Searching over 5,500,000 cases.


searching
Buy This Entire Record For $7.95

Download the entire decision to receive the complete text, official citation,
docket number, dissents and concurrences, and footnotes for this case.

Learn more about what you receive with purchase of this case.

Fraser v. 301-52 Townhouse Corp.

December 30, 2008

COLIN FRASER, ET AL., PLAINTIFFS-APPELLANTS,
v.
301-52 TOWNHOUSE CORP., ET AL. DEFENDANTS-RESPONDENTS.



Order, Supreme Court, New York County (Shirley Werner Kornreich, J.), entered July 9, 2007, which granted plaintiffs' motion for reargument and renewal of a prior order, same court and Justice, entered October 5, 2006, which, after a Frye hearing, granted defendants' motion to preclude plaintiffs from offering certain expert evidence at trial and granted defendants summary judgment dismissing plaintiffs' causes of action based on personal injury, and, upon reargument and renewal, adhered to the original determination, affirmed, without costs. Appeal from the aforesaid order entered October 5, 2006, unanimously dismissed, as academic, without costs.

Published by New York State Law Reporting Bureau pursuant to Judiciary Law § 431.

This opinion is uncorrected and subject to revision before publication in the Official Reports.

Mazzarelli, J.P., Friedman, Nardelli, Williams, Freedman, JJ.

113586/02

Plaintiffs, former residents of a unit in the cooperative apartment building owned by defendant 301-52 Townhouse Corp., assert causes of action against defendants for, inter alia, 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. Upon defendants' motion seeking summary judgment and preclusion of plaintiffs' expert evidence purporting to establish that the building's alleged dampness and mold condition caused their health problems, the motion court directed that a Frye hearing be held to determine whether plaintiffs' causation theory was generally accepted as reliable within the relevant scientific community. After the Frye hearing, the court granted defendants' motion, precluding the expert evidence and dismissing the personal injury claims (other causes of action were severed for further proceedings). The court subsequently granted plaintiffs reargument and renewal, and, upon reargument and renewal, adhered to the prior determination. We now affirm.

Contrary to the dissent's contention, defendants' experts did deny that it is generally accepted within the scientific community that it has been established that indoor dampness and mold "cause" health problems like plaintiffs'. While there is general agreement that indoor dampness and mold are "associated" with upper respiratory complaints, defendants' experts took the position, consistent with the literature they submitted, that the observed association between such conditions and such ailments is not strong enough to constitute evidence of a causal relationship*fn1. In other words, " association' is not equivalent to causation'" (Green, Freedman & Gordis, Reference Guide on Epidemiology, in Federal Judicial Center, Reference Manual on Scientific Evidence, at 336 [2d ed 2000] [emphasis in original]; see also id. at 348 ["Although a causal relationship is one possible explanation for an observed association between an exposure (to an agent) and a disease, an association does not necessarily mean that there is a cause-effect relationship"]). In this regard, even plaintiffs' main expert, Dr. Eckardt Johanning, testified that "association" is not the same concept as "causation." Given that plaintiff failed to demonstrate general acceptance of the notion that a causal relationship has been demonstrated between the conditions and ailments in question, Dr. Johanning's claim to have established causation in this case by means of "differential diagnosis" is unavailing (see Marso v Novak, 42 AD3d 377, 378 [2007] [expert's opinion as to causation, at which he arrived through differential diagnosis, was not admissible where the resulting conclusion was not accepted in the medical community]; see also Lara v New York City Health & Hosps. Corp., 305 AD2d 106 [2003] [affirming preclusion of expert testimony that "relied solely on a theory . . . neither recognized nor accepted" in the medical community]). Thus, on the record presented to us, plaintiffs have failed to meet their burden of establishing general acceptance of the theory on which the specific claims at issue are based. We note that whether plaintiffs' theory of causation is scrutinized under the Frye inquiry applicable to novel scientific evidence (see Parker v Mobil Oil Corp., 7 NY3d 434, 446-447 [2006]) or under the general foundational inquiry applicable to all evidence (see id. at 447), the conclusion is the same: the proffered expert evidence must be precluded on the ground that the underlying causal theory lacks support in the scientific literature placed before us in the present record. We stress that our holding does not set forth any general rule that dampness and mold can never be considered the cause of a disease, only that such causation has not been demonstrated by the evidence presented by plaintiffs here.

Nothing said here "set[s] an insurmountable standard" (Parker, 7 NY3d at 447) for the reception of scientific evidence. In particular, we disclaim the suggestion attributed to us by the dissent that "Frye requires that the medical literature conclusively establish that an allegedly offending substance not only have the potential to cause illness but that it always causes illness" (emphasis in original). To be clear, the deficiency of plaintiffs' expert evidence is not that the medical literature fails to "conclusively establish" their causal theory or to show that indoor dampness and mold "always cause[] illness."*fn2 Rather, plaintiffs' expert evidence falls short because none of the medical literature in the record supports the stated position of plaintiffs' expert that the observed association between damp or moldy indoor environments and upper respiratory symptoms is strong enough to be considered, under generally accepted principles of scientific analysis, evidence that the former causes the latter. Aside from referencing two studies that Dr. Johanning mischaracterized as demonstrating a causal link, the dissent does not identify any study concluding that indoor dampness and mold have been shown to cause upper respiratory symptoms such as plaintiffs'*fn3. Without any warrant in the scientific literature in the record, the dissent, like Dr. Johanning, simply asserts that "the association' between building dampness and illness is one of causation," thereby conflating the distinct concepts of association and causation.*fn4

Even if it is assumed that plaintiffs' experts established the general acceptance of their view that indoor dampness and mold is capable of causing plaintiffs' health problems (general causation), the experts failed to specify the threshold level of exposure to dampness or mold needed to produce these effects. Without evidence that they were exposed to a level of dampness or mold sufficient to cause their alleged injuries (specific causation), plaintiffs cannot prevail on their personal injury claims (see Parker, 7 NY3d at 448 [plaintiff must show not only exposure to the toxin and that the toxin is capable of causing the particular illness alleged, i.e., general causation, but also that plaintiff was exposed to sufficient levels of the toxin to cause the illness, i.e., specific causation]). It appears from plaintiffs' own literature that there is no standardized or recognized method of measuring "dampness," thus rendering it impossible for plaintiffs' experts to compare the level of dampness in plaintiffs' apartment to that in the studies (cf. id. at 449). Nor would plaintiffs' experts be able to make any reasoned comparison of plaintiffs' exposure to the by-products of dampness to those in other studies. While plaintiffs did offer a measure of the level of mold present in the apartment, their experts did not testify to any threshold level at which mold is capable of causing the injuries of which plaintiffs complain. Finally, while "it is not always necessary for a plaintiff to quantify exposure levels precisely or use the dose-response relationship" (id. at 448), we do not believe that, under the circumstances, plaintiffs' reliance on the method of differential diagnosis was an adequate substitute for quantitative proof.

An additional ground for granting summary judgment dismissing the personal injury claims is that plaintiffs failed to offer a reliable measurement of the level of mold in the subject apartment. That is to say, even if plaintiffs' theory of causation satisfied the Frye test, the mold measurement they offered does not meet the standard of reliability set forth in the record and therefore fails to satisfy the post-Frye foundational inquiry into "whether the accepted methods were appropriately employed in a particular case" (Parker, 7 NY3d at 447, citing People v Wesley, 83 NY2d 417, 429 [1994])*fn5. A textbook that plaintiffs placed into evidence at the hearing states that an estimate of average inhalation exposure should be based on sampling at least three times a day for at least three consecutive, representative days, with duplicate samples for all analyses (Macher, ed., Bioaerosols: Assessment and Control, at 5-10 [1999]). Plaintiffs' environmental expert, however, collected only two indoor air samples within a short time span on the same day, which, according to plaintiffs' own authority, was insufficient.

Finally, although defendants filed their motion for summary judgment 300 days after the filing of the note of issue, defendants have demonstrated good cause for the delay in that disclosure had been completed only two weeks before the motion was made. Accordingly, the motion was properly considered on the merits (see Pena v Women's Outreach Network, Inc., 35 AD3d 104, 108 [2006]).

All concur except Mazzarelli, J.P. and Nardelli J., who dissent in a memorandum by Mazzarelli, J.P. as follows:

MAZZARELLI, J. (dissenting)

Plaintiffs allege that they suffered adverse health effects as a result of chronic water leaks into their cooperative apartment. The leaks began in 1996. In their bill of particulars plaintiffs asserted that, as a result of the leaks, damp conditions prevailed in the apartment and promoted the generation of "toxic mold, toxic fungi, [and] other microbial life." They further claimed that the damp conditions caused them to suffer, among other things, repetitive upper respiratory infections, asthmatic symptoms, severe allergic reactions and allergy symptoms, rashes and fatigue. In addition, plaintiffs claimed certain cognitive and fertility problems, but subsequently withdrew those claims.

Plaintiffs identified five expert witnesses who they expected to testify at trial. Included among those experts was Dr. Eckardt Johanning, a medical doctor who had examined plaintiffs and who has extensively studied in the field of "health effects of microbiological exposure." The disclosure statement indicated that Dr. Johanning was expected to testify that the damp conditions inside the apartment exposed plaintiffs to "excessive and atypical microbiological contamination." Dr. Johanning was further expected to testify that such exposure can cause serious health effects in humans and that plaintiffs were harmed by the damp conditions in their apartment.

Defendants moved for summary judgment and, in the alternative, for preclusion of plaintiffs' medical experts, or a hearing pursuant to Frye v United States (293 F 1013 [DC Cir 1923]). With respect to summary judgment, defendants argued that plaintiffs could not prove that, generally speaking, "the presence of, or exposure to, mold in an indoor residential setting causes the types of ailments" alleged by plaintiffs. They argued that plaintiffs could not specifically prove they were exposed to "mycotoxins" in the apartment and that, even if they could, they could not prove when the exposure took place or the "dose or duration" of any such exposure.

With respect to preclusion, defendants specifically sought to bar testimony "to the extent the plaintiffs intend to have [their expert] witnesses provide scientific evidence' or opinions that: (a) the presence of, or exposure to, mold in an indoor residential setting causes the types of ailments for which [p]laintiffs are seeking money damages (such evidence' or opinions are not generally accepted as reliable by the scientific community); and (b) the presence of, or the exposure of [p]laintiffs to, mold in the Apartment caused [p]laintiffs' specific alleged injuries (such evidence' or opinions cannot be provided with a reasonable degree of medical certainty)."

Defendants submitted affidavits from three physicians in support of the motion. One of the affidavits, that of a neuropsychologist, became irrelevant once plaintiffs withdrew their claim that the damp condition in their apartment caused them to suffer cognitive deficits. The first was by Ronald E. Gots, M.D., Ph.D., a toxicologist who does not purport to have any expertise in mold sampling methodology. He devoted three paragraphs to critiquing mold sampling performed inside the apartment and offered some generalities purporting to support his opinion that the sampling data "is not reliable for determining exposure." Dr. Gots failed to discuss any of the specific findings in any of the mold sampling reports exchanged by plaintiffs during discovery.

Dr. Gots opined that it is highly unlikely that the levels of mold humans can be exposed to in residential or commercial buildings can ever be enough to cause mycotoxicosis, that is, illness caused by the biochemical products produced by molds as part of their life cycle. However, he acknowledged that indoor mold can cause allergic effects "manifest[ed] primarily as respiratory allergies" and that, although uncommon, "[i]rritant effects may occur when there is significant mold growth (thousands of mold spores per cubic meter of air)." At best, he stated, household mold can cause allergic reactions in the 5% of people who are allergic to mold in the first place. Dr. Gots cited to two published scientific works to support his theory that any relation between building dampness and illness is essentially hypothetical. These were a 2002 paper by the American College of Occupational and Environmental Medicine (ACOEM) entitled Adverse Human Health Effects Associated with Molds in the Indoor Environment, and a 2004 book entitled Damp Indoor Spaces and Health, which reflected findings of a study conducted by the Institute of Medicine of the National Academies (IOM).

Dr. Gots also opined that under "causation analysis" plaintiffs could not prove their claim. He described the basic principle of such analysis as (1) identifying what is wrong with the patient, (2) whether the "agent at issue" can produce the given disorder, and (3) whether the agent did indeed cause the disorders at issue in the case. He claimed that plaintiffs could not have had an allergic reaction to mold because "RAST" blood testing performed on them, which looked for allergen-specific IgE-mediated antibodies, was negative. He discounted IgG testing results*fn6 as irrelevant to respiratory allergies and stated that, in any event, positive IgG results could not prove the time and place of exposure. He described the complaints of plaintiffs recorded in their medical records as subjective and not contemporaneous with medical visits. He further questioned why the symptoms persisted even after plaintiffs vacated the apartment. Dr. Gots concluded that plaintiffs' complaints had to have been related to conditions other than exposure to the damp conditions in the apartment. He did not offer any opinion as to what could have caused plaintiffs' symptoms.

The second affidavit was by S. Michael Phillips, M.D. He conceded that indoor mold can cause some of the symptoms asserted in plaintiffs' bill of particulars. For example, Dr. Phillips stated that plaintiffs "may have been exposed to molds and had minor allergic/irritant reactions resulting from such exposure." He further noted that "[e]pidemiologic studies indicate that the presence of mold in indoor environments is associated with upper respiratory symptoms, cough, wheeze, asthma symptoms in sensitized asthmatic persons, and hypersensitivity pneumonitis in susceptible persons." He cited to one of the two scientific publications relied upon by Dr. Gots to support this conclusion. Dr. Phillips also stated that "some of [plaintiffs'] complaints are compatible with irritant or allergic reactions to molds."

However, Dr. Phillips concluded that plaintiffs could never prove that mold caused their symptoms because they could not establish that the level of mold in the apartment was sufficient to result in adverse health effects. However, much like Dr. Gots, Dr. Phillips failed to compare the actual mold measured by plaintiffs to what, in his expert opinion, would be a sufficient level to cause illness. Rather, he described the levels of "expected indoor molds" recorded inside the apartment as "modest," and asserted that "[n]o convincing evidence of high-level exposures via actual air sampling data was available in the materials available for my review." Also, similarly to Dr. Gots, Dr. Phillips noted that plaintiffs' "alleged allergic symptoms have more likely explanations than mold," and suggested that perhaps dust mites and/or plaintiffs' cats were the culprits. Finally, Dr. Phillips asserted that the ill effects of mold exposure are transitory and could not have persisted in plaintiffs after they moved out of the apartment.

In opposition to defendants' motion, plaintiffs submitted the affidavit of Dr. Johanning. In reviewing the state of scientific thought on the relationship between building dampness and illness, Dr. Johanning, who is Board certified in Family Practice and in Occupational and Environmental Medicine, focused on two "large-scale, peer-reviewed epidemiological studies." First, he discussed Respiratory Morbidity in Office Workers in a Water Damaged Building, commissioned by the National Institute of Health and published on line in January 2005. Second, he discussed Home Dampness and Molds, Parental Atopy, and Asthma in Childhood: A Six-Year Population Based Cohort Study. This was published in the March 2005 edition of the peer-reviewed journal Environmental Health Perspectives. Dr. Johanning represented that these two studies:

"showed that the association' between damp buildings, mold, and respiratory morbidity, including new-onset asthma, is one of causation, a fact that had been apparent to clinicians for years. More importantly, they show that building dampness and mold cause permanent irritative and allergic-type problems, including new-onset asthma. Because these studies answered questions left open by the ACOEM and IOM papers*fn7, they were widely publicized and discussed. Neither Dr. Gots nor Dr. Phillips are aware of these studies, or if they are, they chose not to reveal them to the Court, and instead assert that the biased ACOEM 2002 paper and the IOM 2004 paper are the only and final word' on the matter. They are not. Occupational and Environmental physicians involved in direct patient care and research disagree with the conclusions by scientists' with mostly theoretical or peripheral experience about these clinical matters. The defendants' experts' ignorance (or concealment) of the current relevant medical literature is no basis to exclude my testimony. These papers directly contradict the assertions of Drs. Gots and Phillips that irritative and/or allergic-type reactions caused by damp buildings are always transitory in nature."

Unlike defendants' experts' submissions, Dr. Johanning explained in detail the significance of the mold samplings taken by plaintiffs. For example, in attempting to discredit Dr. Gots's statement that indoor air sampling levels in the apartment were below outdoor levels, he pointed out that the indoor air samples were "approximately triple and five times higher than the outdoor sample in terms of levels." He further noted the significance of the fact that the indoor samples were dominated by Aspergillus versicolor, "an atypical, hydrophilic... mold not commonly found in the outdoor air in any significant concentration." According to Dr. Johanning:

"From a medical perspective, its presence and predominance in the Fraser home was very significant because it reveals the presence of atypical species, meaning that our bodies are not used to breathing it in significant concentrations, and it or its by-products are therefore highly allergenic and irritative. This testing is indeed relevant from a health and exposure assessment perspective, as it is indicative of exposure by elevated levels of atypical molds, as a consequence of water events that preceded the testing."

Dr. Johanning further disputed Dr. Gots's statement that in order for mold to exert physical effects on a person that person must be one of the 5% of the general population who are generally susceptible. He explained that, contrary to Dr. Gots's position, mold irritation is not necessarily an allergic reaction but can come about because of chronic irritation caused by inhalation of mold. Accordingly, Dr. Gots's observation concerning the absence of elevated IgE levels was, Dr. Johanning observed, irrelevant. It was sufficient that Colin and Pamela Fraser "showed clear evidence of microbial specific IgG antibodies (typical in Type III or Type IV reactions) to a number of organisms commonly found in damp buildings. ...


Buy This Entire Record For $7.95

Download the entire decision to receive the complete text, official citation,
docket number, dissents and concurrences, and footnotes for this case.

Learn more about what you receive with purchase of this case.