Plaintiffs, former residents of a unit in the cooperative apartment building owned by defendant 301-52 Townhouse Corp., as[417]*417sert 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.1 In other words, “ ‘association’ is not equivalent to ‘causation’ ” (Green, Freedman and Gordis, Reference Guide on Epidemiology, in Federal Judicial Center, Reference Manual on Scientific 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 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, [418]*418Dr. 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, 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.” 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.”2 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 [419]*419demonstrating 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’.3 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.4
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’ apart[420]*420ment 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.
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Plaintiffs, former residents of a unit in the cooperative apartment building owned by defendant 301-52 Townhouse Corp., as[417]*417sert 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.1 In other words, “ ‘association’ is not equivalent to ‘causation’ ” (Green, Freedman and Gordis, Reference Guide on Epidemiology, in Federal Judicial Center, Reference Manual on Scientific 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 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, [418]*418Dr. 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, 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.” 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.”2 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 [419]*419demonstrating 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’.3 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.4
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’ apart[420]*420ment 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]).5 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, 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]). Concur—Friedman, Williams and Freedman, JJ.