| Fraser v 301-52 Townhouse Corp. |
| 2008 NY Slip Op 10208 [57 AD3d 416] |
| December 30, 2008 |
| Appellate Division, First Department |
| Colin Fraser et al., Appellants, v 301-52 Townhouse Corp.et al., Respondents. |
—[*1] Schechter & Brucker, P.C., New York (Thomas V. Juneau, Jr. of counsel), forrespondents.
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 courtand 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 defendantssummary judgment dismissing plaintiffs' causes of action based on personal injury, and, uponreargument and renewal, adhered to the original determination, affirmed, without costs. Appealfrom the aforesaid order entered October 5, 2006, unanimously dismissed, as academic, withoutcosts.
Plaintiffs, former residents of a unit in the cooperative apartment building owned bydefendant 301-52 Townhouse Corp., assert causes of action against defendants for, inter alia,personal injuries (specifically, respiratory problems, rash and fatigue) allegedly caused bydampness in the building and the mold infestations that allegedly resulted from such dampness.Upon defendants' motion seeking summary judgment and preclusion of plaintiffs' expertevidence purporting to establish that the building's alleged dampness and mold condition causedtheir health problems, the motion court directed that a Frye hearing be held to determinewhether plaintiffs' causation theory was generally accepted as reliable within the relevantscientific community. After the Frye hearing, the court granted defendants' motion,precluding the expert evidence and dismissing the personal injury claims (other causes of actionwere severed for further proceedings). The court subsequently granted plaintiffs reargument andrenewal, 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 acceptedwithin 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 dampnessand mold are "associated" with upper respiratory complaints, defendants' experts took theposition, consistent with the literature they submitted, that the observed association between suchconditions and such ailments is not strong enough to constitute evidence of a causal [*2]relationship.[FN1]In other words, " 'association' is not equivalent to 'causation' " (Green, Freedman andGordis, Reference Guide on Epidemiology, in Federal Judicial Center, Reference Manual onScientific Evidence, at 336 [2d ed 2000] [additional quotation marks added]; see also id.at 348 ["Although a causal relationship is one possible explanation for an observed associationbetween an exposure (to an agent) and a disease, an association does not necessarily mean thatthere is a cause-effect relationship"]). In this regard, even plaintiffs' main expert, Dr. EckardtJohanning, testified that "association" is not the same concept as "causation." Given that plaintifffailed to demonstrate general acceptance of the notion that a causal relationship has beendemonstrated between the conditions and ailments in question, Dr. Johanning's claim to haveestablished 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, 106 [2003][affirming preclusion of expert testimony that "relied solely on a theory . . . neitherrecognized 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 onwhich the specific claims at issue are based. We note that whether plaintiffs' theory of causationis scrutinized under the Frye inquiry applicable to novel scientific evidence (see Parker v Mobil Oil Corp., 7 NY3d434, 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 beprecluded on the ground that the underlying causal theory lacks support in the scientific literatureplaced before us in the present record. We stress that our holding does not set forth any generalrule that dampness and mold can never be considered the cause of a disease, only that suchcausation has not been demonstrated by the evidence presented by plaintiffs here.
Nothing said here "set[s] an insurmountable standard" (Parker, 7 NY3d at 447) forthe reception of scientific evidence. In particular, we disclaim the suggestion attributed to us bythe dissent that "Frye requires that the medical literature conclusively establish that anallegedly offending substance not only have the potential to cause illness but that italways causes illness." To be clear, the deficiency of plaintiffs' expert evidence is not thatthe medical literature fails to "conclusively establish" their causal theory or to show that indoordampness and mold "always cause[ ] illness."[FN2]Rather, plaintiffs' expert evidence falls short [*3]becausenone 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 upperrespiratory symptoms is strong enough to be considered, under generally accepted principles ofscientific analysis, evidence that the former causes the latter. Aside from referencing two studiesthat Dr. Johanning mischaracterized as demonstrating a causal link, the dissent does not identifyany study concluding that indoor dampness and mold have been shown to cause upper respiratorysymptoms 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 viewthat indoor dampness and mold is capable of causing plaintiffs' health problems (general [*4]causation), the experts failed to specify the threshold level ofexposure to dampness or mold needed to produce these effects. Without evidence that they wereexposed to a level of dampness or mold sufficient to cause their alleged injuries (specificcausation), plaintiffs cannot prevail on their personal injury claims (see Parker, 7 NY3dat 448 [plaintiff must show not only exposure to the toxin and that the toxin is capable of causingthe particular illness alleged, i.e., general causation, but also that plaintiff was exposed tosufficient levels of the toxin to cause the illness, i.e., specific causation]). It appears fromplaintiffs' 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 dampnessin plaintiffs' apartment to that in the studies (cf. id. at 449). Nor would plaintiffs' expertsbe able to make any reasoned comparison of plaintiffs' exposure to the by-products of dampnessto those in other studies. While plaintiffs did offer a measure of the level of mold present in theapartment, their experts did not testify to any threshold level at which mold is capable of causingthe injuries of which plaintiffs complain. Finally, while "it is not always necessary for a plaintiffto 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 differentialdiagnosis was an adequate substitute for quantitative proof.
An additional ground for granting summary judgment dismissing the personal injury claimsis that plaintiffs failed to offer a reliable measurement of the level of mold in the subjectapartment. That is to say, even if plaintiffs' theory of causation satisfied the Frye test, themold measurement they offered does not meet the standard of reliability set forth in the recordand therefore fails to satisfy the post-Frye foundational inquiry into "whether theaccepted methods were appropriately employed in a particular case" (Parker, 7 NY3d at447, 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 averageinhalation exposure should be based on sampling at least three times a day for at least threeconsecutive, representative days, with duplicate samples for all analyses (Macher, Bioaerosols:Assessment and Control, at 5-10 [1999]). Plaintiffs' environmental expert, however, collectedonly two indoor air samples within a short time span on the same day, which, according toplaintiffs' own authority, was insufficient.
Finally, although defendants filed their motion for summary judgment 300 days after thefiling of the note of issue, defendants have demonstrated good cause for the delay in thatdisclosure had been completed only two weeks before the motion was made. Accordingly, themotion was properly considered on the merits (see Pena v Women's Outreach Network, Inc., 35 AD3d 104, 108[2006]). Concur—Friedman, Williams and Freedman, JJ.
Mazzarelli, J.P., and Nardelli, J., dissent in a memorandum by Mazzarelli, J.P., as follows:Plaintiffs allege that they suffered adverse health effects as a result of chronic water leaks intotheir cooperative apartment. The leaks began in 1996. In their bill of particulars plaintiffs [*5]asserted that, as a result of the leaks, damp conditions prevailed inthe apartment and promoted the generation of "toxic mold, toxic fungi, [and] other microbiallife." They further claimed that the damp conditions caused them to suffer, among other things,repetitive upper respiratory infections, asthmatic symptoms, severe allergic reactions and allergysymptoms, rashes and fatigue. In addition, plaintiffs claimed certain cognitive and fertilityproblems, but subsequently withdrew those claims.
Plaintiffs identified five expert witnesses who they expected to testify at trial. Includedamong those experts was Dr. Eckardt Johanning, a medical doctor who had examined plaintiffsand who has extensively studied in the field of "health effects of microbiological exposure." Thedisclosure statement indicated that Dr. Johanning was expected to testify that the dampconditions inside the apartment exposed plaintiffs to "excessive and atypical microbiologicalcontamination." Dr. Johanning was further expected to testify that such exposure can causeserious health effects in humans and that plaintiffs were harmed by the damp conditions in theirapartment.
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 Cir1923]). With respect to summary judgment, defendants argued that plaintiffs could not provethat, generally speaking, "the presence of, or exposure to, mold in an indoor residential settingcauses the types of ailments" alleged by plaintiffs. They argued that plaintiffs could notspecifically prove they were exposed to "mycotoxins" in the apartment and that, even if theycould, they could not prove when the exposure took place or the "dose or duration" of any suchexposure.
With respect to preclusion, defendants specifically sought to bar testimony "to the extent theplaintiffs 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 ailmentsfor which [p]laintiffs are seeking money damages (such 'evidence' or opinions are not generallyaccepted 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 theaffidavits, that of a neuropsychologist, became irrelevant once plaintiffs withdrew their claim thatthe damp condition in their apartment caused them to suffer cognitive deficits. The first was byRonald E. Gots, M.D., Ph.D., a toxicologist who does not purport to have any expertise in moldsampling methodology. He devoted three paragraphs to critiquing mold sampling performedinside the apartment and offered some generalities purporting to support his opinion that thesampling data "is not reliable for determining exposure." Dr. Gots failed to discuss any of thespecific 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 inresidential or commercial buildings can ever be enough to cause mycotoxicosis, that is, illnesscaused by the biochemical products produced by molds as part of their life cycle. However, heacknowledged that indoor mold can cause allergic effects "manifest[ed] primarily as [*6]respiratory allergies" and that, although uncommon, "[i]rritanteffects may occur when there is significant mold growth (thousands of mold spores per cubicmeter of air)." At best, he stated, household mold can cause allergic reactions in the 5% of peoplewho are allergic to mold in the first place. Dr. Gots cited to two published scientific works tosupport his theory that any relation between building dampness and illness is essentiallyhypothetical. These were a 2002 paper by the American College of Occupational andEnvironmental Medicine (ACOEM) entitled Adverse Human Health Effects Associated withMolds 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 NationalAcademies (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 thepatient, (2) whether the "agent at issue" can produce the given disorder, and (3) whether the agentdid indeed cause the disorders at issue in the case. He claimed that plaintiffs could not have hadan allergic reaction to mold because "RAST" blood testing performed on them, which looked forallergen-specific IgE-mediated antibodies, was negative. He discounted IgG testingresults[FN1]as irrelevant to respiratory allergies and stated that, in any event, positive IgG results could notprove the time and place of exposure. He described the complaints of plaintiffs recorded in theirmedical records as subjective and not contemporaneous with medical visits. He furtherquestioned why the symptoms persisted even after plaintiffs vacated the apartment. Dr. Gotsconcluded that plaintiffs' complaints had to have been related to conditions other than exposureto the damp conditions in the apartment. He did not offer any opinion as to what could havecaused plaintiffs' symptoms.
The second affidavit was by S. Michael Phillips, M.D. He conceded that indoor mold cancause some of the symptoms asserted in plaintiffs' bill of particulars. For example, Dr. Phillipsstated that plaintiffs "may have been exposed to molds and had minor allergic/irritant reactionsresulting from such exposure." He further noted that "[e]pidemiologic studies indicate that thepresence of mold in indoor environments is associated with upper respiratory symptoms, cough,wheeze, asthma symptoms in sensitized asthmatic persons, and hypersensitivity pneumonitis insusceptible persons." He cited to one of the two scientific publications relied upon by Dr. Gots tosupport this conclusion. Dr. Phillips also stated that "some of [plaintiffs'] complaints arecompatible with irritant or allergic reactions to molds."
However, Dr. Phillips concluded that plaintiffs could never prove that mold caused theirsymptoms because they could not establish that the level of mold in the apartment was sufficientto result in adverse health effects. However, much like Dr. Gots, Dr. Phillips failed to comparethe actual mold measured by plaintiffs to what, in his expert opinion, would be a sufficient levelto cause illness. Rather, he described the levels of "expected indoor molds" recorded inside theapartment as "modest," and asserted that "[n]o convincing evidence of high-level exposures via[*7]actual air sampling data was available in the materialsavailable for my review." Also, similarly to Dr. Gots, Dr. Phillips noted that plaintiffs' "allegedallergic symptoms have more likely explanations than mold," and suggested that perhaps dustmites and/or plaintiffs' cats were the culprits. Finally, Dr. Phillips asserted that the ill effects ofmold exposure are transitory and could not have persisted in plaintiffs after they moved out of theapartment.
In opposition to defendants' motion, plaintiffs submitted the affidavit of Dr. Johanning. Inreviewing the state of scientific thought on the relationship between building dampness andillness, Dr. Johanning, who is board certified in family practice and in occupational andenvironmental medicine, focused on two "large-scale, peer-reviewed epidemiological studies."First, he discussed Cox-Ganser et al., Respiratory Morbidity in Office Workers in aWater-Damaged Building, commissioned by the National Institute of Health and publishedon line in January 2005 (113 Envtl Health Persp 485 [2005]). Second, he discussed Jaakkola etal., Home Dampness and Molds, Parental Atopy, and Asthma in Childhood: A Six-YearPopulation-Based Cohort Study (113 Envtl Health Persp 357 [2005]). This was published inthe March 2005 edition of the peer-reviewed journal Environmental Health Perspectives. Dr.Johanning represented that these two studies: "showed that the 'association' between dampbuildings, mold, and respiratory morbidity, including new-onset asthma, is one of causation, afact that had been apparent to clinicians for years. More importantly, they show that buildingdampness and mold cause permanent irritative and allergic-type problems, including new-onsetasthma. Because these studies answered questions left open by the ACOEM and IOMpapers,[FN2]they were widely publicized and discussed. Neither Dr. Gots nor Dr. Phillips are aware of thesestudies, or if they are, they chose not to reveal them to the Court, and instead assert that thebiased 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 andresearch disagree with the conclusions by 'scientists' with mostly theoretical or peripheralexperience about these clinical matters. The defendants' experts' ignorance (or concealment) ofthe current relevant medical literature is no basis to exclude my testimony. These papers directlycontradict the assertions of Drs. Gots and Phillips that irritative and/or allergic-type reactionscaused by damp buildings are always transitory in nature."
Unlike defendants' experts' submissions, Dr. Johanning explained in detail the significance ofthe mold samplings taken by plaintiffs. For example, in attempting to discredit Dr. Gots'sstatement that indoor air sampling levels in the apartment were below outdoor levels, he pointedout that the indoor air samples were "approximately triple and five times higher than the outdoorsample in terms of levels." He further noted the significance of the fact that the indoor sampleswere dominated by Aspergillus versicolor, "an atypical, hydrophilic . . . mold notcommonly 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 wasvery significant because it reveals the presence of atypical species, meaning [*8]that our bodies are not used to breathing it in significantconcentrations, and it or its by-products are therefore highly allergenic and irritative. This testingis indeed relevant from a health and exposure assessment perspective, as it is indicative ofexposure by elevated levels of atypical molds, as a consequence of water events that preceded thetesting."
Dr. Johanning further disputed Dr. Gots's statement that in order for mold to exert physicaleffects on a person that person must be one of the 5% of the general population who are generallysusceptible. He explained that, contrary to Dr. Gots's position, mold irritation is not necessarilyan allergic reaction but can come about because of chronic irritation caused by inhalation ofmold. 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 clearevidence of microbial specific IgG antibodies (typical in Type III or Type IV reactions) to anumber of organisms commonly found in damp buildings. This means that their bodies producedantibodies in response to an exposure to these organisms prior to the testing and consistent withthe patient's history and timeline of exposure." Defendants did not submit any papers in reply toplaintiffs' opposition.
Without discussion of the parties' respective positions and submissions, the motion courtdenied the summary judgment motion and directed a hearing pursuant to Frye v UnitedStates (293 F 1013 [1923], supra). The court stated: "The submissions have raised anissue [of fact] as to whether the theory of plaintiffs—that mold in their apartment causedthem respiratory problems—is generally accepted in the relevant scientific community andwhether the methodology used by plaintiffs to measure the mold was within generally acceptedscientific methods."
The Frye hearing was conducted on 10 days between July 27, 2005 and March 28,2006. Dr. Johanning and Paul Ehrlich, M.D., a clinician specializing in pediatric allergies andasthma, testified on plaintiffs' behalf. Dr. Gots and Dr. Phillips testified for defendants. Plaintiffsplaced in evidence nearly 40 articles, treatises and other published studies concerning therelationship between building dampness and mold and sickness in humans. Defendants placedapproximately 15 such publications in evidence.
Dr. Johanning testified that the symptoms with which plaintiffs presented to him were causedby the damp conditions in the apartment. He stated that he utilized a differential diagnosismethodology, which he described as: "using a comprehensive occupational and environmentalhistory, physical examination, laboratory tests, review of environmental data, looking at medicalreports and test results from other providers, and looking at any information that can help me torule in or out diagnosis or differential diagnostic considerations." Dr. Johanning then explainedthat, in diagnosing Colin Fraser, he consulted the various environmental reports created byOlmsted Environmental Service, as well as medical reports generated by other medical providerswho had examined or treated Mr. Fraser. He also viewed [*9]photographs showing stains and discoloration inside the subjectapartment.
Dr. Johanning took his own history of Mr. Fraser. Mr. Fraser related that he never smoked orabused alcohol or drugs, and that he had never been exposed to organic dust or significantbioaerosols such as those associated with garden work, pesticides, heavy metals or chemicals.Although Mr. Fraser worked as a stamp broker, he denied working with wet or moldy stamps orworking in anything but "clean" environments. Mr. Fraser filled out an eight-page questionnaireregarding his health. He reported that he felt generally better since vacating the apartment.
Dr. Johanning also performed a complete physical examination of Mr. Fraser. He orderedlaboratory testing, the results of which revealed that Mr. Fraser was not suffering from aninfection or any other identifiable condition. His total immunoglobin count was normal,indicating that he had an appropriate and normal level of immune parameters. However, Mr.Fraser had IgG subclass abnormalities "which showed an altered immune response similar as itcan be seen in people who have allergy." Dr. Johanning specified that these IgG levels (which hedescribed as "striking") indicated "hypersensitivity to a number of fungi and bacteria, precisely. . . six out of eight; specifically, Micropolyspora, Thermoactinomyces, Alternaria,Aureobasidium, Phoma herbarum, Trichoderma." Two of those organisms, Micropolyspora,Thermoactinomyces, were described by Dr. Johanning as being more akin to bacteria than mold,and he testified that they were commonly found in people who are exposed to wet organicmaterial, including wood. Dr. Johanning described all of these organisms as being capable ofcausing allergic, irritative and toxic reactions. Three of them, which are molds, were found in theapartment, according to laboratory reports reviewed by Dr. Johanning. The fact that the particularmold- and bacteria-antibody-specific IgG levels were high indicated to Dr. Johanning that Mr.Fraser had been exposed to those particular organisms for a lengthy period of time. Dr.Johanning stated that it was not necessary to perform skin prick testing to further confirm thesignificance of abnormal IgG results.
When asked to describe his diagnosis of Mr. Fraser, Dr. Johanning testified as follows:"Essentially, again, based on the history, the presentation, past medical history, family history,review of systems, the work history, the results of physical examination, laboratory test results asI outlined earlier, the environmental information, consultation reports from other specialists, Iconcluded, using a differential diagnosis approach, that the best explanation for Mr. Fraser'sproblem is the history of acute irritant allergic type reaction while he was living in his previousapartment at 301 East 52nd Street."
Regarding plaintiff Pamela Fraser, Dr. Johanning recounted a similar history related by thepatient. The information elicited was also designed to rule out other possible causes of thereported symptoms including nasal problems, itchy and teary eyes, shortness of breath, burningsensation in the throat, sore throat, wheezing and tightness in the chest. IgG testing showedreaction to Micropolyspora, Thermoactinomyces and Trichoderma. Dr. Johanning testified thatrepeated general blood count and differential and platelet counts did not indicate any othermedical problems. Accordingly, Dr. Johanning recorded in his records that, based on all thelaboratory and clinical findings: "and the differential diagnosis approach, I conclude with areasonable degree of medical certainty that Miss Fraser had a history of allergic and irritant type[*10]reactions while she was residing at her previous apartmentwhich had water damage and microbial growth problems."
Finally, Dr. Johanning testified about his examination of the infant plaintiff, who, because ofher age, could not be subjected to the same diagnostic tests as her parents (including testing forIgG levels). The parents related a history of respiratory problems which dissipated after theyvacated the apartment. Dr. Johanning concluded that, based upon his differential diagnosisapproach, the child had respiratory problems which seemed to be ongoing and episodic and that,while she was too young to determine specific allergies, it was "reasonable to assume" that whereshe lived "caused some respiratory inflammation and allergic response."
Dr. Phillips testified that Dr. Johanning did not record the presence of IgE antibodies in anyof the plaintiffs. While he described IgG as having the capability to cause certain diseases inpeople, he characterized it as "common" and "not unexpected." Moreover, he testified that IgGtest results provide no clues as to when a person was exposed to a particular antigen, the lengthof exposure or the amount of exposure. He stated that approximately 10% of people havedeveloped antibodies to mold, but less than 50% of those people have showed clinical problemsrelated to mold.
Dr. Phillips asserted that IgG is not correlated in any way or related to an allergy. Hecriticized the manner in which Dr. Johanning tested for IgG, claiming that his technique wouldalways yield a positive result. Moreover, because he did not see the presence in Dr. Johanning'sreport of any clinical symptoms associated with IgG exposure, he concluded that it wasimpossible to tell whether the conditions reported in plaintiffs' apartment contributed to anyillness.
Subsequent to the Frye hearing, the court issued an order holding that "plaintiffs areprecluded from introducing testimony demonstrating that mold caused their health complaintsand plaintiffs' causes of action based upon personal injury are dismissed with prejudice." Theorder contained a lengthy recitation of facts that summarized in detail the initial mold samplingreport secured by plaintiffs, the medical reports prepared by Dr. Johanning upon his examinationof plaintiffs, the testimony of all the witnesses, and the scientific publications submitted by bothsides. The court discredited the testimony of both Dr. Johanning and Dr. Gots as beingcompromised by their "strongly held views on the subject of mold and a stake in advancing thoseviews." It credited the testimony of Dr. Phillips, whom it found to be "very impressive," andfound that "plaintiffs failed to demonstrate that the community of allergists, immunologists,occupational and environmental health physicians and scientists accept their theory—thatmold and/or damp indoor environments cause illness."
The court summarized the scientific writings submitted by the parties, which it described as"peer-reviewed and published in journals generally accepted in the medical and/or scientificcommunity," and concluded that they: "demonstrate that, with the exception of one article, thescientific research has not established that indoor exposure to mold causes the symptoms forwhich the plaintiffs seek to recover in this action. Although some of the literature found thatindoor mold exposure or dampness had an 'association' with transient upper respiratory problemsin adults (symptoms similar to those of the common cold), or a 'strong association with asthma inchildren, these findings fall short of a finding of 'causation.' "[*11]
The court then ruled that, even if plaintiffs hadestablished at the hearing that, generally, there is a causal link between building dampness/moldand illness, the case could not go forward. According to the court: "It became clear at the hearingthat plaintiffs wished to argue that moisture in the Fraser apartment caused them ill health.Plaintiffs contended that a damp indoor environment produced bacteria, mold, endotoxins, BetaGlucans, MVOCs and other toxic materials, which caused the Frasers' complained of symptoms.However, moisture, bacteria, endotoxins, MVOCs and Beta Glucans were never measured in theFraser apartment. Moreover, the scientific literature and the testimony of Dr. Phillips establishedthat two measurements for mold in a short time span, the method of measurement used here, wasinsufficient to give a valid mold reading. Then too, the hearing evidence demonstrated that: thereare no standards for what amount of mold was excessive in terms of human health and the indoorenvironment; there are no generally accepted standards for measuring indoor airborne mold;there are no generally accepted standards for the acceptable amount of mold in indoor air; thereare many types of mold, each of which have different or no health effects; there are no standardscientific definitions for "dampness" or "moisture"; skin prick tests for allergy, which were notdone here, were deemed the most reliable way to test for allergy by the literature, Dr. Ehrlich, Dr.Gots and Dr. Phillips; and the IgE test performed on Colin and Pamela Fraser, which is related toallergies, did not show allergy to mold."
Plaintiffs moved to reargue and renew the order. They sought reargument based on a varietyof asserted defects. This was granted, solely to modify the order to eliminate any reference to themanner in which air testing of plaintiffs' apartment was conducted, which the court recognizedwas improper in a Frye hearing. Renewal, based on the intervening Court of Appealsdecision in Parker v Mobil OilCorp. (7 NY3d 434 [2006]), was also granted. However, based on Parker, thecourt held that plaintiffs had failed to lay a proper foundation for their experts' testimony. Thecourt determined that Dr. Johanning's differential diagnosis, which it defined as "a list of possiblecauses of a symptom," was an inadequate foundation for a finding of specific causation. Thecourt wrote: "Dr. Johanning testified without underlying proof of causation or strong association,without proof of mold allergies, without reliable standards for measurement of airborneexposure, and without measurements of mold by-products that plaintiffs' symptoms must havebeen caused by airborne mold and mold by-products. On the other hand, with respect to Mrs.Fraser, he failed to rule in cat and dust allergies." The court further stated that Parkerimplies that only a "significant association" between a substance asserted to cause illness andillness itself is enough to pass the Frye test. It found that this is "consistent with Dr.Phillips' testimony that a strong association occurs all of the time."
The court acknowledged that some courts had found Dr. Johanning's differential diagnosisvalid, but failed to provide any case citations. However, it stated that "other courts, which thiscourt finds more persuasive, have disagreed," citing Jazairi v Royal Oaks Apt. Assoc.,L.P. (217 Fed Appx 895 [11th Cir 2007]) and Roche v Lincoln Prop. Co. (278 FSupp 2d 744 [ED [*12]Va 2003]). For a second time, the courtgranted summary judgment to defendants dismissing all of plaintiffs' personal injury claims.
Defendants' submissions on their original motion plainly did not, in the first instance, supportthe need for the Frye hearing directed by the motion court. Accordingly, I would reverse.Neither Dr. Gots nor Dr. Phillips ever stated in their respective affidavits that it is not generallyaccepted by scientists that indoor mold or damp conditions can cause the allergies and irritationexperienced by plaintiffs. To the contrary, both stated, Dr. Phillips in unambiguous terms, thatindoor mold and building dampness have the potential to cause the health conditions alleged byplaintiffs.
Defendants also failed to rebut Dr. Johanning's criticism of the scientific studies upon whichthey relied, nor did they even attempt to refute the studies cited by Dr. Johanning in his ownaffidavit. Defendants' failure to call into question the studies submitted by plaintiffs is mostsignificant, because it left the court with two studies ostensibly doubting any link between indoormold and illness and two which supported such a link. Even one of defendants' experts reliedfavorably on the IOM study—which defendants submitted in support of theirmotion—as supporting his statement that "the presence of mold in indoor environments isassociated with upper respiratory symptoms, cough, wheeze, asthma symptoms in sensitizedasthmatic persons, and hypersensitivity pneumonitis in susceptible persons."
The purpose of a Frye hearing is not to prove by any particular evidentiary standardthat proposed scientific evidence is sound. Rather, it is to establish that a theory has gainedgeneral recognition in the scientific community. To be sure, the proponent of scientific evidencebears the burden of establishing Frye admissibility (Marso v Novak, 42 AD3d 377, 378 [2007]). However, before thatburden is ever imposed the party contesting the proffered evidence must first make a prima faciecase that the theory has not gained general recognition in the scientific community(see Middleton v Kenny, 286 AD2d 957, 958 [2001]). Here, defendants' submissionsfailed to make a prima facie case that there is not a consensus in the scientific community thatbuilding dampness and mold can cause illness. In fact, their experts conceded this point.
As for the second issue defined by the motion court in its order directing a Fryehearing, defendants similarly failed to make a prima facie showing that the methodology bywhich plaintiffs measured mold in the subject apartment was not generally accepted by therelevant scientific community. Defendants' experts never identified how plaintiffs'mold-measuring methodology was "novel" such that plaintiffs should have been required toestablish general acceptance. Indeed, in the original order to show cause submitted bydefendants, they did not even seek a Frye hearing on this subject. Ultimately, the mannerin which plaintiffs collected mold samples was a minor factor in the court's decision to precludeplaintiffs' experts. Indeed, in the decision on reargument the court modified the original order toeliminate any reference to the manner in which mold was sampled. Nevertheless, the court'sdirective that the Frye hearing include mold sampling methodology within its scope isindicative of the large gap between what defendants argued in their submissions and the issuesthat the court decided were the proper subject of a Frye hearing. As discussed below, thisresulted in a great deal of confusion at the hearing as to what precisely was at issue.
Plaintiffs met their burden of establishing the admissibility of evidence that the conditions intheir apartment caused their illness. The conclusion by the motion court, adopted by the majority,that plaintiffs failed to establish at the hearing that exposure to building dampness and mold cancause illness is based on too restrictive an application of Frye. Frye hearings areto test [*13]the reliability of novel scientific evidence (Parkerv Mobil Oil Corp., 7 NY3d at 446). Frye itself held that "while courts will go a longway in admitting expert testimony deduced from a well-recognized scientific principle ordiscovery, the thing from which the deduction is made must be sufficiently established to havegained general acceptance in the particular field in which it belongs." (Frye, 293 F at1014.) As Judge Kaye stated in her concurrence in People v Wesley (83 NY2d 417, 439[1994]), Frye "emphasizes 'counting scientists' votes, rather than on verifying thesoundness of a scientific conclusion."
Courts have warned against an over-restrictive use of Frye. For example, the Court ofAppeals stated in Parker that "As with any other type of expert evidence, we recognizethe danger in allowing unreliable or speculative information (or 'junk science') to go before thejury with the weight of an impressively credentialed expert behind it. But, it is similarlyinappropriate to set an insurmountable standard that would effectively deprive toxic tort plaintiffsof their day in court. It is necessary to find a balance between these two extremes." (7 NY3d at447.) The Second Department, in reversing a preclusion order after a Frye hearing,observed that: "the trial court, while purporting to credit the deductive reasoning of the plaintiff'sexperts, apparently believed that the Frye test could only be satisfied with medical texts,studies, or other literature which supported the plaintiff's theory of causation under circumstancesvirtually identical to those of the plaintiff. However, the Frye test is not that exacting."(Zito v Zabarsky, 28 AD3d 42,46 [2006].)
Here, the majority has "set an insurmountable standard." (Parker, 7 NY3d at 447.) Itessentially posits that in a case such as this, Frye requires that the medical literatureconclusively establish that an allegedly offending substance not only have the potential to causeillness but that it always causes illness. Indeed, the motion court, in interpretingParker to require at least a "significant association" between an allegedly harmfulsubstance and illness, endorsed Dr. Phillips's position that a "strong association occurs all of thetime." This is far too rigorous an application of Frye.
In this case, plaintiffs submitted at least 20 peer-reviewed publications describing anassociation or strong association between building dampness and mold and the type of irritativesymptoms described by plaintiffs. Collectively, these studies establish that the "association"between building dampness and illness is one of causation, not one of coincidence. In histestimony, Dr. Phillips stated that an "association" is probative of nothing. In other words, heexplained that if one observes a man in a black suit get struck by a car, and observes the samething a few blocks later, it would not be logical to conclude that one should not wear a black suitwhile crossing the street. "Association," however, is a continuum, which spans from thecoincidence described in the above scenario to unquestionable causation. The evidence submittedby plaintiffs here, while perhaps not establishing that building dampness always causes illness, isfar closer to the causation end of the continuum than the coincidence end.
Moreover, it is not plaintiffs' contention that building dampness and mold alwayscause [*14]illness, and that is not required. Rather, plaintiffsclaim, and the literature confirms, that more than an outlying segment of the scientificcommunity has concluded that there is evidence that building dampness and mold have thepotential to cause allergic and irritative reaction in sensitized people. Plaintiffs simply seekan opportunity to prove to a jury that the dampness and mold in their apartment caused theirsymptoms.
Indeed, Dr. Phillips's testimony concerning the causal relationship between buildingdampness and illness reveals that he considers the "association" described in the literaturesubmitted by plaintiffs as being on the causation end of the continuum discussed above. Dr.Phillips stated that because science has only identified an "association" between dampness andillness, a doctor treating a patient complaining of mold-related illness must perform a completeevaluation of the patient and his environment to confirm his claim. In other words, he said thatbecause science has not established that mold always causes illness, the doctor may not simplyaccept that the patient is sick from mold. In his practice, Dr. Phillips has treated "thousands" ofpatients complaining of respiratory problems associated with a damp building. He testified thatwhen a patient presents with such a complaint:
"[y]ou evaluate the patient, you try to see how ill they are, what the clinical manifestationsare. You try to establish the presence or absence of mold sensitization. I give them instructions interms of what they can do to control, for example, the moisture, the dehumidification. . .
"Because excess moisture increases growth of mites and mold and bacteria and other things.So high amounts of moisture is an adverse environment in which that patient is going to live.You are going to try to help them in any way you can. You give them proper medicine and testthem if in fact they are sensitive to mold, and in some cases do desensitization shots."
This is the precise approach Dr. Johanning took with plaintiffs. It recognizes that buildingdampness can cause illness but that the link between the two is not so consistent that a doctor candispense with a detailed examination into whether it did in fact cause illness. In employing thisapproach, Dr. Phillips recognizes that the theory that there is a link between building dampnessand illness is not the type of "theoretical speculation, or . . . scientific 'hunch' " thatFrye hearings are designed to weed out (Zito v Zabarsky, 28 AD3d at 46).
Finally, to the extent that this Court has in recent history precluded expert testimony underFrye, it has based such decisions upon a complete absence of literature or studiessupporting the claim (see e.g. Marso vNovak, 42 AD3d 377 [2007], supra; Lara v New York City Health & Hosps.Corp., 305 AD2d 106 [2003]; Selig v Pfizer, Inc., 290 AD2d 319 [2002], lvdenied 98 NY2d 603 [2002]; Stanski v Ezersky, 228 AD2d 311 [1996], lv denied89 NY2d 805 [1996]). Here, a plethora of peer-reviewed articles supports plaintiffs'claim.
The motion court was correct in stating that Parker v Mobil Oil Corp. required it notonly to consider the general question of whether the link between building dampness and illnessis generally accepted, but also that a scientific foundation existed for plaintiffs' experts'conclusion that plaintiffs were sickened by the conditions in their apartment. However,Parker's applicability here is limited to that general proposition. Indeed, there is no basisfor the motion court's statement that "[t]here is a striking similarity between the testimony ofplaintiffs' experts [*15]and the vague expert testimony rejected bythe Court of Appeals in Parker."
In Parker, the plaintiff, a former gasoline station attendant, claimed to havedeveloped acute myelogenous leukemia as a result of exposure to benzene contained in gasoline.The defendants sought to dismiss the case on the theory that the plaintiff could not establish acausal link between the exposure and his illness. The Court of Appeals held that a traditionalFrye analysis was unnecessary because the plaintiff's scientific theory was not "novel."However, it further held that the trial court still had a gatekeeping role of ensuring the reliabilityof the proposed scientific evidence. In Parker, that required ensuring that the plaintiff'sexperts could demonstrate the threshold of exposure to benzene below which leukemia would notoccur, as well as the exposure level to which the plaintiff was subjected. The Court rejected theplaintiff's experts' opinions because they failed to offer any scientific measure of the level of theplaintiff's exposure in other than the most general and conclusory terms.
In contrast to Parker, here plaintiffs are not claiming that they were harmed by thetoxic effects of mold. Rather, they claim to have been sickened by those properties ofmold and building dampness which have an irritative and allergic effect. Accordingly, as Dr.Johanning explained, ascertaining the specific levels of a particular mold in a building is notdeterminative of whether the mold caused irritative or allergic effects. This is because, heexplained, as long as a person has become sensitized to the mold, he or she may react to a smallamount of exposure. In any event, Dr. Johanning objectively determined that there was sufficientmold in the apartment for plaintiffs to have become sensitized. Specifically, he viewedphotographs demonstrating the significant mold growth in the apartment. More importantly, herelied on the Olmsted report showing levels of atypical organisms existing in the apartment ashigh as five times the levels in which they are normally encountered outdoors. This was in sharpcontrast to the facts in Parker, where the record was devoid of any specific articulation ofthe plaintiff's exposure.
In any event, even if quantifying mold levels was critical to plaintiffs' case, Parkerdoes not help defendants here. The holding in Parker put rest to the notion that toestablish an appropriate reliability foundation, plaintiffs in a toxic tort case must establishprecisely quantified exposure levels or a dose-response relationship, provided, the Court wrote,that "whatever methods an expert uses to establish causation are generally accepted in thescientific community" (7 NY3d at 448). Here, Dr. Johanning's differential diagnosis satisfied thattest. Differential diagnosis has been recently accepted by the Fourth Department as a generallyaccepted method for establishing specific causation in mold cases. That court found in B.T.N. v Auburn Enlarged City SchoolDist. (45 AD3d 1339 [2007]), a case involving atypical mold in a school building, that adifferential diagnosis was an adequate basis for opining that the mold caused the plaintiffs'symptoms.
Here, defendants never argued in their initial motion papers that the differential diagnosisperformed by Dr. Johanning was not a generally accepted methodology. Moreover, to the extentthat the motion court can be read as holding that differential diagnosis is not a generally acceptedmethodology in mold cases, that was patently unfair. The order directing the Frye hearingcannot possibly be read to include within its scope the issue of whether differential diagnosis isgenerally accepted in such cases.
Dr. Johanning's differential diagnosis was scientifically valid and the motion court articulatedno basis for concluding otherwise. A differential diagnosis has been described as "apatient-specific process of elimination that medical practitioners use to identify the 'most likely'[*16]cause of a set of signs and symptoms from a list of possiblecauses" (Ruggiero v Warner-Lambert Co., 424 F3d 249, 254 [2d Cir 2005] [internalquotation marks and citation omitted]). Indeed, Jazairi v Royal Oaks Apt. Assoc., L.P.(217 Fed Appx 895 [2007], supra), one of the cases upon which the motion court reliedin rejecting Dr. Johanning's differential diagnosis approach, noted that "[t]he record reflects thatdifferential diagnosis is widely accepted by the medical community" (id. at 898).
Here, Dr. Johanning specifically ruled in the damp conditions in the subject apartment to bethe cause of plaintiffs' symptoms, based not only on the history related by plaintiffs, but also onspecific immunological markers which demonstrated lengthy exposure by plaintiffs to specificorganisms related to irritants that were found to be inside the apartment in levels greater thanoutdoors. In addition, he ruled out all other causes, such as smoking, other allergens and irritantsunrelated to mold or building dampness, or even other possible dampness-related conditions suchas those related to Colin Fraser's vocation as a stamp broker.
In contrast, the 11th Circuit in Jazairi rejected the differential diagnosis (alsoperformed by Dr. Johanning) because he: "apparently did not conclude that [the plaintiff]suffered symptoms due to exposure to any of the molds that were present in her apartment. Tothe extent that Dr. Johanning was prepared to testify that the mold in [the plaintiff's] apartmentcaused her conditions, Dr. Johanning's testimony would have been based solely ontemporal proximity and anecdotal evidence." (Jazairi, 217 Fed Appx at 898 [emphasisadded].) In other words, the differential diagnosis in Jazairi was not one at all, because itwas based on no objective medical data and because it ruled nothing in and nothing out. Here,that was far from the case. Indeed, the motion court's statement that "Dr. Johanning's opinion wasbased solely on temporal proximity to mold and anecdotal evidence" is plainly contradicted byhis testimony.
Moreover, nearly all of the factors which the motion court identified as demonstrating thatDr. Johanning's opinion had no reliable scientific foundation were erroneous. First, the courtstated that Dr. Johanning testified "without underlying proof of causation or strong association."As discussed above, however, plaintiffs established that it is generally accepted that buildingmold and dampness can generally cause illness. The court also stated that Dr. Johanning testified"without proof of mold allergies." However, Dr. Johanning did base his conclusion on plaintiffs'physiological reaction to mold and other dampness-related organisms. While this may not havebeen the "traditional" IgE-mediated allergy, which the court was focused on, the fact thatdiagnostic tests revealed an IgG-mediated response to dampness-related irritants was probative ofa causal link between the conditions in the apartment and plaintiffs' symptoms. Moreover, whiledefendants tangentially questioned the reliability of IgG readings in their initial motion and at thehearing, they did not ask for a ruling that using IgG testing for diagnostic purposes in mold casesis not generally accepted, nor can the order directing the hearing be interpreted as requiringplaintiffs to establish the reliability of such testing.
Second, the court treated as fatal plaintiffs' failure to measure for moisture and nonmoldby-products of moisture identified by Dr. Johanning as contributing to illness, such asendotoxins, mycotoxins, or Beta-D-glucans. However, such measurements were not critical toDr. Johanning's differential diagnosis because, as he testified, the level of organisms sufficient tosensitize plaintiffs could vary significantly depending on the individual. In any event, Dr. [*17]Johanning did have objective evidence of significant mold growthin the apartment from the photographs he viewed and the Olmsted report. Moreover, the fact thatthere were significant water intrusions into the subject apartment was apparently never in dispute.
As for the court's statement that Dr. Johanning failed to rule in cat and dust allergies as apossible cause of Pamela Fraser's symptoms, there is no evidence in the record that she had catallergies. Dr. Johanning did note that she had a reaction to dust mites. However, he stated that itwas "slight," which hardly suggests that he would have ever ruled it in as the most likely cause ofher symptoms. Moreover, there is no requirement that the proponent of expert scientifictestimony prove the ultimate theory of the case during a Frye hearing. Rather, he or shemust only establish the basic reliability of the methodology utilized to reach that conclusion. Aswe recently held, any further challenges to an expert's methodology and/or conclusions above andbeyond its basic reliability are more "properly the subject of cross-examination at trial, as they goto credibility and to the weight to be given to the evidence" (Nonnon v City of New York, 32 AD3d 91, 108 [2006], affd9 NY3d 825 [2007]).
Here, Dr. Johanning's use of the methodology of differential diagnosis was reliable as it wasbased on the confirmed presence of dampness and mold in plaintiffs' apartment and the presencein plaintiffs' systems of antibodies to organisms typically associated with mold and dampness.Moreover, plaintiffs exhibited symptoms consistent with dampness-related illness, and related noother source of exposure to dampness-related antigens. Once Dr. Johanning established thisbaseline of reliability, defendants were relegated to challenging his conclusions before the trier offact.
Finally, plaintiffs not only met their burden at the hearing in this case, they did so in the faceof substantial confusion fostered by the motion court. The order directing the hearing was vagueand overbroad in terms of what plaintiffs were required to establish. Moreover, the order requiredthem to prove the general acceptance of mold sampling methodology when not even defendantshad asked for such relief. Because of the court's ambiguous order, a significant portion of thehearing was devoted to argument between the parties and the court over precisely what was atissue. For example, the parties and the court differed over whether plaintiffs were required toestablish the general acceptance of a causal link between damp buildings and sickness or, morespecifically, mold in general. They argued about whether plaintiffs were required to identify aspecific "disease" caused by the conditions in their apartment, or merely the presence of physicalsymptoms. They also debated whether plaintiffs were required to establish the general acceptanceof differential diagnosis as a methodology for establishing specific causation.
As a result, the scope of the hearing was continuously defined and redefined over its course.This left plaintiffs at sea, without the ability to divine the path the court required for them tosatisfy their burden. In spite of this confusion, plaintiffs established the reliability of their experts'opinions. Nevertheless, the motion court usurped the function of the jury here and became thefinder of fact, not as to whether or not plaintiffs' theories and evidence satisfied the Fryeand Parker tests, but of the ultimate question as to whether defendants were responsiblefor [*18]plaintiffs' injuries. Accordingly, I would reverse theorders appealed and reinstate plaintiffs' personal injury claims. [See 2007 NY Slip Op32086(U).]
Footnote 1: For example, a review of therelevant scientific literature published by the Institute of Medicine of the National Academies,Damp Indoor Spaces and Health (National Academies Press 2004), concluded that there was"sufficient evidence of an association" between upper respiratory (nasal and throat) tractsymptoms, on the one hand, and damp indoor environments and the presence of mold, on theother hand, but found that it could not be said that there was "sufficient evidence of acausal relationship" between any set of health outcomes and such conditions (id. at253-254 [tables 5-12, 5-13]).
Footnote 2: Obviously, there is no rule that ajury may hear only theories that are either "conclusively establish[ed]" by the scientific literatureor unanimously supported by the scientific authorities. Further, we do not suggest, nor did themotion court suggest, that a substance cannot be considered the cause of a health outcome unlessthe substance "always" causes that health outcome.
Footnote 3: Contrary to Dr. Johanning'sassertion, neither of the two studies referenced in the first excerpt from his opposition affidavitquoted by the dissent reached the conclusion that a causal relationship has been demonstratedbetween indoor dampness and mold and the upper respiratory symptoms of which plaintiffscomplain. The first study referenced in the excerpt from Dr. Johanning's affidavit (Cox-Ganser etal., Respiratory Morbidity in Office Workers in a Water-Damaged Building, 113 EnvtlHealth Persp 485 [2005]) concluded only that "[o]ccupancy of the water-damaged building wasassociated with onset and exacerbation of respiratory conditions" (id. at 485[emphasis added]). The authors of Respiratory Morbidity acknowledged that the "majorlimitation" of the study, which was based on voluntary responses to a questionnaire, was "thepossible influence of participation bias" (id. at 490). The other study referenced in thequoted excerpt from Dr. Johanning's affidavit (Jaakkola et al., Home Dampness and Molds,Parental Atopy, and Asthma in Childhood: A Six-Year Population-Based Cohort Study, 113Envtl Health Persp 357 [2005]) focused on risk factors for the development of childhood asthma,and is therefore of little relevance to this case, which does not involve a child suffering fromasthma.
Footnote 4: We have no argument with thedissent's statement that " '[a]ssociation' . . . is a continuum . . .span[ning] from . . . coincidence . . . to . . . causation."This observation is of little help to plaintiffs, however, because the dissent points to nothing inthe record, other than Dr. Johanning's unsupported assertions, that justifies the conclusion thatthe observed association between the conditions and ailments in question is strong enough toconstitute evidence of causation.
Footnote 5: Although the Fryeinquiry and the foundational inquiry are distinct, they may proceed simultaneously (seePeople v Wesley, 83 NY2d at 436 n 2 [Kaye, Ch. J., concurring]).
Footnote 1: "IgE" and "IgG" refer toimmunoglobulin types which reflect the level of antibodies developed by the body in response toexposure to antigens such as allergens and foreign organisms. IgG is a delayed marker, whichindicates that the antibody to the inducing matter was developed over an elongated period oftime. This contrasts with IgE, which is indicative of an immediate allergic reaction to a foreignbody.
Footnote 2: That is, the papers discussed byDr. Gots in his affidavit.