Allen v Consolidated Edison of N.Y.
Annotate this CaseDecided on December 12, 2019
Supreme Court, Bronx County
Tanita Allen, Plaintiff,
against
Consolidated Edison of New York, BH 520 W 175, LLC, 520 West 175th Street LLC, and David Samson, Defendants.
BH 520 W 175, LLC, Third Party Plaintiff,
against
Speedway Plumbing Corp., Third Party Defendant.
301631/2012
Attorney for Plaintiff
Michael A. Rose
Hach & Rose LLP
185 Madison Avenue 14th Floor
New York, New York 10016
Attorneys for Defendant
Michael Caulfield, Esq.
White & McSpedon, P.C.
875 Avenues of the Americas, Suite 800
New York, New York 10001
Attorney for Defendant
Carole A. Bornstein, Esq.
4 Irving Place
New York, New York 10003
Attorney for Defendant
Daniel G. Minnella, Esq
Lester Schwab Katz & Dwyer, LLP
100 Wall Street
New York, New York 10005
Attorneys for Third-Party Defendant
Eric Bailey, Esq.
Mulholland, Minion, Davey, McNiff & Feyrer
374 Hillside Avenue
Williston Park, New York 11595
Kenneth L. Thompson Jr., J.
The following papers numbered 1 to 10 read on this interim order On Calendar of December 12, 2019 PAPERS NUMBERED
Notice of Motion-Order to Show Cause - Exhibits and Affidavits Annexed 1-10Upon the foregoing papers and due deliberation thereof, the Decision/Order on this motion is as follows:
Defendants, 520 West 175th Street, LLC, (520 West) and David Samson, (Samson), move pursuant to CPLR 3212 for summary judgment dismissing the plaintiff's complaint and all cross-claims and counterclaims. Defendant, BH 520 W 175 LLC, (BH) moves pursuant to CPLR 3212 for summary judgment dismissing the complaint and all cross-claims as against it. Third-party defendant, Speedway Plumbing Corp., (Speedway), moves pursuant to CPLR 3212 for summary judgment, dismissing the third-party complaint.
A Frye Hearing was held by submitted papers and videotaped depositions of the party's experts, regarding the admissibility of plaintiff's experts' testimony on the issue of whether the onset of plaintiff's Huntington's Disease, (HD), was triggered by plaintiff's exposure to natural gas and carbon monoxide in plaintiff's leased apartment. Natural gas is primarily methane with some ethane and possibly some propane.[FN1]
Plaintiff, Tanita Allen, (Allen), leased an apartment from 520 West beginning on August 18, 2009. She resided in the apartment until January of 2012. Samson was the owner and manager of 520 West. Plaintiff testified that during the winter of 2010 to 2011, she smelled gas, and had problems with the operation of her stove and the carbon monoxide detector sounded once.[FN2]
In January of 2011, plaintiff complained to Samson of the smell of gas. If one can smell natural gas, there is at least 1% natural gas presence in the air.[FN3] Samson examined plaintiff's stove and being unable to stop the smell of gas, contacted Polie Service Co., Inc., (Polie), to service the stove. Subsequent to Polie's service, plaintiff continued to smell gas and Polie returned to plaintiff's apartment and replaced the igniter in plaintiff's stove.
BH purchased the apartment building from 520 West on February 16, 2011. On February [*2]24, 2011 Ricky Romano, (Romano), a Con Ed mechanic, responded to a call from plaintiff who complained of the smell of gas in her apartment. Romano also smelled gas in her apartment until he shut off the gas at the meter control valve.[FN4] Romano shut off the gas meter "because the house pipe was leaking."[FN5] No gas meter indicator, (GMI), readings were taken.[FN6] He placed an A red tag on the gas meter or stove because there was an immediate hazard in the apartment, a gas leak between the meter and the stove.[FN7] "An A classification red tag would be for immediate hazard that you shut off and left locked, disconnected and plugged. It's your most serious of tags."[FN8]
John Bradley, (Bradley), a service mechanic for co-defendant, Con Edison, (Con Ed), placed a second A red tag in plaintiff's apartment on July 28, 2011.[FN9] Bradley smelled natural gas in the apartment,[FN10] and had a positive GMI reading, near plaintiff's stove.[FN11] Natural gas in the air was measured at 3%.[FN12] Bradley confirmed that the meter control valve was leaking gas into the apartment with a "soapy water test."[FN13] Bradley then plugged the meter control valve to stop the flow of natural gas.[FN14]
FRYE HEARING The focus of the Frye test is to distinguish between scientific principles which are "demonstrable" and those which are "experimental" (see People v Wesley, 83 NY2d 417, 422 [1994], quoting Frye, 293 F at 1014). The Wesley court went on to emphasize that "the particular procedure need not be 'unanimously indorsed' by the scientific community but must be 'generally acceptable as reliable'" (83 NY2d at 423, quoting People v Middleton, 54 NY2d 42, 49 [1981]). (Marsh v. Smyth, 12 AD3d 307, 310 [1st Dept 2004]). It is well-established that an opinion on causation should set forth a plaintiff's exposure to a toxin, that the toxin is capable of causing the particular illness (general causation) and that plaintiff was exposed to sufficient levels of the toxin to cause the illness (specific causation) (see e.g. McClain v. Metabolife Intl., Inc., 401 F.3d 1233, 1241 [11th Cir.2005]; Wright v. Willamette Indus., Inc., 91 F.3d 1105, 1106 [8th Cir.1996] ). Parker v. Mobil Oil Corp., 7 NY3d 434, 448 [2006]). GENERAL CAUSATION
Dr. Enrico Fazzini, (Fazzini), plaintiff's treating neurologist and expert witness, testified that HD is a genetically transmitted disorder. "[W]hat's transmitted is an abnormal sequence, [*3]CAG, repeating units."[FN15] Plaintiff has 39 CAG repeat units, and "if you have 39, the probability is that you're not going to show—manifest the phenotype of Huntington's until you're in your 60s."[FN16]
Dr. Fazzini is a board-certified neurologist with subspecialty training in movement disorders. He also has a PhD in behavioral neuroscience. He specializes mostly in Parkinson's disease and other movement disorders, which includes dystonia, chorea form movements, mile clonus, tic disorders, tremors and restless leg syndrome.[FN17] He did a fellowship in movement disorders at Columbia University. Fazzini authored 20 peer reviewed publications. Fazzini is an associate professor of neurology at St. John's University, teaching neurology to ophthalmology residents. Fazzini testified that of the 30,000 to 40,000 patients he has treated approximately 12 have had HD.[FN18] Plaintiff was the only patient with HD Fazzini was treating at the time of his deposition.[FN19]
Fazzini cites to the Venezuelan study,[FN20] for the proposition that the environmental factors, including pollutants from the oil industry and poor sanitation could contribute to an overall earlier onset of HD. The mean age of onset in the Venezuelan study was compared to the mean age of onset in USA and Canadian populations.[FN21] The mean age of HD onset were 34.35 for the Venezuelans and 37.47 for the USA and 40.36 for Canadians.[FN22] Fazzini also found significant that none of the 80 persons with reduced/variable penetrance for the HD alleles, (35-39 CAG repeats), had been diagnosed with HD at the conclusion of the 23 year study.[FN23] With respect to the Venezuela study, Dr. Marvin Pietruszka, (Pietruszka), plaintiff's expert forensic toxicologist, testified that "[i]ndividuals who may not be necessarily symptomatic when exposed to environmental substances may then become symptomatic, and that is the point of that very large study."[FN24] Defendants' neurological expert, Dr. Pietro Mazzoni, (Mazzoni), also testified that "it is possible, quite possible that environmental factors influence the age of onset" of HD.[FN25] Mazzoni cited to the Venezuela study as "the entire body of evidence that I use in deciding this question."[FN26]
Plaintiff's and defendants' experts appear aligned that the Venezuelan study is evidence that environmental factors may influence the age of onset of HD. The experts differ on whether it is possible to use generally accepted scientific principles and methodology to conclude that [*4]natural gas or carbon monoxide exposure can trigger the onset of HD.
Pietruszka, plaintiff's expert, is a board certified pathologist in anatomic pathology and clinical pathology and is board certified by the American Board of Forensic Toxicology. He is board certified by the American Board of Preventive Medicine and Occupational Medicine and works as a clinician in that specialty.[FN27] He is a clinical associate professor of pathology at USC Keck School of Medicine, where he teaches pathology to medical students. Pietruszka has a clinical practice which was a combination of internal medicine and family medicine though over the last 15 to 20 years it is oriented more towards occupational medicine.[FN28] His pathology practice consists of autopsies. He is medical expert with the Superior Court of Los Angeles in the area of forensic pathology and forensic toxicology.[FN29] Pietruszka is a graduate of law school but is not a practicing attorney.[FN30]
Dr. Mazzoni, defendant's expert, is a board certified neurologist and associate professor of neurology at Washington University in St. Louis for the last three years. He was a faculty member of Columbia University Medical Center for the prior 14 years. His medical degree is from Harvard and he has a PhD in neuroscience from MIT. He did a fellowship in movement disorders at Columbia University. He is associated with the Centers for Excellence for Huntington's Disease at both Columbia and Washington Universities.[FN31] The Centers for Excellence exclusively treat patients with HD and employs clinical data for research into topics such as "how Huntington's disease starts, manifests itself and progresses."[FN32]
Defendants' toxicologist, Dr. Ronald Gots, MD, (Gots), testified that:
natural gas is not a direct toxin. It has absolutely no effect on the brain. It has no effect on the nervous system. It has no effect on any part of the body itself. The only way it produces toxicity is by displacing the oxygen sufficiently so that a person becomes hypoxemic and then hypoxic, and that can cause, obviously, problems. That almost never occurs.[FN33]Dr. Gots is a board certified toxicologist. He had teaching positions at Georgetown and George Washington medical schools, teaching environmental toxicology. He has published 80 to 90 papers and 16 books or chapters in books.[FN34]
The science of the age of onset was addressed by Fazzini with a cite [FN35] to the Quarrell observational study of 176 patients with reduced penetrance who had a 40% chance the person will be asymptomatic at age 65 and 30% chance to be asymptomatic at age 75.[FN36] Mazzoni also cited to the Quarrell observational study, indicating that table one provides the data that for a [*5]repeat length of 39 the range of age of onset was 31-89 years old.[FN37] Plaintiff was approximately 35 years old at the onset of her HD symptoms and 37 when diagnosed with HD.[FN38]
Mazzoni testified that a study relied upon by plaintiff [FN39] , merely "addresses the question of modifying the length of the repeat. This article does not speak to whether the age of onset can be advanced, and I'm not aware of articles that now show factors that affect the age of onset."[FN40] The study concerns mutagenesis of CAG repeats in cell cultures.
With respect to the studies cited by plaintiff, Fazzini agreed that the main point of those studies is that low oxygen level resulted in hypoxemia or hypoxia. Fazzini also agreed that the levels of oxygen used in such studies were substantially less than the 20.9 percent present in the atmosphere.[FN41] Fazzini further testified that it is not known what reduced oxygen levels are required to trigger the expression of HD in a person with reduced penetrance HD.
Mazzoni testified that there were no scientific studies supporting the notion that carbon monoxide or natural gas can cause 1) "Huntington's Disease" 2) "modification in the genetic mutation that causes Huntington's Disease" 3) "triggering the onset of Huntington's Disease" or 4) "accelerating the course of Huntington's Disease."[FN42] Mazzoni explained that he has never seen an article that associated methane gas or carbon monoxide with the onset of Huntington's Disease, nor attended a scientific meeting in which such an association was discussed.[FN43]
Fazzini testified that there are no studies relating natural gas to HD,[FN44] and there are no studies linking carbon monoxide to HD.[FN45] Fazzini also testified he had never been to a conference where there was any discussion of a link between HD and methane or carbon monoxide.[FN46] Fazzini also testified that he treated plaintiff for seven years and never presented a case study orally or in writing of Ms. Allen's case to be peer reviewed.[FN47] Pietruszka also testified that there are no studies connecting methane with Huntington's disease and no studies connecting carbon monoxide with HD.[FN48]
Mazzoni testified that a common way for a factor to be accepted as affecting the age of onset for HD is for "a review article [to look] back at the body of evidence that says, yes, we now believe this factor is important for age of onset because there are these lab studies, animal studies, human studies."[FN49] However, there are no studies linking natural gas or carbon monoxide to the early onset of HD to be reviewed.
"[W]hile courts will go a long way in admitting expert testimony deduced from a well-recognized scientific principle or discovery, the thing from which the deduction is made must be sufficiently established to have gained general acceptance in the particular field in which it belongs." (Frye v US, 293 F 1013, 1014 [DC Cir 1923]). "Plaintiff's experts were unable to identify a single epidemiologic study finding an increased risk of AML as a result of exposure to gasoline Thus, the experts' opinions were properly excluded." (Parker v. Mobil Oil Corp., 7 NY3d 434, 450 [2006]). It is noted that the Venezuelan study did not identify natural gas, methane or carbon monoxide as the cause of triggering early onset of HD.
Fazzini testified, "I don't know the exact levels [of natural gas] that would be needed to cause someone with 39 repeat units to —to manifest the disease. I don't know what level of hypoxemia, hypoxia, what type of hypoxic environment for how long would do it. But we know in this case that it seems like it did."[FN50] In contrast, Mazzoni testified that "I think that one has to independently establish exposure to the toxic factor and, secondly establish the onset of symptoms, but I don't think it's correct to link them...because there were symptoms there must have been exposure [to natural gas]."[FN51]
"It was plaintiff's burden to show that the methodology his experts employed was generally accepted in the scientific community." (Sean R. ex rel. Debra R. v. BMW of N. Am., LLC, 26 NY3d 801, 812 [2016]). Accordingly, plaintiff has not met her burden to show that her expert's methodology is generally accepted.
SPECIFIC CAUSATIONIn response to questioning as to why he opines that plaintiff's HD was triggered by exposure to natural gas, Fazzini testified as follows:
Because she has the genetics for Huntington's Disease and the probabilities were that she should have not gotten Huntington's Disease until her late 60s or after or not at all. And we have evidence that there was a malfunctioning gas valve in her apartment and people smelling gas. And we know that hypoxemia can stress out the basal ganglia, which is an already sensitive brain structure, and her Huntington's Disease developed coincidentally temporally with the gas exposure.[FN52]Fazzini avers that plaintiff's mother is 64 years old and is free of HD symptoms, even though, like plaintiff, she has reduced penetrance 39 repeat CAG units.[FN53] Nevertheless, Fazzini did testify that plaintiff had a 2% chance of manifesting HD at the age she did.[FN54]
Fazzini testified that plaintiff had sleep apnea from 2005 or 2006 and probably still has it,[FN55] and testified that sleep apnea "can cause low oxygen to the brain."[FN56] Fazzini also testified that he did not take plaintiff's sleep studies into consideration in determining the causation of her early manifestation of HD, because he did not think it was significant. "If it was significant, then [*6]she would have brought it up with me a lot more."[FN57] At his deposition, Fazzini read from the results of a sleep apnea study from 2005-2006, that stated that plaintiff had "significant apnea syndrome."[FN58] Pietruszka testified that sleep apnea that is not ameliorated with a CPAP machine, can cause hypoxia.[FN59] Plaintiff testified to using the CPAP machine "religiously."[FN60] Plaintiff also testified that she has asthma induced by an allergic reaction to pollen. Use of an inhaler resolves her asthma.[FN61]
With respect to plaintiff's carbon monoxide detector, since plaintiff's carbon monoxide detector went off only once,[FN62] and no carbon monoxide had otherwise been detected, Gots concludes that the single alarm was "consistent with a faulty carbon monoxide detector that detected something that wasn't there."[FN63]
Plaintiff's engineering expert, Mr. Michael Tobias, (Tobias), is a licensed professional engineer in New York State as well as other states. He has written several hundred engineering articles for various engineering magazines.[FN64] Tobias testified that he has dealt with "gas leak situations from design, from leak testing to mitigation. Every aspect of it."[FN65]
Tobias testified that there was a natural gas leak in plaintiff's apartment from "December of 2010, for several months through when Con Ed shut everything off in July 28, 2011."[FN66] Pietruszka testified that plaintiff may have had symptoms of HD prior to the alleged time of exposure.[FN67] Pietruszka testified from the medical report of Dr. Frucht that plaintiff experienced headaches, nose bleeds, dizzy spells, nausea, hair loss, rashes and cough in early 2010, prior to her exposure to natural gas or exposure to carbon monoxide.[FN68] Fazzini testified that plaintiff's medical record indicates that plaintiff noticed involuntary movements of her toes and fingers in the summer of 2010.[FN69] Mazzoni also testified that plaintiff's medical records indicate that she had involuntary movement of her feet and fingers in March or April of 2010 which are symptoms of HD.[FN70]
Plaintiff's experts Fazzini and Pietruszka are admitting that the onset of plaintiff's symptoms may have preceded her exposure to natural gas and her possible exposure to carbon monoxide. If this is so, then plaintiff's HD was not triggered by her exposure to natural gas and/or carbon monoxide in the time period established by plaintiff and Tobias' testimony.
Pietruszka testified that a person can get HD only once.[FN71] Mazzoni, who performed an Independent Medical Examination of plaintiff on December 16, 2014 also averred that "the onset of Huntington's disease cannot be triggered twice."[FN72] Therefore, if plaintiff's HD was triggered in early 2010 or the summer of 2010, it was not triggered by the gas leak and/or carbon monoxide in her apartment.
Pietruszka avers that the Bradford Hill Criteria has "extensive, peer-reviewed scientific literature on assessing whether a causal connection can be supported by the available scientific and medical evidence.[FN73] Pietruszka avers that the "Bradford Hill can be utilized in this case to establish causation of Ms. Allen's symptomatology."[FN74]
However, with respect to one of the Bradford Hill factors, "temporality," (did exposure occur before disease developed),[FN75] plaintiff did not smell gas in her apartment until December of 2010, while there is medical evidence, she manifested symptoms of HD in early to mid-2010. When Pietruszka was questioned regarding this lack of temporality, Pietruszka speculated as follows: "I think that she could have theoretically been exposed earlier but we can't prove that."[FN76] The fact that the evidence indicates that plaintiff experienced symptoms of HD prior to her exposure to natural gas undermines plaintiff's expert's opinion that the facts of this action comport with the Bradford Hill criteria.
Tobias testified that it would take ten days to fill plaintiff's apartment with gas from the ¾ inch pipe delivering gas to the stove. However, Tobias testified that "there's obviously a leak much smaller than that,"[FN77] rendering his opinion regarding filling up the apartment in ten days irrelevant to the specific facts of this case, and therefore, not supportive of any mathematical modeling of exposure to natural gas. The testimony is also irrelevant as "natural gas explodes at about 5 percent."[FN78] Therefore, plaintiff's apartment was never full of natural gas.
Tobias also testified that "all buildings have air leakage through the envelope of the building, through little cracks in the windows, in the walls. There is always air infiltration."[FN79] Tobias never inquired of plaintiff how frequently she opened her windows.[FN80] Tobias admitted that the sole natural gas reading in the apartment was 3% and that was a reading in the vicinity of plaintiff's stove, while there was no atmospheric reading of natural gas was taken in plaintiff's apartment. Tobias testified that a 3% natural gas reading near a stove is different than a 3% natural gas reading in the apartment.[FN81] Bradley confirmed that he took the sole reading of natural gas in plaintiff's apartment in the vicinity of the stove, which is not an "atmospheric reading."[FN82]
Gots testified that a level of 3% natural gas would not be enough to produce hypoxemia.[FN83] Three percent natural gas would reduce the available oxygen from 20.9 percent to 20.3 or 20.4 percent.[FN84] Gots testified that in order for an individual to have cerebral hypoxia as a result of exposure to natural gas "you'd have to reduce the oxygen level from 20.9 percent in the air to about 6—-17, 16 percent. And then, if you go down to 13 or 12 percent, you will have very serious problems and can be comatose."[FN85] In order to lower the oxygen level in the air to about 16 to 17 percent the air would have to be about 15 percent natural gas to produce some degree of hypoxia. Three percent natural gas was the only measurement ever taken of plaintiff's apartment. "[N]atural gas explodes at about 5 percent."[FN86] No explosion occurred in plaintiff's apartment.
Fazzini testified that there are no studies that indicate that hypoxia can be caused by less than 5 percent displacement of oxygen.[FN87] "Parker by no means dispensed with a plaintiff's burden to establish sufficient exposure to a substance to cause the claimed adverse health effect (see id. at 449 [suggesting alternative ways to do this, such as estimating exposure by means of mathematical modeling])." (Cornell v. 360 W. 51st St. Realty, LLC, 22 NY3d 762, 784 [2014]).Fazzini avers that the MRI of plaintiff's "brain in December 2012 also has the structural findings at that time of toxic exposure, as well as, HD."[FN88] Both the May 2011 and December 2012 MRI report finds abnormal white matter signal of plaintiff's brain. The May 2011 brain MRI was ordered by Dr. Steven Facia and the MRI report did not indicate that the MRI findings were related to exposure to carbon monoxide or methane gas.[FN89] While there is overlap in the possible causes of the abnormal white signal matter, the December 2012 MRI ordered by Dr. Fazzini differs in the inclusion of the possibility of exposure to toxic materials "in view of clinical history".[FN90] (emphasis added). Mazzoni testified that the abnormal white matter signal may be seen in patients with migraine headaches, vasculitis, demyelinating disease, lime disease and viral illness.[FN91]
Mazzoni also testified that plaintiff's symptoms of nausea, headache, dizziness, hair loss, forgetfulness, skin rashes, confusion are also symptoms of a myriad of other diseases or problems.[FN92] Pietruszka testified that one can have headaches, dizziness, nausea, confusion and forgetfulness without exposure to natural gas or carbon monoxide.[FN93]
[T]he Appellate Division is incorrect to the extent that it suggests that performance of a differential diagnosis establishes that a plaintiff has been exposed to enough of an agent to prove specific causation. This is not what we meant when we stated that "precise [*7]quantification" of exposure was not necessary, and there exist alternative "potentially acceptable ways to demonstrate [specific] causation" (Parker, 7 NY3d at 448, 449). In any event, this record does not supply a proper foundation for Dr. Johanning's differential diagnosis.(Cornell v. 360 W. 51st St. Realty, LLC, 22 NY3d 762, 784—85 [2014]).With respect to differential diagnosis in this action, Fazzini testified that "[w]e have not ruled out intoxication by some other substance in this case. It's always a possibility that there could have been something else. Who knows. Arsenic. Who knows."[FN94]
Both Fazzini and Pietruszka employ what has been described as "backwards" reasoning by the Court of Appeals.[FN95] As previously stated, Fazzini testified, "I don't know the exact levels [natural gas] that would be needed to cause someone with 39 repeat units to —to manifest the disease. I don't know what level of hypoxemia, hypoxia, what type of hypoxic environment for how long would do it. But we know in this case that it seems like it did."[FN96]
Pietruszka, similarly to Fazzini, works backwards from plaintiff's symptoms to the cause of plaintiff's onset of HD:
In this case, we are demonstrating exposure by the effects of the exposure, we do not have the measurements, we will not have the measurements, but we can reasonably assume what those measurements would have been had the individual been exposed.[FN97]After testifying to plaintiff's asthma and sleep apnea as predisposing factors for hypoxia, Pietruszka further testified, "[s]o is that amount, that one to three percent, sufficient to cause this disease? I don't know a hundred percent for sure. All I know is that in this case that amount was sufficient.[FN98]
Pietruszka testified that:
So any risk analysis, any toxicologic risk analysis that's being done is incomplete. We're looking basically at end results and going backward and trying to essentially make a statement about what is reasonably believed to be the exposure considering the fact that there's no other exposure.[FN99]The Court of Appeals has disapproved of "working backwards" from symptoms:
We don't disagree with the scientific validity of controlled studies or their ability to measure symptoms in response to a given exposure. But those controlled studies do not support the inverse approach Dr. Frazier employed in this case—working backwards from reported symptoms to divine an otherwise unknown concentration of gasoline vapor. Dr. Frazier has not identified on this record any study, report, article or opinion that admits or employs such a methodology.(Sean R. v BMW, 26 NY3d 801, 810 [2016]).Drawing on the ventilation analysis of Tobias and the record, Fazzini, avers that there was between a 1 to 3% natural gas in the apartment between December 2010 through July of [*8]2011.[FN100] Fazzini avers that the National Institute of Occupational Safety and Health, (NIOSH) Threshold Limit Value, (TLV), for natural gas/methane/carbon monoxide is 0.1% over an 8 hour period.[FN101] Fazzini further opined that the time period of exposure for 8 months at a time plaintiff was unemployed, was "multiple orders of magnitude greater than NIOSH"[FN102] standard. However, "standards promulgated by regulatory agencies as protective measures are inadequate to demonstrate legal causation." (Parker v. Mobil Oil Corp., 7 NY3d 434, 450 [2006]).
CONCLUSIONThere are no studies linking exposure to natural gas or carbon monoxide triggering the early onset of Huntington's Disease, nor is there evidence of any discussion in the relevant scientific community of such a possibility. Moreover, under the facts of this action, plaintiff manifested symptoms of Huntington's Disease prior to her exposure to natural gas and her alleged exposure to carbon monoxide.
The Bradford Hills criteria was not met as there is no temporality. The mathematical model of exposure is undercut by calculations made that do not reflect the facts of this action. The differential diagnosis of the trigger for HD suffers from lack of temporality, or elimination of other possible environmental triggers as attested to by plaintiff's expert.[FN103]
Accordingly, as a result of the Frye hearing defendants' motions are granted to the extent that plaintiff's experts are precluded from testifying that expression of plaintiff's Huntington's Disease was triggered by her exposure to natural gas and/or carbon dioxide.
The motions in this action are adjourned to December 4, 2020 for further submissions limited to the issue of whether plaintiff has incurred damages from her exposure to natural gas and/or carbon monoxide apart from triggering the onset of Huntington's Disease. Since this action has not been converted to an E-file action, please direct briefs or a stipulation if there is agreement on this issue, to Chambers at this email: NMBenjamin@nycourts.gov.
The foregoing constitutes the interim order of the Court.
Dated: December 12, 2019KENNETH L. THOMPSON JR. J.S.C. Footnotes
Footnote 1:Gots, deposition, p. 12-13.
Footnote 2:Plaintiff, deposition, pp. 35-36.
Footnote 3:Pietruszka, affidavit, April 14, 2017, par. 65-66.
Footnote 4:Romano, deposition, pp. 48-53.
Footnote 5:Romano, deposition, p. 57.
Footnote 6:Romano, deposition, p. 59.
Footnote 7:Romano, deposition, p. 46.
Footnote 8:Romano, deposition, p. 41.
Footnote 9:Bradley, deposition, p.55.
Footnote 10:Bradley, deposition, p. 121.
Footnote 11:Bradley, deposition, p. 110.
Footnote 12:Bradley, deposition, p. 118.
Footnote 13:Bradley, deposition, p. 112.
Footnote 14:Bradley, deposition, p. 73.
Footnote 15:Fazzini, deposition, p. 13.
Footnote 16:Fazzini, deposition, p. 17.
Footnote 17:Fazzini, deposition, p. 9.
Footnote 18:Fazzini, deposition, p. 260-261.
Footnote 19:Fazzini, deposition, p. 196.
Footnote 20:Wexler NS, et al, Venezuela Collaborative Research Project. Venezuelan kindreds reveal that genetic and environmental factors modulate Huntington's disease age of onset. Proc. Natl. Acad. Sci. USA. 2004; 101:3498-3503.
Footnote 21:Venezuelan study, p. 3503.
Footnote 22:Venezuelan study, p. 3502.
Footnote 23:Fazzini, affidavit, April 17, 2017, par. 79.
Footnote 24:Pietruszka, deposition, pp. 89-90.
Footnote 25:Mazzoni, deposition, p. 162.
Footnote 26:Mazzoni, deposition, p. 163.
Footnote 27:Pietruszka, deposition, p. 9.
Footnote 28:Pietruszka, deposition, p. 10.
Footnote 29:Pietruszka, deposition, p. 10.
Footnote 30:Pietruszka, deposition, p. 9.
Footnote 31:Mazzoni, deposition, pp. 12-17.
Footnote 32:Mazzoni, deposition, p. 20.
Footnote 33:Gots, deposition, p. 13.
Footnote 34:Gots, deposition, pp. 9-10.
Footnote 35:Fazzini, affidavit, April 17, 2017, par. 84.
Footnote 36:Quarrell O, et al, Reduced penetrance alleles for Huntington's disease: a multi-centre direct observational study. J Med Genet 2007: 44 e68.
Footnote 37:Mazzoni, deposition, pp. 55-57.
Footnote 38:Allen, deposition, p. 362.
Footnote 39:Chatterjee N, et al, Environmental stress induces trinucleotide repeat mutagenesis in human cells. Proc Natl Acad Sci, 112(12) 3754-3769, 3765.
Footnote 40:Mazzoni, deposition, p. 113.
Footnote 41:Fazzini, deposition, pp. 252-253.
Footnote 42:Mazzoni, deposition, p. 73.
Footnote 43:Mazzoni, deposition, p. 74.
Footnote 44:Fazzini, deposition, p. 196.
Footnote 45:Fazzini, deposition, p. 69.
Footnote 46:Fazzini, deposition, p. 69.
Footnote 47:Fazzini, deposition, pp. 71-72.
Footnote 48:Pietruszka, deposition, p. 320.
Footnote 49:Mazzoni, deposition, p. 66.
Footnote 50:Fazzini, deposition, p. 181.
Footnote 51:Mazzoni, deposition, p. 124.
Footnote 52:Fazzini, deposition, p. 181.
Footnote 53:Fazzini, affidavit, April 17, 2017, par. 24-25.
Footnote 54:Fazzini, deposition, p. 54.
Footnote 55:Fazzini, deposition, p. 178.
Footnote 56:Fazzini, deposition, p. 178.
Footnote 57:Fazzini, deposition, pp.202-203.
Footnote 58:Fazzini, deposition, p. 355.
Footnote 59:Pietruszka, deposition, p. 407.
Footnote 60:Allen, deposition, p. 478.
Footnote 61:Allen, deposition, pp. 504-505.
Footnote 62:Allen, deposition, p. 51.
Footnote 63:Gots, deposition, p. 16.
Footnote 64:Tobias, deposition, p. 8.
Footnote 65:Tobias, deposition, p. 9.
Footnote 66:Tobias, deposition, pp. 10-11.
Footnote 67:Pietruszka, deposition, pp. 387-388.
Footnote 68:Pietruszka, deposition, pp. 225-226.
Footnote 69:Fazzini, deposition, pp. 227-228.
Footnote 70:Mazzoni, deposition, pp. 117-120.
Footnote 71:Pietruszka, deposition, p. 299.
Footnote 72:Mazzoni, affidavit dated January 24, 2017, par. 9.
Footnote 73:Pietruszka, affidavit, April 14, 2017, par. 12.
Footnote 74:Pietruszka, affidavit April 14, 2017, par. 129.
Footnote 75:Pietruszka, affidavit, April 14, 2017, par. 15.
Footnote 76:Pietruszka, deposition, p. 274.
Footnote 77:Tobias, deposition, p. 34.
Footnote 78:Gots, deposition, pp. 17-18.
Footnote 79:Tobias, deposition, p. 26.
Footnote 80:Tobias, deposition, pp. 85-86.
Footnote 81:Tobias, deposition, pp. 191-193. Referencing Bradley, deposition, p. 65.
Footnote 82:Bradley, deposition, pp. 65-68.
Footnote 83:Gots, deposition, p 18.
Footnote 84:Gots, deposition, pp. 18-19.
Footnote 85:Gots, deposition, pp. 80-81.
Footnote 86:Gots, deposition, pp. 17-18.
Footnote 87:Fazzini, deposition, p. 132-133.
Footnote 88:Fazzini, affidavit, April 17, 2017, par. 106.
Footnote 89:Mazzoni, deposition p. 100.
Footnote 90:Mazzoni, deposition, p. 104.
Footnote 91:Mazzoni, deposition, p. 100.
Footnote 92:Mazzoni, deposition, p. 285.
Footnote 93:Pietruszka, deposition, pp. 346-348.
Footnote 94:Fazzini, deposition, p. 275.
Footnote 95:Sean R. v BMW, 26 NY3d 801, 810 [2016].
Footnote 96:Fazzini, deposition, p. 181.
Footnote 97:Pietruszka, deposition, p. 203.
Footnote 98:Pietruszka, deposition, p. 207.
Footnote 99:Pietruszka, deposition, p. 308.
Footnote 100:Fazzini, affidavit, April 17, 2017, par. 107.
Footnote 101:Fazzini, affidavit, April 17, 2017, par. 105.
Footnote 102:Fazzini, affidavit, April 17, 2017, par. 105.
Footnote 103:Fazzini, deposition, p. 275.
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