Opinion
NO. 2015-CA-001545-WC
06-10-2016
ARMSTRONG COAL COMPANY, INC. APPELLANT v. NATHAN ATTEBURY; HON. CHRIS DAVIS, ADMINISTRATIVE LAW JUDGE; AND WORKERS' COMPENSATION BOARD APPELLEES
BRIEF FOR APPELLANT: Will E. Messer Lexington, Kentucky BRIEF FOR APPELLEE, NATHAN ATTEBURY: Jerry P. Rhoads Madisonville, Kentucky
NOT TO BE PUBLISHED PETITION FOR REVIEW OF A DECISION OF THE WORKERS' COMPENSATION BOARD
ACTION NO. WC-14-90179 OPINION
AFFIRMING
** ** ** ** **
BEFORE: KRAMER, TAYLOR AND THOMPSON, JUDGES. THOMPSON, JUDGE: Armstrong Coal Company, Inc. appeals from an opinion and order of the Workers' Compensation Board affirming a decision of the Administrative Law Judge (ALJ) finding that Nathan Attebury suffered permanent brain damage from exposure to toluene contained in cans of spray paint he used in the course and scope of his employment with Armstrong. Armstrong argues the Board erred by affirming the ALJ's award because the ALJ relied on the testimony of neurologist Dr. Michael Mayron to support the medical causation element of his claim. We affirm.
Attebury worked at Armstrong's Kronos coal mine from June 8, 2012, to January 22, 2014. One of his duties was to mark the face of the mine using orange Krylon spray paint containing toluene. In a typical ten-hour shift, he used two to four cans of spray paint.
Attebury testified that about six months after he began working for Armstrong, he suffered intermittently from shortness of breath. He testified that it usually started when he was spraying the paint and improved when outside the mine. He testified that in January 2013, he returned from the mine every workday with headaches, sickness to his stomach and dizziness, and sometimes experienced momentary black outs. His headaches would usually begin about halfway into his shift while he was using the spray paint, would sometimes last all day, and eventually began occurring on his days off. Attebury testified that he began losing his ability to concentrate and experienced confusion. At some point during his employment with Armstrong, he began experiencing hand tremors.
After a series of temporary periods being off work due to his symptoms, Attebury permanently quit work on January 22, 2014. Attebury testified that his blackouts ceased in March or April of 2014. His headaches ceased for a few months but returned and have been consistent since September or October 2014. He testified his confusion has remained.
Attebury first sought treatment for his symptoms in January 2014, with his regular physician, Dr. Jayna Jones. Dr. Jones referred him to Dr. Mayron, who initially examined him on February 17, 2014.
Dr. Mayron opined that the cause of Attebury's symptoms was exposure to industrial paint containing toluene. He testified that he had reviewed scientific reports regarding the effect of exposure to paint containing toluene, including the Annals of Neurology. Dr. Mayron opined that Attebury's condition is irreversible and permanent and, according to the American Medical Association's Guides to the Evaluation of Permanent Impairment, Fifth Edition, he has a 30 to 49% impairment. He testified he would assign Attebury a 49% impairment.
In its post-hearing brief, Armstrong argued Dr. Mayron's findings and conclusions should be disregarded for lack of scientific reliability and relevancy pursuant to Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993).
The ALJ found Dr. Mayron's opinions to be scientifically reliable and relevant and, relying on his opinions, found Attebury suffers from toluene-induced toxic encephalopathy caused by his work. The ALJ stated as follows:
Dr. Mayron states that one of the potential side effects of the Krylon paint is toxic encephalopathy. This is the diagnosis he makes for [Attebury]. He states the toxic encephalopathy is work-related. Dr. Mayron testified in his deposition that he extensively reviewed the Krylon
paint, particularly the toluene. It can cause the toxic encephalopathy and it can cause all of [Attebury's] neurologic symptoms. The damage is permanent.
In short [. . .] I am more inclined to find the opinion of Dr. Mayron persuasive. He is a treating physician with no known or demonstrated bias. His is a very specific field and area of expertise to which he devotes his practice, i.e. neurological conditions. He has demonstrated the scholarly texts he relies upon. There is no other known source of causation for [Attebury's] symptoms, as I agree that the ADHD, anxiety or depression is not causing them.
I am not persuaded by [Armstrong's] argument that Dr. Mayron had insufficient knowledge regarding the amount of toluene exposure. [Attebury] testified to me and related to Dr. Mayron his exposure levels. That it was not measured in parts per milliliter or some other scientifically exact amount is not decisive.
I find, based on the foregoing, that [Attebury] does have toxic encephalopathy and it is work-related.
The Board reviewed Armstrong's objections to the ALJ's reliance upon Dr. Mayron's findings and conclusions and determined Armstrong's objections merely concerned the weight of the evidence rather than its admissibility. The Board affirmed, and this appeal followed.
The Board pointed out that Armstrong did not file a petition for reconsideration and, therefore, ruled it was bound by the ALJ's findings of fact. Kentucky Revised Statutes (KRS) 342.285(1) provides: "An award or order of the administrative law judge as provided in KRS 342.275, if petition for reconsideration is not filed as provided for in KRS 342.281, shall be conclusive and binding as to all questions of fact[.]" In other words, this Court cannot substitute those findings with those of its own.
Armstrong argues that whether the ALJ's decision was based on substantial evidence is a question of law and, therefore, a petition for reconsideration was not required. It contends the Board erroneously failed to consider the merits of its argument that substantial evidence did not support the ALJ's decision.
We disagree that the Board did not consider the merits of Armstrong's arguments. The Board's opinion and order reveals that it carefully considered the merits of Armstrong's challenge to the reliability and relevancy of Dr. Mayron's opinions. The Board merely observed that it could not substitute its findings of fact for those of the ALJ. We likewise turn to the merits of Armstrong's challenge to Dr. Mayron's opinions.
"The claimant bears the burden of proving every element of a workers' compensation claim, including causation." Lane v. S & S Tire, Inc., No. 15, 182 S.W.3d 501, 505 (Ky. 2005). "In order for that burden to be sustained, no less than substantial evidence of each element of the claim must be introduced. Substantial evidence has been defined as some evidence of substance and relevant consequence, having the fitness to induce conviction in the minds of reasonable people." Magic Coal Co. v. Fox, 19 S.W.3d 88, 96 (Ky. 2000). Because it would not be apparent to a layperson whether Attebury's medical condition was caused by repeated exposure to a toxic substance during the course of his employment, he was required to support his theory of medical causation with expert medical testimony. Megel v. Hawaiian-Tropic Northwest and Central Distributors, Inc., 618 S.W.2d 184, 187 (Ky.App. 1981).
Armstrong contends that Dr. Mayron was unaware of Attebury's exact level of exposure to toluene and his exposure was within the acceptable level according to the published OSHA standards. Armstrong also challenges the reliability of the study submitted by and relied upon by Dr. Mayron claiming the article examines only abusive exposure to toluene and links toluene exposure to central nervous system damage, not toxic encephalopathy. Essentially, it invites this Court to conduct a de novo review of the relevancy and reliability of Dr. Mayron's expert opinion.
Under our civil rules, the admission of expert testimony is governed by Kentucky Rules of Evidence (KRE) 702 which states:
If scientific, technical, or other specialized knowledge will assist the trier of fact to understand the evidence or to determine a fact in issue, a witness qualified as an expert by knowledge, skill, experience, training, or education, may testify thereto in the form of an opinion or otherwise, ifKentucky's Supreme Court has adopted the factors enumerated in Daubert for determining the reliability and relevancy of expert testimony. "Generally, when a party proffers expert testimony, the trial court must determine in a preliminary hearing—a so-called Daubert hearing—whether the expert is indeed proposing to testify to the knowledge meeting the criteria of KRE 702 and KRE 104." Epperson v. Commonwealth, 437 S.W.3d 157, 164 (Ky.App. 2014). Among the factors that have been recognized as pertinent to the court's inquiry are:
(1) the testimony is based upon sufficient facts or data,
(2) the testimony is the product of reliable principles and methods, and
(3) the witness has applied the principles and methods reliably to the facts of the case.
1) whether the theory or technique can be and has been tested;Burton v. CSX Transp., Inc., 269 S.W.3d 1, 7 (Ky. 2008).
2) whether the theory or technique has been subjected to peer review and publication;
3) the known or potential rate of error in using a particular scientific technique and the existence and maintenance of standards controlling the technique's operation; and
4) whether the theory or technique has been generally accepted in the particular field.
In City of Owensboro v. Adams, 136 S.W.3d 446, 450 (Ky. 2004), the Court held that Daubert is applicable to workers' compensation proceedings. The Court noted that the "the difference between the application of Daubert in a jury trial and its application in a bench trial or a workers' compensation proceeding is only procedural." Id. The Court continued and gave further explanation:
In a jury trial, a Daubert hearing, is usually required "to protect juries from being bamboozled by technical evidence of dubious merit." However, in a bench trial, the trial court, without a Daubert hearing, will often admit the
evidence first and then disregard it upon deciding that it is unreliable.Id. at 451. The ALJ properly addressed Armstrong's post-hearing challenge to Dr. Mayron's testimony by conducting a Daubert analysis. The issue is whether the ALJ's determination that his testimony was scientifically reliable and relevant should be disturbed.
In Miller v. Eldridge, 146 S.W.3d 909 (Ky. 2004), our Supreme Court went to great lengths to instruct appellate courts on the appropriate standard when reviewing a Daubert determination. Our Supreme Court stressed that "clear error and abuse of discretion are separate standards of review" and that the "distinct aspects of the Daubert analysis—the findings of fact, i.e., reliability or non-reliability, and the discretionary decisions, i.e., whether the evidence will assist the trier of fact and the ultimate decision as to admissibility—must be reviewed under different standards." Id. at 915. Consequently, "an error that is alleged in the trial court's findings of fact must be reviewed for clear error before the appellate court can reach the discretionary aspects of the trial court's decision." Id. When reviewing a trial court's finding that testimony is reliable or unreliable, the trial court must be afforded great deference. Id at 917. Our Supreme Court cautioned that the appellate court's must avoid "unfettered review of the record[.]" Id. As stated by the Court:
[A]ppellate courts must recognize the unfortunate but necessary corollaries of deference to the trial court: that it is possible for a trial court to rule contrary to what an appellate court would rule without abusing its discretion
or being clearly erroneous, and that an appellate court is powerless to disturb such rulings. The abuse of discretion and clear error standards allow an appellate court to walk this fine line—to engage in a meaningful review without resorting to retrying the issue—by requiring a thorough but deferential examination of the record and the trial court's findings of fact and rulings.Id.
Dr. Mayron is a board certified neurologist who has practiced for over thirty-five years and treated Attebury regularly. He provided a description of the diagnostic testing performed and the research he conducted to support his opinion. Dr. Mayron's opinion as to the cause of Attebury's condition is not the type of "pseudoscientific quackery" that Daubert is intended to exclude from evidence. Id. at 922. Although "toxic encephalopathy is a somewhat controversial diagnosis[,]" Burton, 269 S.W.3d at 4, n.5, it is nevertheless one recognized by some in the medical community. The "minor problems" with Dr. Mayron's "qualifications, his use of scientific principles to arrive at his opinions, or his application of the variables specific to [Attebury's] case were fertile ground for a robust cross-examination by [Armstrong's] attorneys—not reasons to exclude his testimony at trial." Miller, 146 S.W.3d at 922.
Based on the foregoing, the opinion and order of the Workers' Compensation Board is affirmed.
TAYLOR, JUDGE, CONCURS.
KRAMER, JUDGE, DISSENTS AND FILES SEPARATE OPINION.
KRAMER, JUDGE DISSENTING: Respectfully, I dissent. In my opinion, the record compels the conclusion that the ALJ committed reversible error by considering and relying upon Dr. Mayron's flawed methodology to reach his findings and conclusions as evidence of work-relatedness and medical causation in this matter.
To begin, the ALJ recited in his opinion that the reason he found Dr. Mayron's findings and conclusions persuasive and reliable was "His is a very specific field and area of expertise to which he devotes his practice, i.e. neurological conditions." This reasoning is unsound because it is well settled that the admissibility and reliability of an expert's opinion do not turn on the quality of the proffered expert's credentials. See FRE 702 adv. committee note (2000 Amendment) ("The trial court's gatekeeping function requires more than simply 'taking the expert's word for it.'") (quoting Daubert v. Merrell Dow Pharmaceuticals, Inc., 43 F.3d 1311, 1319 (9th Cir. 1995); see also Tamraz v. Lincoln Elec. Co., 620 F.3d 665, 671 (6th Cir. 2010), ("No matter how good experts' credentials may be, they are not permitted to speculate. . . . Dr. Carlini may be a distinguished doctor, and his conjecture about causation may be worthy of careful attention. . . . But the courtroom is not the place for scientific guesswork, even of the inspired sort.") (citations and internal quotations omitted); Burton v. CSX Transp., Inc., 269 S.W.3d 1, 10 (2008) ("Certainly, a trial court as the gatekeeper should exclude a so-called expert's unsupported assertions[.]").
What is critically important-- and what is tellingly absent from the ALJ's, Board's and majority's respective analyses in this matter--is an examination of Dr. Mayron's methodology, which is entirely proper--and in fact necessary-- on initial determination by the ALJ and by the Court on review thereafter. Contrary to blindly accepting credentials, a searching examination of the data and other materials underpinning a challenged expert's conclusions is in keeping with the gate-keeping function required by Daubert. See, e.g., Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146, 118 S.Ct. 512, 139 L.Ed.2d 508 (1997):
Conclusions and methodology are not entirely distinct from one another. Trained experts commonly extrapolate from existing data. But nothing in either Daubert or the Federal Rules of Evidence requires a district court to admit opinion evidence which is connected to existing data only by the ipse dixit of the expert. A court may conclude that there is simply too great an analytical gap between the data and the opinion offered.
Consistently with this principle, the Sixth Circuit has instructed district courts that "[expert] testimony must 'fit' the facts of the case, that is, there must be a connection between the scientific research or test result being offered and the disputed factual issues in the case in which the expert will testify." Pride v. BIC Corp., 218 F.3d 566, 578 (6th Cir. 2000) (citing Daubert, 509 U.S. at 592).
Furthermore, where an expert draws an inference from his experience, the proponent must establish "appropriate validation" for the application of the expert's theory to the matter at hand. 1 McCormick on Evidence, § 13 (7th ed.1999); In re Scrap Metal Litigation, 527 F.3d 517, 529 (6th Cir. 2008). The judge's role is to ensure the theory or technique "works":
The foundation must include a showing of the results when the technique was used on prior occasions . . . [n]either the expert's personal voucher nor general acceptance in the field nor even long-term, repeated use of the theory suffices.McCormick, supra.
. . . .
It is also clear that it is not enough for the witness to assert in conclusory fashion that she is relying on her general 'expertise,' 'knowledge,' or 'education.' Those considerations can qualify the witness as an expert, but they do not speak to the validity of the expert's theory or technique. To provide a useful expert insight, the witness must identify a more specific technique or theory. The witness must articulate that technique or theory. Otherwise, the witness is venturing nothing more than a guess.
With the above in mind, the methodology underpinning of Dr. Mayron's findings and conclusions requires scrutiny.
It is helpful to note some of the methodologies courts have, for purposes of Daubert, found reliable in proving permanent injury resulted from gradual toxic exposure. Generally speaking, litigants who assert they suffered injury in this manner must establish both general and specific causation through proof that the toxic substance is capable of causing and did cause the alleged injury. See, e.g., Burton, 269 S.W.3d at 7-8 and n.19 (discussing proof of specific and general causation in toxic tort case involving injury allegedly sustained by exposure to solvents); see also Pluck v. BP Oil Pipeline Co., 640 F.3d 671 (6th Cir. 2011) (discussing general burden of proving general and specific causation regarding claims alleging injury due to toxic substance exposure).
To do so, one accepted methodology borrows from toxicological principles and focuses upon the relationship in which a change in amount, intensity, or duration of exposure to a chemical is associated with a change in risk of disease. Under this methodology,
[f]irst, the expert should analyze whether the disease can be related to chemical exposure by a biologically plausible theory. Second, the expert should examine if the plaintiff was exposed to the chemical in a manner that can lead to absorption into the body. Third, the expert should offer an opinion as to whether the dose to which the plaintiff was exposed is sufficient to cause the disease.Federal Judicial Center, Reference Manual on Scientific Evidence 419 (2d ed. 2000). An example of this methodology, and a court's scrutiny of it, is found in Nelson v. Tennessee Gas Pipeline Co., 243 F.3d 244 (6th Cir. 2001). There, several plaintiffs alleged that the defendant released toxic substances, including polychlorinated biphenyls (PCBs), into the atmosphere, water, and soil of the area in which they lived and that these substances had injured them. In reviewing the magistrate judge's decision to exclude one of the plaintiffs' experts (Kaye Kilburn, M.D.) on Daubert grounds, the Sixth Circuit held:
In examining the scientific validity of the methodology Kilburn used to conclude that the plaintiffs were injured as a result of exposure to PCBs, the magistrate judge focused most heavily upon Kilburn's failures to account
for "confounding factors" that could have caused similar symptoms, establish a temporal relationship between exposure to PCBs in Lobelville and the reported maladies, demonstrate that the plaintiffs received doses of PCBs sufficient to make them ill, or show that his theories enjoyed general acceptance. We agree that the flaws in the methodology underlying Kilburn's opinion that PCB exposure caused the plaintiffs' impairments, as well as a lack of support for the proposition that environmental PCB exposure can cause the impairments Kilburn found in the Lobelville subjects, render his opinion unreliable.Id. at 252.
Another example of an accepted methodology is a "differential diagnosis," which is "[t]he method by which a physician determines what disease process caused a patient's symptoms. The physician considers all relevant potential causes of the symptoms and then eliminates alternative causes based on a physical examination, clinical tests, and a thorough case history." Best v. Lowe's Home Centers, Inc., 563 F.3d 171, 178 (6th Cir. 2009) (internal quotations and citations omitted). For Daubert purposes, the Sixth Circuit deems a proffered differential diagnosis reliable and admissible where the doctor:
(1) objectively ascertains, to the extent possible, the nature of the patient's injury, see [In re Paoli Railroad Yard PCB Litigation, 35 F.3d 717, 762 (3d. Cir. 1994)] ("A physician who evaluates a patient in preparation for litigation should seek more than a patient's self-report of symptoms or illness and . . . should . . . determine that a patient is ill and what illness the patient has contracted."), (2) "rules in" one or more causes of the injury using a valid methodology, and (3) engages in "standard diagnostic techniques by which doctors normally rule out alternative causes" to reach a conclusion as to which cause is most likely. Id. at 760.
In connection with the third "rules out" prong, if the doctor "engage[s] in very few standard diagnostic techniques by which doctors normally rule out alternative causes," the doctor must offer a "good explanation as to why his or her conclusion remain[s] reliable." Id. Similarly, the doctor must provide a reasonable explanation as to why "he or she has concluded that [any alternative cause suggested by the defense] was not the sole cause." Id. at 758 n. 27.Best, 563 F.3d at 179.
With that said, the bulk of Dr. Mayron's findings and conclusions are recited in a May 2, 2014 report he composed at the request of Attebury's attorney, and this forms the bases of Armstrong's argument. In relevant part, his report states:
The following is a fair summary of what we discussed in our conference on April 25, 2014.
My medical specialty is neurology and I have been practicing neurology for thirty-five (35) years.
In connection with my practice, I began treating Mr. Nathan Attebury on referral from Dr. Jana [sic] Jones. Mr. Attebury was referred because of symptoms of memory loss, dizziness, headaches, confusion, and blackouts. The history that he gave me was that from June 8, 2012, until January 22, 2014, Mr. Attebury was exposed to toxic spray paint and during this period, he suffered shortness of breath, dizziness, headaches, confusion, blackouts, and memory loss. I first saw him for these problems on February 18, 2014.
On the initial visit, I suspected his problems very well may relate to toxic encephalopathy from exposure to dust or paint. After further visits and additional research, I have come to the opinion that the most likely cause of Mr. Attebury's symptoms that he described to me would be due to the exposure to this industrial paint.
The rationale for this opinion is that he never had any blackout spells prior to this exposure. He never had any problems with memory loss or headaches until he was exposed to the industrial paint. When he did not any longer go down to the mines, and therefore was not exposed to paint, his headaches disappeared, but his memory problems persisted.
You asked me to identify the type of paint that Mr. Attebury was exposed to that would be the kind of paint that would cause these problems. Mr. Attebury was exposed to Krylon industrial paint and it contains Toluene, which is implicated in exactly the kind of problems that Mr. Attebury has been suffering. There are articles in authoritative publications that support this proposition. You have asked me to give the specific periodical and page number that supports my opinion in this area. The information is set forth in the Annals of Neurology, June, 1988, Volume 23, Page 611 to 614 supports my opinion. The title of one article is entitled "Toluene Abuse" and that is abuse from sniffing. It causes diffuse central nervous system white matter changes.
In my opinion, all of Mr. Attebury's symptoms are causally related to his exposure to the toxic paint.
Regarding my initial findings and current treatment, when I first saw Mr. Attebury, the history was that of severe headaches at the time that he was exposed to the overhead marking paint made by Krylon. Following this exposure, he would get lost easily in the mines or not know how to get there and it was a route that he had taken many times before. He described headaches on the right side of his head, as a pressure feeling. He had several episodes of loss of consciousness that were, in fact, witnessed by his wife, that were associated with fluttering of the eyelids and stiffening of his extremities and confusion afterward. His physical exam showed neuropathy, which is decreased sensation in his left arm and leg and he had a tremor in both hands. We also did a memory test on him that showed a severe impairment
that was comparable to a person with very severe Alzheimer's disease. I ordered a brain scan and the brain wave test that we call an EEG. The results of his brain scan was normal and the brain wave test results were normal. At the point in time that he had those tests performed, he had stopped going down to the mines. When he stopped going down into the mines, his headaches went away. He went back down into the mines one time and his headaches came back. Then when he finally stopped for good, the headaches went away and stayed away. His memory problems, however, have not improved.
In my opinion, these serious memory problems are irreversible and it is too early to tell what other problems that he is experiencing will be irreversible.
. . .
I believe it would be helpful to refer Mr. Attebury to a neuropsychologist. The neuropsychologist's testing is very detailed and can pinpoint specific areas of the brain that are affected, which would also help to consolidate the opinion of Toluene toxicity. It would also help to further elucidate the severity of his dementia.
. . .
You have asked me to go over testing that I have provided and explain the results. On February 17th, the day we first met, my staff and I performed what's called an MMSE, which is a Mini Mental State Exam, and the highest possible score is 30 and he got a 14. That's very severe.[] Now, on the test itself, it lists 14 as moderate, but I'll tell you from my experience with Alzheimer's patients, 14 is a seriously disabling condition. 14 is what I see in severe Alzheimer's patients, who can barely
function at home and require help with the preparation of meals and dressing themselves. We also have them draw a clock with a specific time on it and there is a total maximum of 4 points for that. He was only able to draw the circle. He couldn't even put the numbers in. He only got a 1 out of a possible 4 on a clock drawing. So he is not a person who can be trained to do any other task.
Despite Dr. Mayron's apparent reliance upon the results of this MMSE, he acknowledged over the course of his deposition that, according to the Fifth Edition of the American Medical Association (AMA) Guides to the Evaluation of Permanent Impairment, p. 319, the MMSE is not a diagnostic tool. Rather, it is a screening test that is merely used to determine whether further evaluation with neuropsychological testing is needed.
Attebury's level of dysfunction and disability, as described by Dr. Mayron (i.e.,"barely function at home and require help with the preparation of meals and dressing themselves" and "he is not a person who can be trained to do any other task"), appears inconsistent with how Attebury actually functions. Having extensively reviewed the record, I note Attebury was capable of recalling facts and extensively and coherently testifying at a lengthy deposition and administrative hearing over the course of these proceedings; and, among other things, he testified he remains able to operate an automobile.
Armstrong first takes issue with the quality of the medical history Dr. Mayron took of Attebury prior to making his diagnosis of toluene-induced toxic encephalopathy. Armstrong points out that during Dr. Mayron's deposition Dr. Mayron acknowledged, contrary to one of the founding premises of his opinion regarding the temporal relationship between Attebury's condition and his alleged exposure to toluene, that Attebury's headaches did not stop when Attebury stopped going down into the mines and using Krylon spray paint, and that they had in fact continued to date and remained constant.
Armstrong also notes that Dr. Mayron's review of Attebury's medical history was based upon his consultation with Attebury and Attebury's wife, but Dr. Mayron provided no analysis of Attebury's prior medical records. Thus, none of Dr. Mayron's findings or conclusions addressed the records of Dr. Jayna Jones (the treating physician who referred Attebury to Dr. Mayron), which noted Attebury had sought treatment prior to his employment with Armstrong for many of the same symptoms Dr. Mayron attributed to toluene exposure. For example, on November 18, 2009, Dr. Jones stated in a treatment note that Attebury "has lighthead, et [sic] feels like he could pass out when pressure is up. pt notes feeling like he is having a heart attack after eating. pt notes chest pain, soa [sic] et dizziness." Her records from 2009 to 2010 further indicate she was treating Attebury for complaints of anxiety, depression, and "lack of focus" relating to ADHD. Thus, to the extent that the ALJ believed Dr. Mayron offered an opinion that preexisting ADHD, anxiety or depression was not causing Attebury's current symptoms, this was a proposition Dr. Mayron's findings and conclusions never addressed.
Attebury testified he could not recall making these complaints to Dr. Jones, but did not deny that he made them.
In this vein, we reference the following portion of the ALJ's opinion which appears to support this may have been what the ALJ believed: "There is no other known source of causation for [Attebury's] symptoms, as I agree that the ADHD, anxiety or depression is not causing them." (Emphasis added).
Likewise, Dr. Mayron's report does not attempt to rule out any alternative explanations for Attebury's alleged condition. This is significant, as Armstrong points out, because Dr. Mayron's record from his initial February 18, 2014 consultation recites Attebury was taking "SUBOXONE 4MG 1 TAB 2-5 TIMES DAILY" due to a prior addiction to Lortab. Lortab is an opiate pain medication. Attebury testified he had been prescribed Lortab after he had sustained an injury to his back in 2006. Attebury's medical records provide that since at least 2009, he has been prescribed suboxone, a synthetic opiate, to wean him off of his addiction to Lortab; and that his dosage was initially "2.5 mg QD," or once per day, which was lower than his prescription of 4 mg 2-5 times per day as noted by Dr. Mayron on February 18, 2014. As to why this is significant, the Food and Drug Administration lists that common side effects of suboxone include many of the symptoms Attebury attributed to toluene exposure: nausea; headache; feelings of lightheadedness; disturbance in attention; irregular heart beat; insomnia; blurred vision; fainting; and dizziness. See http://www.fda.gov/downloads/Drugs/DrugSafety/UCM225677.pdf (last visited May 13, 2016). Dr. Mayron was also questioned about Attebury's continued use of opiates and conceded that abuse of opioids may cause an "altered mental state."
Suboxone is the trade name for a drug containing two active ingredients, buprenorphine and naloxene. Under both Kentucky and federal law, buprenorphine is regulated as a Schedule III drug, having been changed by regulation from a Schedule V drug in 2002. See Commonwealth v. Hamilton, 411 S.W.3d 741 (Ky. 2013).
The medical abbreviation "Q.D.", or "quaque die," means "every day." THE AMERICAN HERITAGE STEDMAN'S MEDICAL DICTIONARY 698 (2001).
Next, Armstrong takes issue with Dr. Mayron's interpretation of the article cited in his report, which is the only medical research Dr. Mayron relied upon in support of his medical causation opinion. As indicated above, the article in question, entitled "Toluene Abuse Causes Diffuse Central Nervous System White Matter Changes," appeared in pages 611 to 614 of Annals of Neurology, June, 1988, Volume 23. The authors summarize this article as follows:
We describe the findings of magnetic resonance imaging (MRI) of the brain in 6 chronic toluene vapor abusers and
the neuropathological findings in 1 abuser not studied by MRI. MRI in 6 chronic toluene abusers revealed the following abnormalities: (1) diffuse cerebral, cerebellar, and brainstem atrophy; (2) loss of differentiation between the gray and white matter throughout the central nervous system; and (3) increased periventricular white matter signal intensity on T2-weighted images. Another chronic toluene abuser (MRI not performed) died as a result of acute toluene overdose. The brain displayed diffuse, ill-defined myelin pallor, maximal in cerebellar, periventricular, and deep cerebral white matter. Neurons were preserved throughout, axonal swelling or beading was not seen, gliosis was minimal, and occasional, scant perivascular macrophage collections were seen. Taken in concert, these findings suggest that the pathological and MRI abnormalities are due to either increased water content of the white matter or subtle toluene-induced metabolic changes in myelin.
In sum: the six living chronic toluene vapor abusers who took part in the study described above had MRI brain scans, and had observable abnormalities in their MRI brain scans. The seventh (the one who died) did not have an MRI but also had observable abnormalities when his brain was later examined. Hence the name of the article: "Toluene Abuse Causes Diffuse Central Nervous System White Matter Changes." (Emphasis added.) All seven participants were also toluene abusers—they were not occupationally exposed to toluene. Indeed, the article itself carefully draws this distinction in its concluding paragraph and notes that other studies are in progress regarding occupational exposure:
The MRI and neuropathological evidence from this study supports prior clinical studies that suggested that abuse of toluene can cause permanent CNS injury. The mechanism of injury is not known, and other solvents in the abused mixtures (e.g., methylene chloride) may enhance the toxicity of toluene. Further studies currently
in progress are attempting to characterize the effects of toluene in minimally affected or neurologically normal toluene abusers. Data obtained from these studies may help establish a dose-response relationship between toluene abuse and permanent CNS injury and yield useful methods for evaluating those individuals who are chronically exposed to toluene at low levels in the workplace.
With this in mind, Dr. Mayron acknowledged in both his report and deposition that Attebury's MRI showed no changes or abnormalities. During his deposition, he asserted that this was enough to rule out epilepsy or a tumor, but did not necessarily refute that Attebury had toluene-induced toxic encephalopathy because Attebury was still alive and, from his reading of "Toluene Abuse Causes Diffuse Central Nervous System White Matter Changes," he understood that all seven of the study participants who had abnormal MRIs had "died, so there's a matter of degree." Immediately after making this statement, however, he acknowledged that six of the seven study participants were actually alive at the time of the study, and that all six of those participants were, thus, likewise alive at the time of their MRIs. Dr. Mayron further acknowledged that the above-referenced article concerned toluene abusers; he testified that he was not aware of any studies "offhand" that supported his theory of Attebury's occupational exposure to toluene, nor did he produce or cite any.
The following exchanges from Dr. Mayron's deposition testimony illustrate these points: Q: Were the subjects in this study individuals who were occupationally exposed to toluene? MAYRON: No, these were drug abusers, people who sniffed glue and paint. Q: So they were, in fact, chronic toluene vapor abusers? MAYRON: Yes. Q: Are you aware of any studies of occupational exposure of toluene? MAYRON: Not offhand but that is in the literature. Q: And I believe you mentioned one individual whose brain was actually examined. That person had died. There were six other individuals that had MRIs performed. All of those individuals, their brains were not normal, is that correct, Doctor? MAYRON: That's correct. Q: But if I understood your testimony earlier, the scans you had performed on Mr. Attebury's brain are normal? MAYRON: The one was normal but he didn't die. Those people died, so there's a matter of degree. (Emphasis added.) Q: Well, the six chronic toluene abusers, they were alive at the time of the study, correct? The seventh was the deceased. MAYRON: That's correct.
Armstrong also notes several other deficiencies in Dr. Mayron's opinion which highlight, contrary to what the ALJ stated in his opinion and award, Attebury did not relate his "exposure levels" to Dr. Mayron in any way Dr. Mayron understood or remembered. Over the course of Dr. Mayron's deposition testimony, Dr. Mayron admitted he had no knowledge of: (1) how many ounces were in each can of the paint Attebury used; (2) how many cans of paint Attebury used in a day, week, or in the eighteen months of his tenure with Armstrong; (3) the quantity of toluene in each can; (4) the manner of Attebury's exposure to the paint (i.e., how Attebury sprayed the paint, the vapor pressure of each can, the ventilation in the mines, whether Attebury wore a mask, or whether absorption of toluene occurred through Attebury's work clothes and skin); (5) whether Attebury had been exposed to toluene prior to his employment with Armstrong; (6) any other diagnosis of toxic encephalopathy that had ever been made due to exposure to Krylon industrial paint; or (7) whether an occupational exposure guideline even existed for toluene.
The evidence of record conflicted regarding whether Attebury wore a mask or respirator while spraying paint. Dr. Mayron testified that "if he had worn a mask that was an adequate protector, I would have to rethink my diagnosis."
At most, Dr. Mayron offered only an unsupported hypothesis in this regard: Q: Is any part of your diagnosis based on his skin coming in contact with this toxin? MAYRON: That's possible. It can be absorbed through the skin. Q: So I guess, if I understand you, would you say the primary cause of your diagnosis is inhalation? MAYRON: No, it's exposure which could be inhalation or exposure through skin. Q: Okay. Do you know what kind of clothing Mr. Attebury would have worn in the mines? MAYRON: No. Q: If any part of his body would have been exposed in the mines? MAYRON: No. Q: If he was wearing longsleeves, gloves, a hat, would you expect his skin to come in contact with much of this toxin? MAYRON: Not much. Clothing would have helped but don't forget that we're talking about a gaseous vapor that can pass through the fibers of clothing. Q: Do you believe that Mr. Attebury was using the paint in a normal manner? MAYRON: I have no idea. I could only—again, I don't like to assume. I was going to say I can only assume that he was, but otherwise I have no idea. --------
The "knowledge" requirement of KRE 702, interpreted consistently with Daubert, requires "more than subjective belief or unsupported speculation." Daubert 509 U.S. at 590, 113 S.Ct. 2786. A plausible hypothesis or a hypothesis that could even be correct does not qualify as "knowledge," nor is it "based upon sufficient facts or data" or the "product of reliable principles and methods . . . applied . . . reliably to the facts of the case." KRE 702. In light of the above, I agree with Armstrong's arguments and believe Dr. Mayron offered nothing more than a hypothesis founded upon his own subjective belief and unsupported speculation regarding the cause of Attebury's condition, as opposed to anything approaching knowledge, sufficient facts, or reliable data. This is not an independent weighing of credibility and/or the evidence. To the contrary, and to reiterate, Dr. Mayron's findings and conclusions give no indication that they are based upon a complete medical history of Attebury; they fail to rule out a very plausible alternative theory raised by the defense; they are based upon an apparent misreading of a medical journal article that addressed findings that do not fit the facts presented in this case; and they ignore the relationship in which a change in amount, intensity, or duration of exposure to toluene is associated with a change in risk of disease. Accordingly, in my opinion, the ALJ erred by relying upon Dr. Mayron's opinion. And, because the ALJ's decision in favor of Attebury otherwise lacks support from any evidence of record, I would reverse. BRIEF FOR APPELLANT: Will E. Messer
Lexington, Kentucky BRIEF FOR APPELLEE, NATHAN
ATTEBURY: Jerry P. Rhoads
Madisonville, Kentucky