health problems” ( see id. at 419.) Two justices dissented.

In the Second Department, the question of the relationship between exposure to indoor mold and illness had been addressed only on motions for summary judgment, with mixed results. In two decisions, the court held that the lower court had properly granted or should have granted the defendants' motion for summary judgment ( see Cubas v. Clifton & Classon Apt. Corp., 82 AD3d 695 [2d Dept 2011]; Travers v. Charles H. Greenthal Mgt. Corp., 66 AD3d 768 [2d Dept 2009] ), whereas in two decisions, the court held that the lower court had properly denied the defendant's motion for summary judgment ( see Cabral v. 570 West Realty, LLC, 73 AD3d 674 [2d Dept 2010]; Rashid v. Clinton Hill Apts. Owners Corp., 70 AD3d 1019 [2d Dept 2010].)

In Cubas v. Clifton & Classon Apt. Corp. (82 AD3d 695), without describing the defendants' prima facie showing that was found sufficient, the court held that the plaintiff had failed to raise a triable issue. The plaintiff's experts “failed to utilize objective standards to show that the toxic mold to which the plaintiff and the decedent were allegedly exposed was capable of causing their injuries or that their exposure to the toxic mold was the actual cause of their illnesses and symptoms.” ( See id. at 696.) In Travers v. Charles H. Greenthal Mgt. Corp. (66 AD3d 768), the court merely stated that defendants had established prima facie that “they neither created nor had actual or constructive notice of an alleged toxic mold condition in the plaintiff's apartment,” and that the plaintiff failed to raise a triable issue. ( See id. at 769.)

In Cabral v. 570 West Realty, LLC (73 AD3d 674), the defendant failed to meet its initial burden in that its expert “did not opine that mold is incapable of causing asthma (general causation) and his affirmations do not address whether the scientific community generally accepts or rejects the theory that mold can cause asthma.” ( See id. at 675.) “The expert affirmations proffered by the defendant were also insufficient to demonstrate a lack of specific causation ( i.e., that the infant plaintiffs were exposed to insufficient levels of mold to cause their asthma, or that their asthma was caused by some other factor).” ( Id.)

In Rashid v. Clinton Hill Apt. Owners Corp. (70 AD3d 1019), the defendant failed to establish prima facie that “it did not have notice of the presence of mold in the plaintiffs' apartment” ( see id. at 1020.) In addition, in opposition to the defendant's prima facie showing that “the existence of mold was not the proximate cause of the plaintiffs' personal injuries, the plaintiffs raised a triable issue of fact by submitting the report of their expert, Dr. Irene Grant, who opined that the mold caused their injuries.” ( See id.)

In B.T.N. v. Auburn Enlarged City School District (45 AD3d 1339 [4th Dept 2007] ), the Fourth Department affirmed denial of the defendant's motion for summary judgment, concluding that although the defendant met its prima facie burden with an expert's affidavit “establishing that there was no scientifically-based causal relationship between plaintiffs' exposure and symptoms” ( see id. at 1339–40), the plaintiffs raised a triable issue. “The record contains sufficient epidemiological evidence to support a finding of general causation, i.e., that the atypical molds found to be present in the school building can cause plaintiffs' symptoms.” ( Id. at 1340.)

In light of Fraser (57 AD3d 416), and the absence of any affirmative appellate court determination that exposure to indoor mold is capable of causing at least certain of the injuries alleged here, the Court ordered the Frye hearing. In addition to the lower court affirmed in Fraser, two other trial courts in the First Department considered motions for a Frye hearing on that issue. In Friedman v. 40 Madison LP (2008 N.Y. Misc. LEXIS 3532 [Sup Ct, Bronx County 2008] ), decided before Fraser, the court denied the motion, concluding that the “plaintiffs have established that the causal relationship between damp and/or moldy indoor environments and respiratory problems is generally accepted in the scientific community” ( see 2008 N.Y. Misc. LEXIS 3533 at * 15), relying on the Fourth Department's decision in B.T.N. v. Auburn Enlarged School District (45 AD3d 1339.) In Cornell v. 360 W. 51st St. Realty, LLC (26 Misc.3d 1211[A], 2009 N.Y. Slip Op 5270 [U] [Sup Ct, N.Y. County, 2009), the court also denied the motion, but concluded that Fraser “mandate[d] ... dismissal of plaintiff's personal injury cause of action” ( see id. at *7.)

Cornell was appealed to the First Department and, in another 3–2 ruling, the court held that the lower court had “incorrectly interpreted” the ruling in Fraser, and that the expert opinion in the case before it satisfied the Frye standard. ( See Cornell v. 360 W. 51st St. Realty, LLC, 95 AD3d 50, 52–53 [1st Dept 2012].) As will appear, Cornell changed the landscape on which this Court ordered the Frye hearing in this case.

The hearing here took place over seven days. The Court heard from two experts on behalf of Plaintiff, Irene Hanchett Grant, M.D., board-certified in internal medicine and infectious diseases; and Theodore J. Harrison, M.D., board-certified in otolaryngology; and from one expert on behalf of Defendants, Stuart H. Young, M.D., board-certified in allergy and immunology. Plaintiff marked 145 exhibits, and Defendants marked 35. Most of the exhibits are journal articles, studies, or other sources that the respective experts relied upon for their opinions, and were marked only “for identification.” ( See People v. Goldstein, 6 NY3d 119, 124–27 [2005];Wagman v. Bradshaw, 292 A.D.2d 84, 89–92 [2d Dept 2002].)

Before a review of that evidence, however, context must be provided by the caselaw applying the Frye standard to issues of causation in tort cases, provided primarily by the Court of Appeals decision in Parker v. Mobil Oil Corp. (7 NY3d 434 [2006].) In considering this caselaw, attention should be paid to the question whether the Frye “general acceptance” standard is applied to the “theory” or conclusion reached by the expert, or to the principles and methodologies used in arriving at that theory or conclusion, or both.

Prior to the Court of Appeals decision in Parker, opinions in the Second Department appeared to require that the plaintiff's “theory of causation” be “generally accepted” in the medical community. ( See Cumberbatch v. Blanchette, 35 AD3d 341, 342 [2d Dept 2006]; Lewin v. County of Suffolk, 18 AD3d 621, 622 [2d Dept 2005]; Del Maestro v. Grecco, 16 AD3d 364, 366 [2d Dept 2005].) And so, the plaintiffs failed to meet their burden at a Frye hearing where their experts “conceded that no scientific organization or national board [had] expressly recognized a causal relationship between in utero exposure to [a pesticide] and birth defects, and the peer-reviewed scientific articles and textbooks relied upon the plaintiffs' experts did not establish the existence of such a relationship.” ( See Lewin v. County of Suffolk, 18 AD3d at 622.) Somewhat in contrast, in Zito v. Zarbarsky (28 AD3d 42 [2d Dept 2006] ), the Second Department concluded that the plaintiff carried her burden at a Frye hearing where her experts supported their theory of a causal nexus between an excessive dose of [a drug] and [disease] with generally accepted scientific principles and existing data” ( see id. at 45; see also id. at 46 [“scientifically accepted methodology and reasoning”]; id. at 46–47 [“medical literature, reasoned methodology, and generally accepted scientific principles”].)

In Parker v. Mobil Oil Corp (16 AD3d 648 [2d Dept 2005], aff'd7 NY3d 434 [2006] ), the plaintiff alleged that he contracted acute myelogenous leukemia (AML) as a result of his 17–year occupational exposure to gasoline containing benzene, a known human carcinogen. On the defendants' motion for preclusion of expert testimony and summary judgment, the Second Department concluded that “the plaintiff's experts failed to make a causal connection, based upon scientifically-reliable methodology, between the plaintiff's specific level of exposure to benzene in gasoline and his AML.” ( See16 AD3d at 653.) The court articulated a “scientifically-reliable methodology,” which had been “acknowledged in numerous [federal] cases as generally accepted and reliable.” ( See id. at 651.) The three-step methodology had been recommended by the World Health Organization and the National Academy of Sciences “for drawing a sound conclusion as to the relationship between an individual's disease and a specific factor suspected of causing that disease.” ( See id.) The methodology includes:

“(1) a determination of the plaintiff's level of exposure to the toxin in question, (2) from a review of the scientific literature, proof that the toxin is capable of producing the illness, or general causation, and the level of exposure to the toxin which will produce that illness ( i.e., the dose-response relationship) must be ascertained, and (3) establishment of specific causation by demonstrating the probability that the toxin caused the particular plaintiff's illness, which involves weighing the possibility of other causes of the illness.” ( See id. [emphasis added]; see also Zaslowsky v. J.M. Dennis Constr. Co. Corp., 26 AD3d 372, 373 [2d Dept 2006].)

The court specifically addressed the contention of one of the plaintiff's experts that “studies have shown that there is no threshold level of benzene exposure below which leukemia cannot result.” ( See Parker v. Mobil Oil Corp., 16 AD3d at 652.) “[T]his approach, referred to as a linear non-threshold model,' assumes that if a lot of something is bad for you, a little of the same thing, while perhaps not equally bad, must be so in some degree'.” ( Id.) But, “the scientific reliability of this methodology has flatly been rejected as merely a hypothesis.” ( Id . at 653.)

On appeal, the Court of Appeals stated the question as “whether the methodologies employed by [plaintiff] Parker's experts lead to a reliable result—specifically, whether they provided a reliable causation opinion without using a dose-response relationship and without quantifying Parker's exposure.” ( See Parker v. Mobil Oil Corp., 7 NY3d at 447.) Since “[t]here is no particular novel methodology at issue for which the Court needs to determine whether there is general acceptance ... the inquiry here is more akin to whether there is an appropriate foundation for the experts' opinions, rather than whether the opinions are admissible under Frye.” ( See id.)

The Court of Appeals held that “an opinion on causation should set forth a plaintiff's exposure to a toxin, that the toxin is capable of causing the particular illness (general causation) and that the plaintiff was exposed to sufficient levels of the toxin to cause the illness (specific causation,” but “it is not always necessary for a plaintiff to quantify exposure levels precisely or use the dose-response relationship, provided that whatever methods an expert uses to establish causation are generally accepted in the scientific community.” ( See id. at 448.)

Parker does not further define or elaborate the term and concept “dose-response relationship.” In a decision after the Second Department's ruling in Parker, but before the Court of Appeals ruling, the First Department adopted a definition that appears in the Reference Manual on Scientific Evidence (Federal Judicial Center, Reference Manual on Scientific Evidence [2d ed 2000] ), i.e., “[t]he extent to which a living organism responds to specific dose of a toxic substance.” ( See Nonnon v. City of New York, 32 AD3d 91, 105 n19 [1st Dept 2006] [quoting Reference Manual on Scientific Evidence, Reference Guide on Epidemiology, at 433], aff'd on other grounds9 NY3d 825 [2007].) “The more time spent in contact with a toxic substance, or the higher the dose, the greater the organism's response.” ( See32 AD3d at 105 n19)

Parker states, “There could be several other ways an expert might demonstrate causation.” (Parker v. Mobil Oil Corp., 7 NY3d at 449.)

“For instance, amici note that the intensity of exposure to benzene may be more important than a cumulative dose for determining the risk of developing leukemia. Moreover, exposure can be estimated through the use of mathematical modeling by taking a plaintiff's work history into account to estimate the exposure to a toxin. It is also possible that more qualitative means could be used to express a plaintiff's exposure. Comparison to the exposure levels of subjects of other studies could be helpful provided that the expert made a specific comparison sufficient to show how the plaintiff's exposure level related to those of the other subjects. These, along with others, could be potentially acceptable ways to demonstrate causation if they were found to be generally accepted as reliable in the scientific community.” ( Id. at 449.)

Although the Court of Appeals in Parker “reject[ed] the Appellate Division's requirement that the amount of exposure need be quantified exactly,” it concluded that the Appellate Division properly precluded the opinions offered by the plaintiff's experts and properly deemed them insufficient to defeat summary judgment. ( See id.) “The experts ... failed to demonstrate that exposure to benzene as a component of gasoline caused [the plaintiff's] AML.” ( Id.) “Plaintiff's experts were unable to identify a single epidemiologic study finding an increased risk of AML as a result of exposure to gasoline.” ( Id. at 450.)

The opinion in Parker appears to generally resolve the question whether the “general acceptance” standard is to be applied to the “theory” or conclusion reached by the expert, or to the principles and methodologies used in arriving at that theory or conclusion, or both. If there is “no particular novel methodology at issue,” neither is “general acceptance” at issue. ( See id. at 447.) Presumably, that applies not only to “general causation,” but also to “specific causation”; in both cases, without novelty in methodology, the “inquiry ... is more akin to whether there is an appropriate foundation for the experts' opinions” ( see id.)

Subsequent to Parker, however, opinions of the First Department applied Frye “general acceptance” to the expert's proffered “theory” or “opinion” as to causation. ( See Matter of Bausch & Lomb Contact Lens Solution Prod. Liab. Litig., 87 AD3d 913, 913 [1st Dept 2011]; Rowe v. Fisher, 82 AD3d 490, 491 [1st Dept 2011] [“novel theory”]; Santos v. Nicolas, 65 AD3d 941, 941 [1st Dept 2009]; Leffler v. Feld, 51 AD3d 410, 410 [1st Dept 2008].) In Nonnon v. City of New York (32 AD3d 91), the majority stated, “ Frye is not concerned with the reliability of a certain expert's conclusions, but instead with whether the experts' deductions are based on principles that are sufficiently established to have gained general acceptance as reliable'.” ( id. at 103.) A subsequent panel, implicitly acknowledging that Nonnon might be understood to mean that “generally accepted methodology ... when properly performed leads to admissible expert conclusions,” was “prompt[ed] ... to add but not when there is a generally or widely held view in the scientific community rejecting such conclusions outright'.” ( See Marso v. Novak, 42 AD3d 377, 378 [1st Dept 2007].)

In the Second Department, however, the opinions appear to more closely adhere to the Frye /foundation distinction emphasized in Parker. Thus, most recently in Ratner v. McNeil–PPC, Inc. (91 AD3d 63 [2d Dept 2011] ), a unanimous panel stated that “where a plaintiff's qualified experts offer no novel test or technique, but intend to testify about a novel theory of causation, where such opinion is supported by generally accepted scientific methods, it is proper to proceed directly to the foundational inquiry of admissibility, which is whether the theory is properly founded on generally accepted scientific methods or principles” ( see id. at 73;see also People v. Oddone, 89 AD3d 868, 869–70 [2d Dept 2011]; Lugo v. New York City Health & Hosps. Corp., 89 AD3d 42, 56–57 [2d Dept 2011]; Ellis v. Eng, 70 AD3d 887, 892 [2d Dept 2010]; Lipschitz v. Stein, 65 AD3d 573, 576 [2d Dept 2009]; Alston v. Sunharbor Manor, LLC, 48 AD3d 600, 602 [2d Dept 2008].)

The differences between the First and Second Departments are particularly significant here because, as noted above, the two appellate opinions that most fully address the relationship between exposure to indoor mold and illness, i.e., Fraser v. 301–52 Townhouse Corp. (57 AD3d 416) and Cornell v. 360 W. 51st St. Realty, LLC (95 AD3d 50) were both decided by the First Department. Consistent with other First Department caselaw, except Nonnon (32 AD3d 91), both opinions appear to apply the Frye standard to the experts' theories and conclusions. In Fraser, as previously noted, the majority concluded that that plaintiffs' experts had not established “the general acceptance of their view that indoor dampness and mold is capable of causing plaintiffs' health problems” ( see Fraser v. 301–52 Townhouse Corp., 57 AD3d at 419 .) In Cornell, the court concluded, “Since plaintiff's expert's opinions relating plaintiff's condition to the mold infestation find some support in existing data, studies and literature, namely, studies that have found a statistically significant relationship between mold and respiratory maladies, the Frye standard is satisfied” ( see Cornell v. 360 W. 51st St. Realty, LLC, 95 AD3d at 53 [internal brackets, quotation marks, and citation omitted].)

In the Second Department, the only opinion that even implicitly addresses the issue in the context of exposure to mold, the court concluded that the defendant failed to meet its initial burden on its motion of summary judgment in that the expert affirmations submitted in support did not address “whether the scientific community generally accepts or rejects the theory that mold can cause asthma.” ( See Cabral v. 570 West Realty, LLC, 73 AD3d at 675.)

This Court, of course, must follow the law as it is articulated by the Second Department, unless and until the Court of Appeals rules otherwise. ( See Stewart v. Volkswagon of America, Inc., 181 A.D.2d 4, 7 [2d Dept 1992], rev'd on other grounds81 N.Y.2d 203 [1993];see also Weiner v. City of New York, 84 AD3d 140, 142 [2d Dept 2011].) To the extent, therefore, that Plaintiff's experts here “offer no novel test or technique,” and offer opinions “supported by generally accepted scientific methods,” the Court will “proceed directly to the foundational minquiry of admissibility.” ( See Ratner v. McNeil–PPC, Inc., 91 AD3d at 73.)

That “foundational inquiry” must include whether Plaintiff's experts “utilize objective standards to show that the toxic mold to which the plaintiff ... [was] allegedly exposed was capable of causing [his] injuries.” ( See Cubas v. Clifton & Classon Apt. Corp., 82 AD3d at 696;see also Cabral v. 570 West Realty, LLC, 73 AD3d at 675 [defendant's expert did not show that the plaintiffs “were exposed to insufficient levels of mold to cause their asthma”].) To that extent, the foundational inquiry is addressed to the element of “specific causation” ( see id.; see also Parker v. Mobil Oil Corp., 7 NY3d at 448 [“plaintiff was exposed to sufficient levels of the toxin to cause the illness (specific causation)”]; Muhammad v. Fitzpatrick, 91 AD3d 1353, 1354 [4th Dept 2012] [“sufficiently harmful event]; Todman v. Yoshida, 63 AD3d 606, 606–07 [1st Dept 2009].)

The trial court determines “as a preliminary matter of law” whether an adequate foundation exists to support the proferred expert opinion as to general causation and specific causation. ( See People v. Wesley, 83 N.Y.2d at 429.) Ordinarily, “[m]atters going to trial foundation” are “not properly addressed” in a pretrial proceeding addressed to that issue. ( See id. at 426.) Where, as here, however, the same evidence will be considered on whether the Frye standard is implicated by an expert's opinion; and, if so, whether it is satisfied; and, if so, whether on adequate foundation supports the opinion; no reason appears why all issues cannot be addressed prior to trial.

Because of the number of exhibits that were marked at the hearing “for identification” as support for the opinions of Plaintiff's and Defendants' respective experts, the parties stipulated that certain questions would be deemed asked and answered in the affirmative, so as to allow the expert to rely on the exhibits as a basis for the expert's opinion.

Specifically:

“MR. XANTHOS: During the lunch break, your Honor, plaintiff and I had an opportunity to hammer out a stipulation to the affect of the following, that four particular questions which I'll go over will be answered in the affirmative by each medical expert, Your Honor, will see in this Frye Hearing, and it will be stipulated these four questions need not be asked specifically with respect to each of the documents enumerated, but that part of the record will be the answer to each of these four questions assuming they were asked and we are going to assume they were will be yes. So the questions are as follows: Is the literature of a type generally relied upon by medical experts in your field in formulating the opinions you have rendered in this proceeding. That's question number one. With respect to plaintiff the literature identified is Exhibit R. It is Exhibit 54 to 128 and 132 to 137, and with respect to defendant the literature is Exhibit A, C, D and E. To the extent that additional medical literature will be supplemented each of the parties will identify whether or not it's covered by this stipulation.

Question number two, is question, is the literature not the sole basis—let me rephrase that. It's true that the literature is not the sole basis of the opinion that you have rendered in this proceeding, correct. The answer will be yes.

Number three, the third question is the methodology utilized by the authors of the literature is generally reliable. Yes, and the answer will be yes.

And question number four is the particular source of the literature is sufficiently reliable. Answer, yes. Yes. And that's the stipulation we hope will save some time.” (Transcript [“T”] at 333–34.)

The Court in effect determined that, except as to specifically noted exhibits—for example, letters to the editor or affidavits—the stipulation was sufficient to allow each expert to rely on the exhibits as a basis for the expert's opinion. ( See People v. Goldstein, 6 NY3d at 124–27;Wagman v. Bradshaw, 292 A.D.2d at 89–92.)

“[T]he rule in New York is that the trial courts must follow an Appellate Division precedent set in any department in the State until its own Appellate Division decides otherwise.” (Stewart v. Volkswagon of America, 181 A.D.2d at 7.) This Court, therefore, must follow the First Department's decision in Cornell v. 360 West 51st St. Realty, LLC (95 AD3d 50), to the extent that it resolves any of the issues presented at the hearing, and except to the extent that it is undermined by controlling authority in the Second Department on any issue ( see Weaver v. State of New York, 91 AD3d 758, 761 [2d Dept 2012].) As will appear, Cornell does not resolve all of the issues before this Court.

In Cornell, the majority concluded that the evidence offered by the plaintiff “easily satisfied the test of scientific reliability set forth in Frye ” ( see Cornell v. 360 West 51st St. Realty, LLC, 95 AD3d at 58.) Specifically, “[t]he scientific evidence shows that exposure to molds, particularly the types of molds whose presence in plaintiff's apartment was confirmed by sampling, i.e., aspergillus/penicillium, stachybotrys and chaetoium, can cause the types of ill effects experienced by plaintiff” ( see id.) In its description of the proceedings below, the court noted testimony by the plaintiff that at one point she “experienced a body rash, shortness of breath, fatigue, disorientation and headaches” ( see id. at 53), and that at a later time she “experienced dizziness, chest tightness, congestion, shortness of breath, a rash, swollen eyes and a metallic taste in her mouth” ( see id.)

To the extent that Cornell addresses the question of general causation, its conclusions must be considered dictum, since “plaintiff's expert and defendant's expert all agree[d] that mold is capable of causing the ill-health effects experienced by plaintiff” ( see id. at 61.) The court pointed to the defendant's expert's opinion that “[m]old can cause a wide spectrum of illness, including allergies, irritation, hypersensitivity pneumonitis and direct infection.” ( See id.) As to specific causation, however, the defendant's expert “conclu[ded] that mold had not caused [the plaintiff's] ailments,” and that “in the case of [the plaintiff], molds caused no significant, objectively documented illness.” ( See id.)

The plaintiff in Cornell relied on the opinion of her treating physician that “plaintiff's irritative and allergic-type symptomatology was caused by exposure to building dampness and excessive and atypical mold exposure, over time, at her apartment.” ( See id. at 55.) “[I]n arriving at a conclusion assessing the health effects of building dampness and mold exposure in plaintiff (or any other plaintiff), [the plaintiff's physician] used a differential diagnosis, the universally accepted methodology used by physicians in assessing causation and diagnosing illness.” ( See id. at 56.) The physician also relied on a number of studies, which are described by the court, and which are also relied upon by Plaintiff's expert here:

“In forming his opinion, Dr. Johanning relied on a number of peer-reviewed studies, including a 2004 publication of the Institute of Medicine in the National Academies, entitled Damp Indoor Spaces and Health, relied upon by the Fraser plaintiffs, as well as two studies which post-date Fraser, a 2007 study entitled Excess dampness and mold growth in homes: An evidence-based review of the aeroirritant effect and its potential causes (28 Journal of Allergy and Asthma Proceedings, May/June 2007), and an article published in 2008 entitled Hydrophilic Fungi and Ergosterol Associated with Respiratory Illness in a Water–Damaged Building (116 Environmental Health Perspectives, June 2008). The first study reviewed the major epidemiological and biological studies, concluding that [t]he preponderance of epidemiological data supports a link between exposure to dampness and excess mold growth and the development of aeroirritant symptoms,' ... The authors noted, in reviewing the data, that [m]ultiple studies [ ] have found a dose-response relationship between the numbers of indicators of dampness present and aeroirritant symptoms.' These studies found statistically significant relationships between visible mold growth and eye, nose and throat/respiratory symptoms.

The second study found that among workers in a building with long-term water damage, respiratory illnesses showed significant linear exposure-response relationships to total culturable fungi.' The authors stated that they had found “significant linear exposure-response relationships between various microbial measurements (total fungi, fungi requiring Awo 0.8, hydrophilic fungi, ergosterol and endotoxin) in dust and health outcomes (respiratory cases, epi-asthma cases, and post-occupancy asthma cases)'.” ( Id. at 56–57.)

Here, the studies referred to were marked as Plaintiff's Exhibits 74, 113, 138.

As to general causation, the Cornell court stated that “the studies relied upon by plaintiff's expert demonstrate a clear relationship between exposure to mold and respiratory and other symptoms” ( see id. at 58), and that the results reported by the studies “were found to be statistically significant, meaning the strength of the association was sufficient to conclude, within the range of probability, that exposure to mold caused the identified ill-health effects” ( see id. at 59.)

As to specific causation, the court recognized differential diagnosis as an accepted methodology, but stated that “in order to be considered as a possible cause, in a differential diagnosis matrix, a given agent must be capable of causing the harm observed.” ( See id. at 61.) The plaintiff would not be required to “set forth her exposure levels to the molds identified in the apartment,” since “in cases involving environmental contamination and exposure to toxic substances, ... it is generally difficult or impossible to quantify a plaintiff's exposure to a toxin.” ( See id. at 59.)

The Cornell court does not specifically address that aspect of specific causation required by Parker v. Mobil Oil Corp. (7 NY3d 434) that “plaintiff was exposed to sufficient levels of the toxin to cause the illness” ( see id. at 448 [emphasis added] ), other than to quote Parker that “it is not always necessary for a plaintiff to ... use the dose-response relationship, provided that whatever methods an experts uses to establish causation are generally accepted in the scientific community” ( see Cornell v. 360 W. 51st St. Realty Corp., 95 AD3d at 59 [quoting Parker v. Mobil Oil Corp., 7 NY3d at 448];see also id. at 60 [quoting B.T.N. v. Auburn Enlarged City School District, 45 AD3d at 1340].)

Two justices dissented on the ground that “plaintiff's expert failed to establish the reliability of his theory under the Frye standard of review-namely that his theory is generally accepted in the scientific community.” ( See id. at 62 [Catterson, J., dissenting in part].)

Applying Cornell here as to general causation, although dictum, this Court would adopt the First Department's stated conclusions to the extent that the ill-health effects identified in Cornell correspond to those alleged by Plaintiff. Contrary to the dissent, and in line with the Second Department authority discussed above, the majority in Cornell appears to apply Frye “general acceptance” to the principles and methodologies used by the expert in arriving at a theory or conclusion, rather than to the theory or conclusion itself. “Epidemiology itself is certainly not novel.” (Nonnon v. City of New York, 32 AD3d at 104.) “Epidemiological studies ... are similarly not novel.” ( Id.) “In addition, numerous courts have held that this field of science is the primary generally accepted methodology for demonstrating a causal relation between a chemical compound and a set of symptoms or a disease.” ( Id. [internal quotation marks and citation omitted].)

As to specific causation, Cornell establishes differential diagnosis as a scientifically-accepted methodology. ( See Cornell v. 360 W. 51st St. Realty, LLC, 95 AD3d at 60–61;see also B.T.N. v. Auburn Enlarged School District, 45 AD3d at 1340.) “A differential diagnosis has been described as a patient specific process of elimination that medical practitioners use to identify the most likely cause of a set of signs and symptoms from a list of possible causes.” (Fraser v. 301–52 Townhouse Corp., 57 AD3d at 435 [Mazzarelli, J., dissenting] [internal quotation marks and citation omitted].) Thus, specific causation determined via differential diagnosis as to one patient, i.e., the plaintiff in Cornell, cannot determine specific causation as to another patient, i.e., Plaintiff here.

Moreover, to the extent that Cornell conflates the two elements of specific causation-the level of exposure and the sufficiency of that level to cause ill-health effects, and/or holds that proof of the latter is not required to establish specific causation, the holding would conflict both with Parker and the Second Department authority reviewed above.

Cornell was decided after the conclusion of the Frye hearing in this action, but before the parties submitted their respective post-hearing memoranda. The Court asked the parties to specifically address the extent to which Cornell had resolved issues of general causation in this case. As might be expected, the parties do not agree. Plaintiff contends, in effect, that Cornell resolves the general causation question as to the injuries he alleges. ( See Plaintiff's Frye Hearing Memorandum ¶¶ 59, 61.) Defendants barely take note of Cornell, addressing only its treatment of the use of differential diagnosis. ( See Defendants' Post- Frye Hearing Brief at 15, 25 n8.) Although disingenuous, Defendants correctly point out, as this Court notes above, that the defendant's expert in Cornell conceded much on the issue of general causation ( see Cornell v. 360 West 51st Street Realty, LLC, 95 AD3d at 61), whereas Defendants here dispute it.

Unfortunately, a simple comparison of the injuries addressed in Cornell and those alleged here is not immediately helpful. Again, the plaintiff in Cornell alleged that at different times she experienced “body rash, shortness of breath, fatigue, disorientation and headaches” and “dizziness, chest tightness, congestion, shortness of breath, a rash, swollen eyes and a metallic taste in her mouth” ( see id. at 53.) Plaintiff here alleges upper respiratory inflamation, bacterial infection, cough, obstructive sleep apnea, mold growing in nose, sinusitis, rhinitis/rhinosinusitis, abscesses in neck/throat, nosebleeds, asthma attacks, and nasal polypsosis. One apparent difficulty arises from a lack of precise delineation between disease and its symptoms.

Indeed, the Cornell court, discussing two peer-reviewed studies relied upon by the plaintiff's expert in that case, characterized one as finding “statistically significant relationships between visible mold growth and eye, nose and throat/respiratory symptoms.” ( See id. at 57.) The other study showed “significant linear exposure-response relationships” between measured mold levels and “respiratory cases, epi-asthma cases, and post-occupancy asthma cases.” ( See id.)

All considered, the most that can be said of the effect of Cornell (95 AD3d 50) on this proceeding is that the three-justice majority neutralized the earlier ruling by the three-justice majority in Fraser (57 AD3d 416), such that Fraser does not require summary dismissal of an action alleging respiratory illness on exposure to indoor mold. Where, as here, the plaintiff's expert and the defendant's expert do not “all agree that mold is capable of causing the ill-health effects experienced by plaintiff” ( see Cornell v. 360 West 51st Street Realty, LLC, 95 AD3d at 61), the Court is not relieved of the task of determining whether the case can go forward on the expert opinion proferred to support it.

In making that assessment, the Court notes that it has not seen any appellate authority that articulates a standard of proof to be applied by the trial court at a Frye hearing. At least two trial courts have adopted the “fair preponderance of credible evidence” standard. ( See Santos v. State Farm Fire & Cas. Co., 28 Misc.3d 1078, 1079 [Sup Ct, Nassau County 2010]; Matter of Seventh Jud. Dist. Asbestos Litig., 9 Misc.3d 306, 312 [Sup Ct, Wayne County 2005].) Not seeing another standard that commends itself, this Court adopts the “fair preponderance of credible evidence standard,” although noting that the standard would more appropriately be applied to an assessment of the accuracy of an expert's conclusions than to the reliability of those conclusions. In this context, the “fair preponderance” standard appears fairly approximated by asking whether a “reasonable quantum of legitimate support exists in the literature for the expert's opinion.” ( See Lugo v. New York City Health & Hosps. Corp., 89 AD3d at 62 [quoting Marsh v. Smyth, 12 AD3d 307, 312 (1st Dept 2004) (Saxe, J., concurring) ].)

In assessing the expert opinion proffered by Plaintiff at the Frye hearing, the Court takes direction from the most recent Second Department authority, Ratner v. McNeil–PPC, Inc. (91 AD3d 63), that “where a plaintiff's qualified experts offer no novel test or technique, but intend to testify about a novel theory of causation, where such opinion is supported by generally accepted scientific methods, it is proper to proceed directly to the foundational inquiry of admissibility, which is whether the theory is properly founded on generally accepted scientific methods or principles” ( see id. at 73.) The Court has also noted, however, that “where an expert seeks to introduce a novel theory of medical causation without relying on a novel test or technique, the proper inquiry begins with whether the opinion is properly founded on generally accepted methodology, rather than whether the causal theory is generally accepted in the relevant scientific community.” ( See id. at 78 [emphasis added].)

Putting aside for the moment questions about the qualifications of the proferred expert and determination of the “relevant scientific community,” the suggestion in Ratner that something more may be required than properly-applied generally accepted methodology may mean nothing more that the foundation for the proffered expert opinion will be considered together with the expert opinion and foundation offered by the party contending for the contrary conclusion. Or it may mean, as one First Department authority holds, that properly-performed generally accepted methodology will not be deemed to lead to admissible expert conclusions “when there is a generally or widely held view in the scientific community rejecting such conclusions outright.” ( See Marso v. Novak, 42 AD3d at 378.)

Here, Plaintiff's primary expert, Dr. Irene Grant, testified in part based upon her own research, which, as will appear, was not conducted in accordance with generally accepted methodology for making determinations about medical causation. But Dr. Grant also testified, as did Plaintiff's other expert, Dr. Theodore J. Harrison, based upon peer-reviewed reports of epidemiological studies. “Epidemiology itself is certainly not novel”; indeed, “[i]t is a science which focuses on the question of general causation.” (Nonnon v. City of New York, 32 AD3d at 104 [internal quotation marks and citation omitted].) “Epidemiological studies ... are similarly not novel”; “numerous courts have held this field of science is the primary generally accepted methodology for demonstrating a causal relation between [an agent] and a set of symptoms or a disease.” ( See id. [internal quotation marks and citations omitted].)

The qualifications of the proffered expert and determination of the “relevant” medical or scientific community are related questions that, too, have not been specifically addressed in the caselaw that this Court has seen. As noted above, Dr. Grant is board-certified in internal medicine and infectious diseases; Dr. Harrison is board-certified in otolaryngology; and Dr. Stuart H. Young, Defendants' expert, is board certified in allergy and immunology. At the hearing, Dr. Grant criticized a paper relied upon heavily by Defendants because the authors did not include “the infectious disease experience,” and “don't know the infectious disease literature.” ( See T. at 519.) Dr. Grant would apparently define the “relevant” community as the “community of infectious disease experts who are working with mold.” ( See T. at 529.) Dr. Young criticized a paper relied upon by Plaintiff because its author was an epidemiologist, and no “medical doctor” participated. ( See T. at 644.) Dr. Young would apparently define the “relevant” community as the “medical community of allergists and immunologists.” ( See T. at 615–16.)

The Court has been given no basis to disqualify any of the experts who testified, or to exclude any of their respective specialties from the “orchestra of specialties,” to use Dr. Grant's phrase ( see T. at 451), that might comprise the “relevant” medical community. The roster of experts in Cornell included environmental consultants and a microbiologist. ( See Cornell v. 360 W. 51st St. Realty, LLC, 95 AD3d at 54.) On the other hand, the Court does not consider the “general primary care, general medicine, general family practice community” to be the “relevant” community for purposes of the “general acceptance” inquiries in this case, and, therefore, Dr. Grant's acknowledgment that the “general community of medicine” does not “yet recognize mold as a problem” does not itself undermine the reliability of her opinions. ( See T. at 406–08.)

Dr. Grant described the species of mold, within the genus of fungi, that are the subject in this case, i.e., aspergillus, penicillium and stachybotrys; the by-products of mold that become airborne, i.e., spores, volatile organic compounds (gases); particulate debris, and mycotoxins; and the nature and mechanisms of injury that can result from exposure to mold. Dr. Harrison described the structures of the upper respiratory system, and the nature and mechanisms of injury that can result from exposure to mold. From the perspectives of their respective specialties, Dr. Grant and Dr. Harrison testified to similar opinions as to the relationship between exposure to indoor mold and illness, and as to the “general acceptance” of those opinions.

Specifically, Dr. Grant or Dr. Harrison, or both, testified to a causal relationship between exposure to indoor mold and the following injuries alleged by Plaintiff: upper respiratory illness generally ( see T. at 40, 45–46, 182, 285–86, 309, 387); sinusitis and/or rhinosinusitis ( see T. at 151–52, 154, 167, 182, 191–92, 269–70, 285, 309, 387); asthma ( see T. at 41, 45–46); infection ( see T. at 46, 154–55, 197, 387); polyps ( see T. at 154–55); mold in nose ( see T. at 155); and sleep apnea ( see T. at 197–98.)

Neither Dr. Grant nor Dr. Harrison testified in terms about a causal relationship between mold and nosebleeds, but Dr. Grant testified that aspergillus and penicillium “have a predilection for invading blood vessels so they are also associated not just with inflamation, they are also associated with bleeding” ( see T. at 46; see also T. at 51.) Nor did either Dr. Grant or Dr. Harrison testify in terms about a causal relationship between mold and cough, but Dr. Harrison testified as to a relationship with bronchitis ( see T. at 281–82, 286.) And neither Dr. Grant nor Dr. Harrison testified in terms as to a causal relationship between mold and abscesses in neck/throat, but both testified that mold can cause infection.

Dr. Grant based her opinions in part on her own clinical research, which she described variously as “observational clinical research” ( see T. at 428), “prospective observational type of research” ( see T. at 435), and “prospective case study” ( see T. at 452.) In oversimplified terms, Dr. Grant treated individuals identified as having “[s]ignificantly heavy mold exposure” ( see T. at 454) with anti-fungal therapy, and tracked the results, concluding that “removal of the fungi removes the trouble” ( see T. at 472; see also Ponikau, Treatment of chronic rhinosinitis with intranasal amphtericin B: A randomized, placebo-controlled, double-blind trial, 115 J Allergy Clin Immunol, No. 1 [Jan 2005].)

Although Dr. Grant would disagree ( see T. at 449, 532–34), courts have determined that “observational studies or case reports are not generally accepted in the scientific community on questions of causation.” ( See Heckstall v. Pincus, 19 AD3d 203, 205 [1st Dept 2005]; see also Pauling v. Orentreich Med. Group, 14 AD3d 357, 358 [1st Dept 2005].) Recent Second Department authority does not entirely dismiss such data, considering them “of a lesser caliber than controlled clinical studies from which results can be reviewed and verified.” ( See Ratner v. McNeil–PPC, Inc., 91 AD3d at 76.) Where an expert's opinion is “primarily based upon case studies,” there may be “too great an analytical gap between the data and the opinion proffered,” and be deemed “fundamentally speculative.” ( See id. 77–78.)

Dr. Grant testified that her research is different from other observational studies. “[I]f this was just an observational study that did not include any anti-fungal treatment it would be like all the other observational studies that just say there's a lot of symptoms in mold which doesn't say anything”; “the clue, the response to therapy, is a robust clue of causation.” ( See T. at 447.) Indeed, when Defendants' expert, Dr. Stuart H. Young, was asked whether it would be methodologically improper to draw a conclusion of causation where “you give medicine, the patient improves,” Dr. Stuart answered affirmatively only if the conclusion was drawn from only one study. ( See T. at 605.) Dr. Young acknowledged such a study could show a “correlation” or “association.” ( See T. at 605, 606.)

In any event, since Dr. Grant's opinions were based on more than her own clinical research, it is unnecessary to resolve whether that research itself would be sufficient to carry Plaintiff's burden on this motion. It seems clear that the research need not be ignored, and, as the only one of the testifying experts to actually conduct research into this crucial issue, her opinions benefit from the knowledge and judgment that come with conducting one's own research.

Although more than 80 exhibits were marked at the hearing, representing the sources upon which Dr. Grant and Dr. Harrison in part based their respective opinions, not all of the items were specifically addressed in testimony, and, of those addressed, a few were given particular prominence. Two papers authored by William J. Fisk and others were given significant attention: Fisk et al, Meta–Analysis of the Associations of Respiratory Health Effects with Dampness and Mold in Homes (Lawrence Berkeley National Laboratory 2006 [“2006 Fisk Paper”] ); Fisk et al, Association of residential dampness and mold with respiratory tract infections and bronchitis: a meta-analysis (Environmental Health 2010 [“2010 Fisk Paper”].)

The 2006 Fisk Paper “report[ed] the results of quantitative meta-analysis of the studies reviewed” in a report of the Institute of Medicine of the National Academy of Sciences, which had in 2004 completed a “critical review of the scientific literature pertaining to the association of indoor dampness and mold contamination with adverse health effects.” ( See 2006 Fisk Paper at 2.) “A meta-analysis uses statistical methods to combine data from different but comparable research studies, in order to provide a quantitative summary on the size and variability of association.” ( Id. at 3.) “Based on the results of the meta-analyses, building dampness and mold are associated with approximately 30% to 80% increases in a variety of respiratory and asthma-related health outcomes.” ( Id. at 2.) Over 40 studies were included, reporting outcomes in categories of upper respiratory tract symptoms, including rhinitis and sinusitis, cough, wheeze, and asthma. All of the reviewed studies were “published in referred archival journals, which is one indicator of study quality.” ( See id. at 8.)

The 2010 Fisk Paper “report[ed] the results of quantitative meta-analyses of published studies that examined the association of dampness or mold in homes with respiratory infections and bronchitis .” ( See 2010 Fisk Paper at 1.) The meta-analyses included 23 studies, all published in “referred archival journals in English.” The review concluded, “Residential dampness and mold are associated with substantial and statistically significant increases in both respiratory infections and bronchitis.” ( See id.) Also, “Additional focused research is necessary to document whether these associations are causal.” ( See id. at 10.)

Meta-analysis is a recognized tool of epidemiology, “most appropriate when used in pooling randomized experimental trials.” ( See Reference Guide on Epidemiology, Federal Reference Manual on Scientific Evidence § VI.) “[W]hen meta-analysis is applied to observational studies—either case-control or cohort—it becomes more problematic,” because “often methodological differences among studies are much more pronounced than they are in randomized trials,” and “the justification for pooling the results and deriving a single estimate of risk, for example, is not always appropriate.” ( See id.)

Where an expert relies on an epidemiological study as part of the foundation for her opinion, including a meta-analysis, and where, as here, the expert expressly assesses the methodology of the study and finds it reliable ( see T. at 282–83, 285, 295–96), the Court will accept that the study was conducted in accordance with general accepted methodology, and the adversary will be expected to show how, if at all, the study was not properly conducted. Here, neither through their expert, Dr. Young, nor otherwise, do Defendants show that the meta-analyses described in the 2006 Fisk Paper and the 2010 Fisk Paper may not appropriately be relied upon by Dr. Grant in her opinions.

The Fisk Papers, however, raise fundamental issues that pervaded the hearing in this case: what do we mean by “causation” when we assess “general causation” in tort cases, and, specifically, how is that assessment affected by the connection of “dampness” to mold in the literature (and, indeed, in certain of the cases)? For example, the 2006 Fisk Paper states:

“We do not distinguish among dampness, mold, dampness or mold, and dampness and mold as risk factors. Our rationale-visible mold is always considered the result of excess dampness, whether or not the dampness is reported, and excess dampness is very often accompanied by mold, although the mold may not be visible. Thus, it is not possible to make a clear distinction among these risk factors .” ( See 2006 Fisk Paper at 3–4.)

“Statistical associations do not prove that dampness and mold are causally related to the health outcomes. Building dampness itself is very unlikely to directly cause adverse health effects ... Building dampness may cause the building to become contaminated with microorganisms such as mold or bacteria, which might in-turn cause adverse health effects ... Research has not yet determined the casual agents ...” ( Id. at 8.)

The 2010 Fisk Paper makes almost identical statements, but continues, “However, the consistent evidence of adverse health effects from a substantial number of studies that have controlled for key potential confounders, along with the moderately strong associations and the limited evidence of publication bias, provide initial evidence for causal links between these health effects and some dampness related agent(s).” (2010 Fisk Paper at 6.)

One of the studies specifically identified in the 2010 Fisk Paper is also relied upon by Dr. Grant: World Health Organization Regional Office for Europe, WHO Guidelines for Indoor Air Quality: Dampness and Mold (2009) (“WHO Guidelines”). “[T]he document provides a comprehensive review of the scientific evidence on health problems associated with building moisture and biological agents,” and “concludes that the most important effects are increased prevalences of respiratory symptoms, allergies and asthma as well as perturbation of the respiratory systems.” (WHO Guidelines, Abstract.) But, “the individual species of microbes and other biological agents that are responsible for health effects cannot be identified.” ( Id., Executive Summary, at XII.)

The WHO Guidelines includes “separate reviews and a synthesis of the epidemiological, clinical and toxicological evidence on the health effects of dampness and mould,” including the 2006 Fisk Paper. (WHO Guidelines at 63.) The document includes “studies involving human volunteers or experimental animals exposed in controlled circumstances, occupational group or clinically”; “both the exposure and the clinical outcomes are characterized better than they are in the epidemiological studies.” ( See WHO Guidelines at 78.) The document also includes a “brief review of toxicological studies on microbial exposure in damp buildings,” both studies in vitro and studies in experimental animals in vivo. ( See id. at 84.) “Toxicology is ... not a novel field of science.” (Nonnon v. City of New York, 32 AD3d at 105.)

The WHO Guidelines reports a “[s]ynthesis of available evidence on health effects,”based initially on the epidemiological and clinical evidence for causal relations between dampness-related factors and specific human health outcomes,” with the toxicological evidence considered “as either supporting or not supporting the biological plausibility of any potentially causal association.” ( See WHO Guidelines at 89.) The results are reported in accordance with a five-category classification scheme: “Sufficient evidence of a causal relationship”; “Sufficient evidence of an association”; “Limited or suggestive evidence of an association”; “Inadequate or insufficient evidence to determine whether an association exists”; and “Limited or suggestive evidence of no association.” ( See id. at 66.)

This classification system is used as well in a report published by the National Academy of Sciences, also relied upon by Dr. Grant for her opinions: Committee on Damp Indoor Spaces and Health of the Institute of Medicine, Damp Indoor Spaces and Health (2007) (“IOM Report”) ( see Executive Summary at 8.) (This appears to be the report that is referenced in the 2006 Fisk Paper, although the copyright date of the IOM Report is later than the date on the Fisk Paper marked at the hearing.) Dr. Grant acknowledged the classification scheme in part in her testimony at the hearing; specifically, the description of the category “Sufficient evidence of a causal relationship.” ( See T. at 300.)

“Sufficient evidence of a causal relationship” in this scheme is evidence that “fulfills the criteria for sufficient evidence of an association' and, in addition, satisfies the following evaluation criteria: strength of association, biological gradient, consistency of association, biological plausibility and coherence and temporally correct association.” (WHO Guidelines at 66.) “Sufficient evidence of an association” is “an association between the agent and the outcome ... observed in studies in which chance, bias and confounding could be ruled out with reasonable confidence,” such as studies that “show an association that is consistent in magnitude and direction.” ( Id.) “The finding of sufficient evidence of a causal relationship ... means that the exposure can cause the outcome, at least in some people under some circumstances.” ( Id.)

Using this classification scheme, the WHO Guidelines states that “[t]he epidemiological evidence is not sufficient to conclude causal relationships between indoor dampness or mould [ sic ] and any specific human health effect,” although “[t]here is sufficient epidemiological evidence of association between dampness or mould [ sic ] and asthma development, asthma exacerbation, current asthma, respiratory infections (except otitis media), upper respiratory tract symptoms, cough, wheeze and dyspnea.” ( Id. at 89.) “In vitro and in vivo studies have demonstrated diverse inflammatory, cytotoxic and immunosuppressive responses after exposure to the spores, metabolites and components of microbial species found in damp buildings, lending plausibility to the epidemiological findings.” ( Id. at 90.)

There are conceptions of “causation” and “association” that are different from those described above, but not necessarily inconsistent with them. The Federal Reference Manual on Scientific Evidence defines “association” as “[t]he degree of statistical relationship between two or more events or variables.” ( See Reference Guide on Epidemiology [“ “Reference Guide”], Glossary of Terms.) “Events are said to be associated when they occur more or less frequently together than one would expect by chance.” ( Id .) “Association does not necessarily imply a causal relationship.”

“Causation ... denotes an event, condition, characteristic, or agent's being a necessary element of a set of other events that can produce an outcome, such as a disease.” ( Id.) “Other sets of events may also cause the disease.” ( Id.) “A cause may be thought of as a necessary link in at least one causal chain that results in an outcome of interest.” ( Id.) “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 with, the familiar but for,' or sine qua non, test is [ sic ] used in law for cause in fact.” (Reference Guide § V.) “This is equivalent to describing the act or occurrence as a necessary link in a chain of events that results in the particular event.” ( Id. [footnote omitted.)

“[E]pidemiology cannot objectively prove causation, rather, causation is a judgment for epidemiologists and others interpreting data.” ( Id.) “[S]cientific determinations of causation are inherently tentative.” ( Id.) “Most researchers are conservative when it comes to assessing causal relationships, often calling for stronger evidence and more research before a conclusion of causation is drawn.” ( Id. [footnote omitted].)

“The factors that guide epidemiologists in making judgments about causation are 1. temporal relationship; 2. strength of the association; 3. dose-response relationship; 4. replication of the findings; 5. biological plausibility (coherence with existing knowledge); 6. consideration of alternative explanations; 7. cessation of exposure; 8. specificity of the association; and 9. consistency with other knowledge.” ( Id.) “There is no formula or algorithm that can be used to assess whether a causal inference is appropriate based on these guidelines.” ( Id.) “While the drawing of causal inferences is informed by scientific expertise, it is not a determination that is made by using scientific methodology.” ( Id.)

Although Dr. Grant acknowledged that “causation” meant something different to an epidemiologist than it meant to her as a clinician ( see T. at 296–98, 316–17), she acknowledged the meaning of “causation” as described in the IOM Report and WHO Guidelines, including the difference between “causation” and “association” ( see T. at 416–18.) Interestingly, Dr. Young also a clinician, characterized “association” as “a lower level of causation.” ( See T. at 565.)

Dr. Grant addressed studies that speak only of dampness, or that do not differentiate in reporting results between dampness and mold, conceding that such studies would be less useful than those that report results specifically as to exposure to mold ( see T. at 473–78, 507–08.) Dr. Grant also testified that, although “the science isn't totally out yet,” exposure to mold by-products can cause an immunosuppressive response ( see T. at 38–39.) The WHO Guidelines noted the “immunosuppressive effects of damp building-associated microbes in experimental animals, which impair immune defences [ sic ] and thus increase susceptibility to infections.” (WHO Guidelines at 91.) “The synergistic interactions among microbial agents present in damp buildings suggest that the immunotoxic effects of the fungal and bacterial strains typically found can be potentiated during concomitant exposure, leading, for instance, to increased cell death or cytotoxic or inflammatory effects.” ( Id.) And the 2010 Fisk Report stated that, “although it has not been demonstrated that exposures to microbial toxins in typical damp or moldy houses can suppress immune response in humans, potential underlying mechanisms can be suggested.” (2010 Fisk Report at 7.) Indeed, joint exposures to the fungal and bacterial strains typically found in damp buildings “could explain lack of evident associations for specific exposures.” ( See id. at 8.)

Although the Court would take some issue with the linearity of the link-in-the-chain metaphor used in the epidemiologic conception of causation, that conception seems closely related to the “substantial factor” formulation of “legal cause.” ( See Derdiarian v. Felix Contracting Corp., 51 N.Y.2d 308, 314–15 [1980];Nallan v. Helmsley–Spear, Inc., 50 N.Y.2d 507, 520 [1980].) That an agent may be one of a “set of other events” and satisfy the epidemiologic conception of causation is consistent with the possibility that there may be more than one legal cause of an injury. ( See Argentina v. World Wide Delivery Corp., 93 N.Y.2d 554, 561 n2 [1999]; Forte v. Albany, 279 N.Y. 416, 422 [1939].)

Were “general causation” necessarily limited to the results of epidemiological studies that show “causation” as determined in accordance with the epidemiologic conception, Plaintiff's position here would be difficult, if not impossible, to sustain. None of the many additional sources that were relied upon by Dr. Grant or Dr. Harrison, or both, in reaching her or his opinions find “causation” in the epidemiologic conception. As recently as last year, a group of authors stated that “there is not sufficient epidemiologic evidence of a causal relationship for any of the reviewed health outcomes, although for asthma exacerbation in children ... the evidence [is] strongly suggestive of causality by dampness-related agents.” (Mendell et al, Respiratory and Allergic Health Effects of Dampness, Mold, and Dampness–Related Agents: A Review of the Epidemiologic Evidence, 119 Environmental Health Perspectives, No. 6 at 755 [June 2011].) Nonetheless, the consistency of the respective conclusions of the published sources gives reliability to the “association” between exposure to indoor mold or dampness and various upper respiratory illnesses, asthma, infections, and bronchitis.

In any event, “general causation” is not limited to the results of epidemiological studies that show “causation” as determined in accordance with the epidemiologic conception. Again, the question is “whether a reasonable quantum of legitimate support exists in the literature for the expert's views.” ( See Lugo v. New York Health & Hosps., Corp., 89 AD3d at 62.) Where a “synthesis” of the medical literature produced by the plaintiff's expert at a Frye hearing “considered in the aggregate ... establish that [the expert's] theory [is] properly based upon far more than theoretical speculation or a scientific hunch',” the expert's opinion will pass the Frye test. ( See id. at 60–61.)

The Frye test determines the admissibility of opinion, which is comprised, not only of the sources relied upon by the expert in formulating the opinion that are themselves not admissible as evidence ( see Hinlicky v. Dreyfuss, 6 NY3d 636, 645–48 [2006];Spensieri v. Lasky, 94 N.Y.2d 231, 236–39 [1999] ), but also of the knowledge, experience, and professional judgment of the expert. As noted above, even the epidemiologic conception of “causation” is a judgment, and not a “formula or algorithim.” ( See Reference Guide § V.) Where, as here, there is substantial and consistent epidemiological evidence of a relationship between exposure to indoor mold and illness, the Court has no warrant to disregard the knowledge, experience, and judgment of an infectious disease specialist or an otolaryngologist who says that the relationship is strong enough to be determined to be causal. Dr. Grant's characterization of the research as showing an “increasingly robust association” ( see T. at 315–16) reflects both the quantitative nature of the assessment, and the development of the foundation for professional judgment.

Defendants' opposition to the admissibility of the expert opinion of Dr. Grant and Dr. Harrison is primarily two-fold. First, Defendants rely on the expert opinion of Dr. Stuart Young, who bases his opinions in part on a “position paper” of the American Academy of Allergy, Asthma and Immunology (Bush, et al, The medical effects of mold exposure [2006] [“AAAAI Position Paper”] ), and a “position statement” of the American College of Occupational and Environmental Medicine (Adverse Human Health Effects Associated with Molds in the Indoor Environment [2011] [“ACOEM Position Statement”].) Second, Defendants contend that Plaintiff has not established a “threshold level by which it has been proven that exposure to indoor residential mold can cause the type of injuries alleged by the plaintiff”; that “[w]ithout the ability to establish specific causation, the plaintiff cannot prevail on a personal injury claim.” ( See Defendants' Post–Frye Hearing Brief at 25.) Defendants rely heavily on the First Department's decision in Fraser v. 301–52 Townhouse Corp. (57 AD3d 416), which has been undermined by that court's later ruling in Cornell v. 360 W. 51st St. Realty, LLC (95 AD3d 50.)

Dr. Young did not testify in terms that exposure to indoor mold does not, or can not, cause illness, although he did disagree that there is a “significant association between mold,” presumably indoor mold, “and adverse health effects, especially upper respiratory disease.” ( See T. at 645.) Dr. Young did acknowledge, however, in certain occupational settings, indoor mold does cause illness ( see T. at 574–78), “mainly farm, agricultural, because that's where you get massive amounts” ( see T. at 578.)

Dr. Young also testified that exposure to “external mold”/”outdoor mold” can cause asthma, and that, “in [his] experience and in what [he] read,” outdoor mold can cause rhinitis. ( See T. at 563, 621.) He acknowledged that most species of mold are found both indoors and outdoors ( see T. at 571), and that “[w]hat is outdoor can become indoor” ( see id.) He stated that the respective levels of exposure are significantly different, but he could not say what level(s) of exposure to outdoor mold could cause illness. ( See T. at 571–74.)

Dr. Young's testimony was primarily a vehicle for review of the conclusions of the AAAAI Position Paper and ACOEM Position Statement. The stated purpose of the AAAAI Position Paper was “to provide a state-of-the-art review of the role that molds are known to play in human disease, including asthma, allergic bronchopulmonary aspergillosis, sinusitis, and hypersensitive pneumonitis.” ( See AAAAI Position Paper at 326.) The AAAAI Position Paper starts with the statement, “Exposure to certain fungi (molds) can cause human illness.” ( See id.) “Molds can cause adverse human health effects through 3 specific mechanisms: generation of a harmful immune response (eg, allergy or hypersensitive pneumonitis (HP), direct infection by the organism, and toxic-irritant effects from mold byproducts.” ( Id.)

The paper addresses a number of pathological responses alleged to result from indoor mold, and either finds support in the literature reviewed, or not. As they appear to relate to the injuries alleged here, “Allergic responses to inhaled mold antigen are a recognized factor in lower airway disease (ie, asthma),” but, “Currently available studies do not conclusively prove that exposure to outdoor airborne molds plays a role in allergic rhinitis, and studies on the contribution of indoor molds to upper airway allergy are even less compelling” and, “Data supporting the role of fungi in [chronic rhinosinusitis] are lacking at this time.” ( See id. at 327.)

In addition, “The occurrence of mold-related toxicity (mycotoxicosis) from exposure to inhaled mycotoxins in nonoccupational settings is not supported by the current data, and its occurrence is improbable,” and, “The occurrence of mold-related irritant reactions from exposure to fungal irritants in nonoccupational settings are theoretically possible, although unlikely to occur in the general population given exposure and dose considerations.” ( See id. at 329.) “Host factors, rather than environmental exposure are the main determinant of opportunistic fungal infection.”

The AAAAI Position Paper is based upon a literature review, a form of research that Dr. Young acknowledged is not conducted pursuant to a generally accepted methodology. ( See T. at 639–40 .) Dr. Young did not know the selection criteria the authors used, “which journal articles would be included and which ones would not be and which ones were to be given credit and which ones were not.” ( See T. at 640.) Nor did Dr. Young know “how many people approved of [the document] before it was allowed to become the position paper of the AAAAI.” ( See T. at 639.) Perhaps most importantly, Dr. Young acknowledged that “there's disagreement among allergists and immunologists whether mold can cause adverse human health effects,” but “it's not a very major disagreement at all.” ( See T. at 638.) There is no evidence, from Dr. Young or otherwise, as to the significance of a “position paper” or “position statement” to the AAAAI or the ACOEM, or the rest of the medical community.

The ACOEM Position Statement was given much less attention at the hearing than the AAAAI Position Statement, perhaps because the copy of the document that was marked is almost illegible. The Summary portion of the document is interesting in its recognition that mold may cause adverse effects in allergic and immuno-compromised persons:

“For almost all allergic individuals, the reactions [to mold] will be limited to rhinitis or asthma; sinusitis may occur secondarily due to obstruction ... To reduce the risk of developing or exacerbating allergies, mold should not be allowed to grow unchecked indoors.

...

Fungal infections of deeper tissues are rare and in general are limited to persons with severely impaired immune systems.

...

Some molds that propagate indoors may, under certain conditions, produce mycotoxins that can adversely affect living cells and organisms by a variety of mechanisms ... Levels of exposure in the indoor environment, dose-response data in animals and dose-rate considerations suggest that delivery by the inhalation route of a toxic dose of mycotoxins in the indoor environment is highly unlikely, even for the most vulnerable subpopulations.

...

[M]old is likely to sensitize and produce allergic responses in allergic individuals. Except for persons with severely impaired immune systems, indoor mold is not a source of fungal infections. Current scientific evidence does not support the existence of a causal relationship between inhaled mycotoxins in home, school, or office environments and adverse human health effects.” (ACOEM Position Statement at 4–5.)

“Causation” in law extends to those injuries that result because of a weakness or predisposition of the plaintiff. ( See McCahill v. New York Transp. Co., 201 N.Y. 221, 223 [1911];Ortiz v. Mendolia, 116 A.D.2d 707, 708 [2d Dept 1986].) It also extends to the aggravation/exacerbation of a pre-existing condition. ( See Edmond v. International Bus. Machs. Corp., 91 N.Y.2d 949, 950 [1998];Doyle v. Am. Home Prods. Corp., 286 A.D.2d 412, 413–14 [2d Dept 2001].) “The causation rule ... in tort law ... is that an accident which produces injury by precipitating the development of a latent condition or by aggravating a preexisting condition is a cause of that injury.” ( See Matter of Tobin v. Steisel, 91 N.Y.2d 254, 259 [1985].) Here, if illness results from exposure to mold in allergic or immunosuppressed persons, or increases that harm from an allergic or immunological response, the mold would be deemed the cause of the illness, notwithstanding the underlying condition, assuming, of course, sufficient proof.

It cannot be said, based upon Dr. Young's testimony and the sources on which he relied, that “there is a generally or widely held view in the [relevant medical] community rejecting ... the conclusions [of Plaintiff's experts] outright.” ( See Marso v. Novak, 42 AD3d at 378.) Indeed, Dr. Young's testimony, the AAAAI Position Paper, and ACOEM Position Statement are consistent with the opinions of Plaintiff's experts in that all agree that exposure to mold, at some level(s) and for some population(s), causes some illness of the types alleged by Plaintiff.

Which brings up Defendants' contention that Plaintiff has not established a “threshold level by which it has been proven that the exposure to indoor residential mold can cause the type of injuries alleged” by him, which Defendants properly recognize is an issue of “specific causation.” (Defendants' Post–Frye Hearing Brief at 25.) As articulated in Parker v. Mobil Oil Corp., (7 NY3d 434), the question is whether the plaintiff “was exposed to sufficient levels of the toxin to cause the illness” ( see id. at 448.) Specifically, the question here is whether Plaintiff's experts “utilize objective standards to show that the toxic mold to which [Plaintiff] ... [was] allegedly exposed was capable of causing his injuries.” ( See Cubas v. Clifton & Classon Apt. Corp., 82 AD3d at 696.) Although it is clear that this aspect of “specific causation” is subject to Parker's foundational inquiry, it is not clear that the inquiry should be resolved in this proceeding.

There is no dispute that neither Dr. Grant nor Dr. Harrison testified to any “dose-response relationship” between exposure to mold and illness, or to any other “threshold” level of exposure necessary to cause illness. Dr. Harrison testified that “no specific microbial metric has been shown to be a consistent risk factor for health” ( see T. at 195), and Dr. Grant acknowledged that “[i]n the published literature” “there are no established mold threshold levels that constitute a high level inside an indoor residential apartment” ( see T. at 457–58.) Dr. Grant and Dr. Young agree that there are ethical limitations on the possibilities of research on such issues ( see T. at 301, 645.) As Dr. Grant put it, “you cannot do an intentional mold study. Tuskegee comes to mind.” ( See T. at 462.)

There are other limitations as well on identifying a dose-response relationship or “threshold” level of exposure. Dr. Grant testified that, unlike exposure to a chemical agent, such as a drug, where “[t]he dose of the drug is so straight forward” ( see T. at 305), infectious disease is complicated and dynamic, involving the pathogenicity of the organism, the toxins it produces, progression over time, and the immune status of the host. ( See T. at 304–05.) “If you're sensitive to mold ... that's the dose.” (T. at 498.)

As previously noted, Parker does not require that a dose-response relationship be established; it is sufficient if “whatever methods an expert uses to establish causation are generally accepted in the scientific community.” ( See Parker v. Mobil Oil Corp., 7 NY3d at 448.) Dr. Harrison testified that, to a clinician, “the presence [of the mold] and the smell and the sense of irritation is—shows the individual is having an effect from the fungus.” ( See T. at 195.) Dr. Grant noted that, in connection with her own studies, she used standards provided by an industrial hygienist, i.e., “[t]en-fold indoor compared to outdoor” as “heavy mold exposure,” and five-fold for “chronic exposure.” ( See T. at 457.) Dr. Grant also described the process of differential diagnosis, including the response to therapy, as a methodology for establishing causation.” ( See T. at 316–17, 420.)

As previously noted, Cornell established differential diagnosis as a scientifically-accepted methodology for determining specific causation. ( See Cornell v. 360 W. 51st St. Realty, LLC, 95 AD3d at 60–61.) “There may be instances where, because of the rigor of differential diagnosis performed, the expert's training and experience, the type of illness or injury at issue, or some other case-specific circumstance, a differential diagnosis is sufficient to support an expert's opinion in support of both general and specific causation.” (Ruggiero v. Warner–Lambert Co., 424 F3d 249, 254 [2d Cir2005].)

Although exhibits were marked at the hearing that would be directed to the issue of specific causation, the hearing proceeded almost entirely as directed to the issue of general causation, in particular the question of whether the opinions of Plaintiff's experts on general causation will be admissible at trial. It would be inappropriate for the Court to rule on specific causation, except to conclude that it cannot be said as a matter of law that Plaintiff cannot establish that he “was exposed to sufficient levels of [mold] to cause the illness” he alleges ( see Parker v. Mobil Oil Corp., 7 NY3d at 448.) Whether there will be adequate foundation for the opinions of Plaintiff's expert(s) on that issue, as well as any other aspects of specific causation, must be determined at trial.

In sum, Plaintiff has shown that “a reasonable quantum of legitimate support exists in the literature for [his] expert[s'] views” as to general causation ( see Lugo v. New York Health & Hosps. Corp., 89 AD3d at 62;see also Cornell v. 360 West 51st St. Realty, LLC, 95 AD3d at 58); and Defendants have not shown that “there is a generally or widely held view in the [medical] community rejecting such conclusions outright” ( see Marso v. Movak, 42 AD3d at 378.) Plaintiff must yet show specific causation, including that he “was exposed to sufficient levels of [mold] to cause the illness” he alleges. ( See Parker v. Mobil Oil Corp., 7 NY3d at 448.)

To the extent Defendants' motion seeks any relief other than the convening of a Frye hearing, the motion is denied. The parties shall appear for a pre-trial conference at 2:30 p.m. on Monday, August 13, at which time a schedule will be adopted for any further pre-trial motions, and a date will be set for jury selection and trial.