Court Opinion

ID: 6345707
Source: CourtListenerOpinion
Date Created: 2022-06-01 15:01:40.275131+00
Date Added: 2024-06-11T09:15:01.773770
License: Public Domain

Cite as 2022 Ark. App. 276
                   ARKANSAS COURT OF APPEALS
                                       DIVISION IV
                                       No. CV-21-611

 MICHAEL BEAN                                   Opinion Delivered June   1, 2022
                                APPELLANT

 V.                                             APPEAL FROM THE ARKANSAS
                                                WORKERS’ COMPENSATION
                                                COMMISSION [NO. G806384]
 REYNOLDS CONSUMER PRODUCTS;
 INDEMNITY INSURANCE COMPANY
 OF NORTH AMERICA/SEDWICK
 CLAIMS MANAGEMENT SERVICES,
 INC.; AND DEATH & PERMANENT
 TOTAL DISABILITY TRUST FUND     AFFIRMED
                       APPELLEES

                                 BART F. VIRDEN, Judge

       Appellant Michael Bean was diagnosed with a rare condition: pauci-immune anti-

neutrophilic cytoplasmic autoantibody (ANCA) vasculitis, also known as granulomatosis

with polyangiitis (GPA), or pulmonary vasculitis, and formerly known as Wegener’s disease.

Bean alleged that the ANCA vasculitis, which caused damage to his kidneys and lungs,

resulted from his exposure to silica dust while working for appellee Reynolds Consumer

Products. The Arkansas Workers’ Compensation Commission denied benefits after finding

that Bean failed to prove that he sustained a compensable accidental injury or that he

sustained a compensable silicosis injury. Bean argues on appeal that (1) his accidental injury
is compensable; (2) his injury was not “legally idiopathic”; and (3) the Commission arbitrarily

disregarded the opinion of his medical expert. We affirm the Commission’s decision.

                                        I. Background

       On May 3, 2018, then thirty-four-year-old Bean was referred by his primary care

physician (PCP) to CHI St. Vincent with the chief complaint of abnormal lab results, which

he had received earlier that day. Specifically, Bean sought an “evaluation of elevated

creatinine and BUNs.” It was noted that Bean is a body builder who uses creatinine, protein

supplements, and Aleve, along with other NSAIDs (nonsteroidal anti-inflammatory drugs)

for his back pain. It was further noted that Bean drinks mostly energy drinks, rather than

water, and that he had gone to his PCP that day complaining of indigestion issues. The

medical records indicate, “Suspect patient’s symptoms are likely coming from his creatinine

and protein intake as well as his NSAID abuse. Although intrinsic kidney function cannot

be excluded.” Bean was admitted to the hospital with acute renal failure—it was noted that

he had a gradual onset of symptoms and “duration: > 1 month.” The hospital gave him

intravenous fluids and conducted studies. Bean was provided a gastroenterology consultation

on May 4. Dr. Sanford Henry Benjamin noted that Bean had chronic back pain for which

he took nonsteroidal medications several times a day and had developed epigastric pain two

months ago. Bean was given a chest x-ray and CT scan on May 5 due to shortness of breath

and coughing up blood. The impression was bilateral upper lobe and right lower lobe

airspace disease consistent with pneumonia. Bean was ultimately diagnosed with acute renal

failure, pulmonary alveolar hemorrhage, and “suspected vasculitis.”

                                              2
        On May 5, Bean was transferred to the University of Arkansas for Medical Sciences

(UAMS) at his request. Dr. Devendra D. Patel noted the earlier symptoms Bean had

described to doctors at St. Vincent, and she pointed out that “[Bean] has exposure to

Aluminum as he has been working in Aluminum plant for 2–3 years.” Dr. Patel’s impression

was acute renal failure “probably related to long term NSAID use vs vasculitis (with

hemoptysis).” She diagnosed anemia, dyspepsia, and hemoptysis. A kidney biopsy was taken

on May 7, the findings of which were consistent with an ANCA-associated disease. A chest

x-ray was taken on May 8, and it was noted that Bean had “significant interval worsening of

patchy consolidation within both lungs . . . this could reflect other hemorrhage versus

multifocal pneumonia.” Bean was transferred to the MICU on May 9 due to “worsening

hypoxic failure which is thought to be due to DAH secondary for vasculitis (pulmonary renal

disease).” Bean was placed in a medically induced coma and later diagnosed with ANCA

vasculitis.

        On May 15, Dr. Manisha Singh, a board-certified nephrologist and internist, reported

that Bean was critically ill. Referring to ANCA vasculitis, Dr. Singh wrote, “This is the one

disease that can fully explain this clinical picture along with biopsy readings . . . The driver

of his clinical condition has to be pauci immune crescentic GN [glomerulonephritis].” Bean

was discharged from UAMS on May 23, 2018; however, Dr. Singh continued to see him for

nearly a year. In late August, Dr. Singh reported that Bean’s renal failure had suddenly

become worse over the last month.

                                               3
       In September 2018, Bean completed a Form AR-C describing an inhalation injury

on May 1, 2018, that had damaged his kidneys and lungs. On a “Workers’ Compensation

First Report of Injury or Illness” form prepared by Georgia Diemer, the same information

from the Form AR-C was reported with additional information that Bean had last worked

at Reynolds on April 18, 2018, and that his disability had begun April 19. It was also reported

that the time of the occurrence could not be determined; that the injury, illness, or exposure

did not occur on the employer’s premises, yet it did occur at the address for Reynolds; that

the specific activity or work process that Bean was engaged in when the accident, illness, or

exposure occurred was driving a forklift; and that he notified his employer of his injury on

September 24, 2018.

       Bean returned to work for Reynolds in January 2019, but his condition deteriorated,

and he underwent a kidney transplant in March 2019. Bean again returned to work at

Reynolds in March 2020.

       On July 25, 2020, Dr. Singh was asked on a questionnaire whether she believed with

a reasonable degree of medical certainty that the injuries/conditions for which she had

treated Bean were caused by exposure to silica at his workplace. She stated, in part, that

       It is difficult to say exactly what caused the [ANCA] GN, but in his history, the only
       thing that we were able to find is known to be associated with this condition – was
       the exposure to silica. This is a rare disease [so] not much is known about it. We
       concluded that this must be the inciting event.

       Dr. William Banner, Jr., was asked to review the case for Reynolds. In a report dated

October 14, 2020, he stated, in part, the following

                                              4
        The key question in this case is whether there is a causal relationship between
Michael Bean’s exposure to silica while working at the Reynolds facility and his
development of a pulmonary-renal syndrome. As can be seen in this case with
conflicting results, testing for ANCA my yield some difficult to interpret results.
Nevertheless, his kidney failure is consistent with a minimal (pauci) immune disorder.
As stated in a recent article by Scott et al. (Scott, Hartnett, Mockler & Little, 2020),
“Like many autoimmune diseases, the exact etiology of AAV (ANCA associated
vasculitis), and the factors that influence relapse are unknown. Evidence suggests a
complex interaction of polygenic genetic susceptibility, epigenetic influences and
environmental triggers.” At this point causal links to these associated “triggers” have
not been well defined and at this point remain associations . . . . A thorough
evaluation of possible exposure in an individual patient would have to also consider
the type of silica including particle size and structure.

....

       To assess the role of exposure time, it is important to consider the exposure
times associated with the development of silicosis . . . . The term acute silicosis which
can occur in shorter periods of time requires extremely high concentrations and
produces severe symptoms. (Pollard, 2016) Mr. Bean by his deposition has indicated
that he worked in this facility for two years. At no point in time did he complain of
acute severe silicosis[,] and his chest CT did not at any point reveal chronic nodular
inflammatory changes associated with silicosis.

....

       [Mr. Bean] had no indication of clinical silicosis either from a complaint
history or from the CT scan that was obtained during his hospitalization. His lung
disease was diffuse alveolar hemorrhage which is related to his autoimmune vasculitis.
That is not surprising in that exposure to silica takes a much longer exposure time to
produce clinical silicosis than Mr. Bean had during his work history. Even without a
mechanistic causal link between silica exposure, silicosis and autoimmune disease
particularly with the anti-nuclear cytoplasmic antibodies[,] the data support that the
pathway to autoimmune disease is via the development of clinical silicosis and not
asymptomatic silica exposure.

       I would conclude to a reasonable degree of medical certainty that Mr. Bean’s
autoimmune vasculitis with pauci syndrome crescentric glomerulonephritis is not
associated with his exposure to silica crystals at his place of employment but is rather
idiopathic. I base this on the length of exposure and the lack of clinical signs and
symptoms of pulmonary silica exposure.

                                        5
             The conclusions reached by Dr. Singh and the clinicians at the University of
      Arkansas Medical School were based on a simplistic review of the literature and did
      not take into account the timing or degree of exposure with clinical symptomatology.
      As exemplified by the list in appendix A, a thorough evaluation would require an in-
      depth occupational history and even with that there may be no specific etiology that
      can be determined in many cases.

      Dr. Singh was deposed on January 21, 2021. The following exchange occurred during

her deposition on direct examination by Bean’s lawyer:

      Q:     So over this year-long treatment that you’d had with Mr. Bean, your conclusion
             was that it was his exposure to silica that caused the ANCA, is that correct?

      A:     That’s correct, yes . . . . Most likely, yes. That’s my take on this, because I
             couldn’t find anything else.

      Q:     Okay. Is it more likely than not that the exposure to silica caused the ANCA?

      A:     At this moment, yes . . . .

      Q:     Other than his exposure to work, could you find any other explanation for his
             diagnosis of ANCA?

      A:     No, I could not . . . .

      Q:     Is it your testimony that you can state within a reasonable degree of medical
             certainty that Mr. Bean’s exposure to silica at work caused his symptoms and
             his autoimmune response of ANCA vasculitis?

      A:     Yes, that’s correct.

      On cross-examination, the following exchange occurred:

      Q:     Do you agree that the cause of ANCA is clinically unknown?

      A:     Cause of all ANCAs? Yes. It’s clinically at this point not known.

      Q:     Okay. Now, what do you know about the silica exposure in this case?

                                            6
A:   From what Mr. Bean told me, he said that he is, there’s a lot of dust around
     him. He physically handles the – and I’m trying to recollect, because in my
     mind, my picture was he’s lifting sacks really, but I don’t think it was sacks.
     But he said that he was physically in contact with it. It was skin-to-skin contact,
     and he was inhaling a lot of it, too. The dust was all around him.

Q:   And how much of the time during the day did he suffer this exposure?

A:   Eight to ten hours.

Q:   Okay. Did you ever get a sample of this silica?

A:   No.

Q:   You’ve not seen it?

A:   No . . . .

Q:   So your opinion is based solely on what Mr. Bean told you?

A:   Yes, that’s correct.

Q:   Would your opinion change if, for example, the period of time he was exposed
     to silica was inaccurate from your information?

A:   So if you tell me that he was exposed for one day that would change. But if it’s
     a year, I have no studies that would tell me that how much this much in a year
     would cause this. You see, for us it’s an association. And all the studies that
     have come off associations have come after, in a different patient group
     altogether. Those are all much older people working for years and years and
     years. There aren’t studies that are looking at one year or, you know, six
     months exposure. We don’t have studies for that . . . .

Q:   And how long was he exposed to silica of any amount?

A:   From my understanding, one to two years . . . .

Q:   Does Mr. Bean have silicosis?

A:   No.

                                      7
       Q:     He does not?

       A:     Not from what we’ve done. We didn’t work him up for silicosis as such. We
              were treating him for ANCA vasculitis, ANCA G, glomerulonephritis. But
              when we are saying silicosis, we are specifically looking at a lung, a very specific
              factor in the lung that happens after years of exposure, acute or chronic
              silicosis. Basically, it’s a family disease, and I’m not an expert on that. It’s a
              lung disease.

       At a hearing before an administrative law judge (ALJ) on January 29, 2021, Bean

testified that he is still working at Reynolds doing the same job despite being warned by his

doctors to avoid exposure to silica. He testified that he was hired to work at Reynolds in June

2016 and that he worked twelve-hour shifts as “general utility” three days on and three days

off. His job duties ranged from running a forklift and crane to just cleaning up in the

breakroom. Bean said that he also worked on a furnace—but not every single day—adding

metal and alloys, including iron, zinc, copper, and silica. He said on cross-examination,

“Silicon, silica, I don’t know but that’s what it says on the bag.” Bean testified that Reynolds

has eight furnaces and that he worked on one, but not more than two, furnaces at a time.

He stated that the alloys are in twenty-five-pound bags and that he added about 300 pounds

of each alloy to the furnace using a front-end loader.

       Bean said that the furnaces were “always” needing to be replaced and that, since he

had been there, every furnace in the cast house had been replaced up to four times. Bean

testified that contractors were brought in to do the job and that they used jackhammers to

“tear down” the furnaces by breaking bricks to take the refractory lining out and replace it.

Bean said that this process takes a few weeks up to a month and that it created a lot of silica

                                               8
dust. Bean said that the silica dust during a “tear down” floated in the air, that it settled onto

surfaces, and that he would sweep it into piles. On cross-examination, Bean conceded that

he was not constantly exposed to dust because he walked outside some and stayed in the air-

conditioned and air-filtered breakroom. Bean testified that he was working next to a furnace

that was being torn down “probably some time in April [2018] maybe” and that he became

sick and had difficulty breathing shortly afterward. He said that he had told someone at work

that his “breathin’ [was] not right” and that, as time went on, he “[didn’t] feel good,” so he

went to see his doctor in early May.

       Brian Elliott, the environmental manager at Reynolds, testified that Reynolds makes

aluminum sheets and coils. He testified that the cast house is a large building containing

eight furnaces. Elliott testified that the bay doors on each end of the cast house typically stay

open most of the day, that side doors can be opened, and that the southern wall of the cast

house is louvered for ventilation. He insisted that the building has good air circulation.

Elliott said that utility workers stayed in the cast house anywhere from three to six hours,

depending on how many furnaces they were running but that they also spent a “fair amount

of time” in the breakroom. Elliott stated that silicon metal is the material added to the

furnaces—not silica—and that this silicon does not have silica granules, particles, or dust. He

described the furnace as basically a steel shell with a refractory lining and said that the

refractory lining of the furnaces needed to be replaced “periodically.” According to Elliott,

outside contractors do the job; they cover everything in plastic to contain the dust during

the job; and they clean up after the job is complete. Elliott said that, when the furnace lining

                                                9
is being replaced, the dust is “very minimal.” When asked if the alloys are still in the furnace

when it is being “torn down,” Elliott said that “there shouldn’t be anything in there. I mean,

there could be very minor amounts of aluminum solidified and stuck to [the refractory

lining].”

                                 II. Appeal to the Commission

         The ALJ addressed four theories of compensability asserted by Bean, which the ALJ

described as “somewhat confusing and, apparently at least, mutually exclusive and

contradictory.” The ALJ addressed accidental injury under Ark. Code Ann. § 11-9-

102(4)(a)(i) (Repl. 2012); a pulmonary injury under Ark. Code Ann. § 11-9-114(a) (Repl.

2012); an occupational disease under Ark. Code Ann. § 11-9-601(a) (Supp. 2021); and a

silicosis injury under Ark. Code Ann. § 11-9-602(a)(2) (Repl. 2012). The ALJ found on each

theory that Bean had failed to prove compensability and, in doing so, repeatedly referred to

Bean’s      “medically   and     legally    idiopathic    autoimmune        disease,    ANCA

vasculitis/GPA/pulmonary vasculitis.” Bean appealed to the Commission. When a

determination by an ALJ is appealed to the Commission, the Commission does not sit as an

appellate court to review the ALJ’s findings; instead, the Commission makes a de novo

determination of the facts. Jackson v. Smiley Sawmill, LLC, 2019 Ark. App. 235, 576 S.W.3d

43.

         The Commission affirmed the ALJ’s decision as modified. At the outset, the

Commission noted that, although Bean had initially claimed that he suffered from an

occupational disease, he had since claimed that he suffered “a compensable injury, not an

                                              10
occupational disease.” Therefore, the Commission did not address occupational disease in

general but did address, specifically, a silicosis injury caused by inhalation of silica dust. 1 The

Commission found that Bean failed to prove that he sustained a compensable injury

pursuant to section 11-9-102(4)(A)(i) and that, alternatively, he failed to prove a compensable

silicosis injury pursuant to section 11-9-602(a)(2). Bean does not challenge the Commission’s

decision that he failed to prove a compensable silicosis injury.

                                     III. Standard of Review

       In reviewing decisions from the Commission, we view the evidence and all reasonable

inferences deducible therefrom in the light most favorable to the Commission’s findings.

Willis v. Ark. Dep’t of Corr., 2021 Ark. App. 50, 616 S.W.3d 679. When the Commission

denies benefits because the claimant has failed to meet his or her burden of proof, the

substantial-evidence standard of review requires that we affirm if the Commission’s decision

displays a substantial basis for the denial of relief. Id. The issue is not whether the appellate

court might have reached a different result from the Commission but whether reasonable

minds could reach the result found by the Commission; if so, the appellate court must

affirm. Id. Questions concerning the credibility of witnesses and the weight to be given to

their testimony are within the exclusive province of the Commission.                Id. Once the

Commission has made its decision on issues of credibility, the appellate court is bound by

that decision. Id.

       1
        A silicosis injury is dealt with separately from a claim for an occupational disease.
Johnson v. Democrat Printing & Lithograph, 57 Ark. App. 274, 944 S.W.2d 138 (1997).

                                                11
                                        IV. Discussion

                                     A. Accidental Injury

       Bean contends that the Commission erred in finding that he failed to prove that he

suffered a compensable injury under Ark. Code Ann. § 11-9-102(4)(A)(i). Compensable

injury means an accidental injury causing internal or external physical harm to the body,

arising out of and in the course of employment and which requires medical services or results

in disability or death. Id. An injury is “accidental” only if it is caused by a specific incident

and is identifiable by time and place of occurrence. Id. The phrase “arising out of the

employment” refers to the origin or cause of the accident, and the phrase “in the course of

the employment” refers to the time, place, and circumstances under which the injury

occurred. J.&G. Cabinets v. Hennington, 269 Ark. 789, 600 S.W.2d 916 (1980). A

compensable injury must be established by medical evidence supported by objective findings.

Ark. Code Ann. § 11-9-102(4)(D). Objective findings are those findings that cannot come

under the voluntary control of the patient. Ark. Code Ann. § 11-9-102(16)(A)(i). Causation

does not need to be established by objective findings, so long as objective medical evidence

establishes the injury’s existence and a preponderance of other nonmedical evidence

establishes a causal relation to a work-related incident. Wal-Mart Stores, Inc. v. VanWagner,

337 Ark. 443, 990 S.W.2d 522 (1999). The burden of proving a compensable injury under

section 11-9-102(4)(A)(i) is on the employee to prove by a preponderance of the evidence.

Ark. Code Ann. § 11-9-102(4)(E)(i).

                                               12
       Bean asserts that he sufficiently identified the time frame of the occurrence as April

2018 because he got sick in early May after a furnace next to him had been “torn down.” He

relies on Pafford Medical Billing Services, Inc. v. Smith, 2011 Ark. App. 180, 381 S.W.3d 921,

for the proposition that he did not have to identify the exact date of injury. The Commission

acknowledged that a precise time and numerical date is not required; however, Bean had

worked at Reynolds for two years and claimed that the furnaces were always being “torn

down.” The Commission referred to Bean’s testimony that he “[did] not believe” that he had

been feeling sick prior to the “tear down” of the furnace in April but that his injury did not

happen in one day. During its recitation of the history of the case, the Commission pointed

out the many inconsistencies in Bean’s reporting of the injury to his employer.

       The Commission found that Bean failed to prove that he sustained an injury as a

result of “acute exposure to the silica dust.” Bean continues to argue on appeal, as he did

below, that his injury resulted from a “single instance” of exposure from which he developed

symptoms within two days. The Commission pointed out that on May 3, Bean sought

medical treatment for symptoms ranging from abnormal creatinine levels to indigestion and

that neither he nor his medical providers attributed those symptoms to his work at Reynolds.

Even on May 4 and 5, Bean’s problems were described as epigastric and back pain over the

past two months and stomach discomfort for about a month.

       Bean insists that Dr. Singh’s opinion established that his injuries were caused by

exposure to silica at work after eliminating all other potential causes. Dr. Singh’s opinion,

however, primarily relied on Bean’s statements to her about his working conditions, which

                                             13
were inaccurate in many respects. For example, he was not physically carrying bags of silica

such that he had “skin-to-skin contact” with the alloy; rather, he was using a front-end loader.

There was even some dispute about whether the substance Bean was exposed to was silica

given that Elliott drew a distinction between silicon and silica. Moreover, there is some

indication in the record that it is crystalline silica that is dangerous, but Dr. Singh had not

examined the substance for herself to determine its type, structure, and size. Also, Bean

described dust all around him and on surfaces, but Elliott said that there was not much dust

in the air during the tear downs and that the air flow is good in the building. Dr. Singh

thought that Bean was exposed to the dust eight to ten hours a day, but Elliott said that,

assuming Bean was working two furnaces, he could be working at the furnaces for six hours

a day, and Bean himself said that he did not work on a furnace every single day. It seems

clear that Dr. Singh considered Bean’s exposure to be the two-year period that he had worked

for Reynolds and not, as Bean insists, “a single instance” of exposure to silica that caused

Bean to develop ANCA vasculitis within two days. In her deposition, Dr. Singh said that her

opinion on causation would change if she were told that Bean had been exposed to silica for

one day.

       Dr. Banner opined that Bean’s condition was idiopathic, and Dr. Singh essentially

agreed that there is no known cause of ANCA vasculitis. Further, Dr. Banner stated that

there was no indication that Bean suffered from clinical silicosis, with which Dr. Singh

agreed, and that “the pathway” to development of ANCA vasculitis is through “the

development of clinical silicosis and not asymptomatic silica exposure.” Bean basically asserts

                                              14
that it is just common sense that he breathed in silica dust and developed ANCA vasculitis.

Speculation and conjecture, even if plausible, cannot take the place of proof. Kimble v. Lab.

Force, Inc., 2013 Ark. App. 601, 430 S.W.3d 156.

       Bean also argues that the Commission erred in finding that there was no “conclusive

evidence” demonstrating that his condition was causally related to the alleged inhalation of

silica dust. The Commission made that statement with respect to its finding that Bean failed

to prove a silicosis injury. See Ark. Code Ann. § 11-9-602(b). Again, that aspect of the

Commission’s decision is not challenged on appeal. We hold that the Commission’s

decision displays a substantial basis for the denial of relief. 2

                         B. Arbitrary Disregard of Medical Testimony

       Bean argues that the Commission arbitrarily disregarded Dr. Singh’s medical

testimony. Although it is true that the Commission may not arbitrarily disregard evidence,

the Commission’s failure to specifically discuss conflicting evidence does not mean that it

was arbitrarily disregarded where there is substantial evidence to support its decision. Est.

of Bogar v. Welspun Pipes, Inc., 2014 Ark. App. 536, 444 S.W.3d 405. In workers’-

compensation cases, arbitrary disregard of evidence is demonstrated when, for example,

       2
        Bean further argues that he suffered an occupational injury as opposed to an
occupational disease. He draws a distinction between the two and asserts that there is
ambiguity in the statutory definitions, which should be resolved in his favor. We note,
however, that he specifically abandoned the theory that he suffered an occupational disease
pursuant to Ark. Code Ann. § 11-9-601 such that the Commission did not address it.
Because the Commission did not address the theory at all, and given that we have affirmed
the Commission’s decision that Bean failed to prove a compensable injury, we need not
further address Bean’s point on the distinction between an injury and a disease.

                                                15
the Commission affirmatively states that there is “no evidence” for a proposition when such

evidence has, in fact, been presented in the proceeding. Id. Arbitrary disregard has also

been described by this court in Lonoke Exceptional School, Inc. v. Coffman, 2019 Ark. App. 80,

569 S.W.3d 378, as follows:

       The Commission cannot disbelieve the testimony of a witness for an irrational or
       whimsical reason; for example, it cannot decide a case on the rationale that witnesses
       with names beginning in vowels are never credible, or that foreign-born doctors always
       offer more accurate medical opinions, or that back injuries are never work-related.

Coffman, 2019 Ark. App. 80, at 4, 569 S.W.3d at 381 (quoting Pyle v. Woodfield, Inc., 2009

Ark. App. 251, at 6, 306 S.W.3d 455, at 459 (Pittman, J., concurring)).

       We hold that the Commission did not arbitrarily disregard Dr. Singh’s opinion. The

Commission quoted from both doctors’ opinions and simply gave more weight to Dr.

Banner’s opinion that Bean’s injury was idiopathic. The Commission has the duty of

weighing the medical evidence as it does any other evidence. Beliew v. Lennox Indus., 2010

Ark. App. 112. The Commission further has the authority to accept or reject medical

opinions, and its resolution of the medical evidence has the force and effect of a jury verdict.

Id. The determination of the credibility and weight to be given a witness’s testimony is within

the sole province of the Commission, which is not required to believe the testimony of the

claimant or any other witness but may accept and translate into findings of fact only those

portions of the testimony it deems worthy of belief. Id.

       Moreover, the Commission is not bound by a doctor’s opinion that is based largely

on facts related to him or her by the claimant where there is no sufficient independent

                                              16
knowledge upon which to corroborate the claimant’s claim. Id. Here, as noted during the

discussion of Bean’s previous point, Dr. Singh in rendering her opinion primarily relied on

what Bean had reported to her, some of which was inaccurate and inconclusive.

                                    C. “Legally Idiopathic”

       An idiopathic injury is one that is personal in nature or peculiar to the individual;

therefore, it is not work-related. Little Rock Convention & Visitors Bureau v. Pack, 60 Ark. App.

82, 959 S.W.2d 415 (1997). Bean argues that, while ANCA vasculitis is medically idiopathic

because its true cause is unknown, it is not legally idiopathic. 3

       The Commission affirmed but did not adopt the ALJ’s decision. While the ALJ called

Bean’s injury “legally idiopathic,” the Commission did not. This court reviews only the

findings of the Commission and ignores those of the ALJ. Graham v. Turnage Emp. Grp., 60

Ark. App. 150, 960 S.W.2d 453 (1998). It is well settled that the ALJ’s findings are irrelevant

for purposes of appeal. Sheridan Sch. Dist. v. Wise, 2021 Ark. App. 459, 637 S.W.3d 280. “As

such, we do not recount the ALJ’s conclusions herein.” Id. at 5 n.5, 637 S.W.3d at 283 n.5.

We give the ALJ’s findings no weight whatsoever. Multi-Craft Contractors, Inc. v. Yousey,

       3
         In his reply brief, Bean raises an argument that this was an aggravation of a
preexisting condition, and he also made an “eggshell skull claimant” argument; however,
Bean did not raise those arguments before the Commission and therefore obtained no
ruling. We have routinely held that we will not consider arguments presented for the first
time on appeal. Harrison v. Street & Performance, Inc., 2017 Ark. App. 611, 533 S.W.3d 648.
Further, we do not consider arguments raised for the first time in a reply brief because
the appellee would have no opportunity to rebut the argument. Helena/W. Helena Schs. v.
Hislip, 78 Ark. App. 109, 79 S.W.3d 404 (2002).

                                               17
2018 Ark. 107, 542 S.W.3d 155; Clark v. Peabody Testing Serv., 265 Ark. 489, 579 S.W.2d

360 (1979); Johnson v. Hux, 28 Ark. App. 187, 772 S.W.2d 362 (1989).

      Affirmed.

      HARRISON, C.J., and VAUGHT, J., agree.

      Laura Beth York, for appellant.

      Michael Ryburn, for appellees.

                                          18