LARRY VANDENBERG, Employee, v. SWANSON & YOUNGDALE, INC., SELF-INSURED/ BERKLEY RISK ADM’RS CO., Employer/Appellant, and ST. MARY’S DULUTH CLINIC HEALTH SYS., DULUTH BLDG. TRADES HEALTH & WELFARE FUND, and HENNEPIN FACULTY ASSOCS., Intervenors.
WORKERS’ COMPENSATION COURT OF APPEALS
SEPTEMBER 18, 2012
CAUSATION - SUBSTANTIAL EVIDENCE; CAUSATION - OCCUPATIONAL DISEASE; EVIDENCE - EXPERT MEDICAL OPINION. Substantial evidence, including adequately founded medical expert opinion, supported the compensation judge’s findings that the employee sustained a work-related injury to his kidneys culminating on or about December 8, 2009, as a result of exposure to paints, specialty coatings, solvents, and chemicals in his occupation as an industrial and commercial painter; that he sustained an acute personal injury to his kidneys on April 30, 2010, as a result of exposure to epoxies and solvents used in his work duties, and that the employee was disabled by an occupational disease to his kidneys on April 30, 2010, arising out of his employment as a commercial and industrial painter.
Hall, J., Milun, C.J., and Wilson, J.
Jerome G. Arnold
Ronald R. Envall, LaCourse & Envall, Duluth, MN, for the Respondent. Richard L. Plagens, Lommen, Abdo, Cole, King & Stageberg, Minneapolis, MN, for the Appellant.
GARY M. HALL, Judge
The self-insured employer appeals from the compensation judge’s findings that the employee sustained a work-related injury to his kidneys culminating on or about December 8, 2009, as a result of exposure to fumes, solvents, and chemicals in his career as a painter; that the employee sustained an acute personal injury to his kidneys on April 30, 2010, as a result of exposure to chemical agents contained in epoxy products and solvents he was using in his work duties; and that the employee was disabled by an occupational disease to his kidneys on April 30, 2010, arising out of his employment as an industrial and commercial painter. We affirm.
Larry Vandenberg, the employee, began working as an industrial and commercial painter in March 1976, working for Stromquist Painting until 1996 and then for Swanson & Youngdale, Inc., the self-insured employer, from 1997 to 2010. The employee testified about 75 percent of his work with Stromquist was industrial and about 50 percent of his work with Swanson & Young was industrial. Industrial work included the application of specialty epoxy or urethane coatings to refinery tanks, structural steel, storage tanks, floors and the like. Commercial work usually involved application of a latex product. Solvents such as xylene were used as thinners for specialty coatings, for cleaning painting equipment, and removing paint and stain from the hands. Safety equipment included glasses, gloves, respirators, and coveralls.
The employee spent most of the summer and fall of 2009 working at BendTec in Duluth, Minnesota, sandblasting and applying epoxy resins and urethane to crane rails. Xylene was also used on the job. In the week prior to December 8, 2009, the employee primarily worked at the Mountain Iron Clinic and the Wieland Building in Duluth. Materials used at these sites included latex paints, oil-based paints including Diamond Vogel Satinenamel, urethane, and paint thinners.
The employee testified that during the week of December 8, 2009, he worked at a residence painting exterior handrails, a stairway, and the landing of an outside deck, applying an oil-based paint he believed was Diamond Vogel Satinenamel. He stated he did not feel good with chills and fatigue and spent Friday and the weekend in bed.
On Monday, December 14, 2009, the employee was seen by a certified nurse practitioner at the Duluth Clinic complaining of a loss of appetite, chills, and lack of sleep. He was transferred to St. Mary’s Medical Center where he was admitted for acute renal failure and anemia. The employee was examined by Dr. Justin Quade on December 15, 2009. The doctor noted the employee denied any recent illness, was taking no medications or nonsteroidal anti-inflammatories (NSAIDs), and had no family history of renal disease or vasculitis, diabetes, or hypertension. Dr. Quade diagnosed probable glomerulonephritis and ordered further laboratory tests and a renal biopsy. Dr. Michael Maddy, a nephrologist, performed the biopsy on December 16, 2009. By report dated December 23, 2009, Dr. David Carter, in consultation with Mayo pathology, diagnosed crescentic glomerulonephritis, pauci-immune, likely related to an ANCA-vasculitis, and, more prominently, acute tubular necrosis (ATN). Clinical correlation was suggested.
The employee was discharged from St. Mary’s on December 18, 2009. The doctor noted that although, initially, it was thought the employee’s condition was secondary to glomerulonephritis, his serologies were negative including a negative ANCA panel. Neither was there evidence of any classic causes of ATN. It was anticipated the acute renal failure would resolve in the next week or two.
On December 26, 2009, the employee was seen in the emergency room at St. Mary’s complaining of increasing shortness of breath along with chest pain and fatigue. His creatinine and BUN labs had increased significantly, and he was readmitted due to worsening renal failure. Dr. Furqan Raja, a nephrologist, examined the employee. Noting the employee was a painter and was in contact with multiple solvents, Dr. Raja raised the possibility of solvent vapor-induced injury to the kidney, among other possible diagnoses. The employee was started on steriods for possible pauci-immune vasculitis and hemodialysis was initiated. The employee was discharged on December 31, 2009.
The employee was seen by Dr. Maddy on January 12, 2010. He had returned to work on January 11 and was feeling quite good. Given the uncertainty of the employee’s diagnosis, Dr. Maddy ordered a biopsy to retest for crescentic glomerulonephritis and ATN. By report dated January 29, 2010, Dr. Geoffrey Witrak identified evidence of ongoing acute tubular necrosis. No active crescentic glomerular lesions were seen and there was no significant interstitial nephritis or evidence of vasculitis. In February 2010, the employee saw Dr. Raja who noted the employee was trying to avoid solvent exposure at work. The doctor diagnosed end-stage renal disease secondary to probable ATN as a result of possible exposure to organic solvents. The employee’s kidney injury appeared to be resolving with maintenance dialysis. In a follow-up visit on March 5, 2010, noting the employee’s creatinine levels had been drifting downward, Dr. Maddy took the employee off dialysis and began tapering down the prednisone.
The employee returned to Dr. Maddy on March 31, 2010. He reported more labored breathing when at work and that he was working with a latex-based epoxy. Dr. Maddy questioned whether the employee was having a chemical reaction and advised the employee to avoid epoxy agents.
On about April 26, 2010, the employee began working at the U.S. Border Patrol station in International Falls, Minnesota. The job involved applying an epoxy coating to floors and baseboards. The employee was also working with xylene. The work took place in areas sealed off with plastic sheeting and in confined areas where the employee was unable to use a respirator. The employee began to experience symptoms similar to those he had experienced in December 2009. At a previously scheduled appointment with Dr. Maddy on April 30, 2010, the employee reported cold-type symptoms, a loss of appetite, nausea, and shortness of breath. The employee’s creatinine levels had increased significantly. Dr. Maddy’s assessment was
[r]ecurrent acute renal failure with the past diagnoses of acute tubular necrosis with the etiology having never been clearly defined, although . . . suspicious for toxic exposure. At this time, given his recurrent toxic exposure, that seems quite likely . . . .
(Pet. Ex. F.) The employee provided Dr. Maddy with material safety data sheets for products the employee had used in December 2009 and April 2010. The doctor initiated a literature search to see if any of the chemicals showed up as a known cause of ATN. The employee was reinitiated on dialysis and put back on a tapering prednisone course.
Dr. Maddy also discussed the case with Dr. Brian Konowalchuk, an occupational medicine specialist at St. Mary’s Duluth Clinic and provided him with copies of the material safety data sheets. After conducting a literature review, Dr. Konowalchuk, in a report dated June 4, 2010, acknowledged that epoxy is a well known sensitizer, but concluded that although low dose sensitization as a result of exposure to such chemicals is an intriguing theory, it “cannot be refuted or substantiated in the literature.” (Pet. Ex. F.)
On June 16, 2010, Dr. Maddy noted the employee was doing reasonably well on dialysis, and diagnosed chronic renal failure due to a toxic acute tubular necrosis. In July 2010, Dr. Raja similarly diagnosed end-stage renal disease secondary to ATN, likely secondary to toxic exposure at work. The employee failed to regain kidney function, and in August 2010, Dr. Maddy referred the employee to Hennepin County Medical Center (HCMC) for consideration of a kidney transplant. The transplant operation was performed on December 30, 2010, without complications. The employee was followed after the surgery by physicians at HCMC, primarily Dr. Jeffrey Connaire and Dr. Meena Sahadevan, both nephrologists.
By report dated November 1, 2010, Dr. Maddy related that at the time of the 2009 hospitalization, the employee was not taking any medications, including over-the-counter, and had not had any insults typically associated with the development of kidney failure. Moreover, the biopsy showed acute tubular necrosis, a condition more often associated with a systemic shock or various medications. Given the employee’s history of acute renal failure after exposure to epoxy materials at work, both in 2009 and April 2010, Dr. Maddy concluded:
I am firmly convinced that the cause of his acute kidney injury is his exposure to the chemicals at work. This is in part because certainly I can come up with no other potential explanation for this type of injury, as he was exposed to no other medications that might be associated with it, and most particularly did not, again, have any episodes of shock or infection which might be associated with this. . . . I am strongly of the opinion that [the employee’s acute tubular necrosis] is related to his exposure to chemicals in December of 2009 and April of 2010.
(Pet. Ex. C.)
Dr. Beth Baker, an occupational medicine and medical toxicology specialist, conducted a medical records review on behalf of the self-insured employer. In a report dated June 2, 2011, Dr. Baker noted it was not clear the employee was using the same epoxy product in December 2009 that he was using in April 2010. Moreover, as he was working outside in December, the exposure was likely low due to the amount of ventilation plus the cold temperatures. Dr. Baker maintained that solvents and epoxies are not a common cause of acute tubular necrosis and concluded that it had not been proven that the employee’s renal failure was due to exposure to solvents or epoxy resins. The doctor acknowledged there was some evidence for ATN or acute renal failure from high dose solvent exposure, but contended it would require a much higher exposure level than the employee would have had in December 2009. Following review of additional material safety data sheets in July 2011, Dr. Baker concluded the paints and other products used in December 2009 were not the same products used in April 2010, and again opined that the employee’s renal failure was not related to products he used in December 2009.
Dr. Maddy reviewed Dr. Baker’s report, including the additional material safety data sheet information for December 2009, and the employee’s deposition, and conducted a literature search. In a report dated September 14, 2011, the doctor stated, “Again, I strongly believe that the most likely cause of his kidney failure is a toxic exposure to chemicals at work.” He disagreed with Dr. Baker’s suggestion that prednisone weaning was a possible cause, stating that acute tubular necrosis was not a disease that responds to prednisone. He concluded,
While I agree that [exposure to solvents or epoxy resins] would be a very uncommon and unlikely cause of acute tubular necrosis . . . there was really at no time any evidence of any of the other well-established causes of acute tubal necrosis, such as other toxins, episodes of shock, or infection. It is also known that there are a variety of chemicals which can lead to acute tubal necrosis . . . . I think in this circumstance, since the other etiologies have been eliminated, the remaining diagnosis, however unlikely, is the appropriate answer.
(Pet. Ex. D.)
Drs. Jeffrey Connaire and Meena Sahadevan, consulting nephrologists at HCMC, provided treatment to the employee, reviewed the employee’s medical records, his occupational exposures, and the reports of Dr. Baker, and conducted a literature review regarding solvent effects on the kidneys. They maintained that both of the diagnoses alluded to in the employee’s initial case, glomerulonephritis and ATN, have been associated with solvent exposure, including specifically xylene, which the employee was exposed to in both 2009 and April 2010. The doctors asserted that kidney toxicity from solvents is supported by medical literature stretching back almost 40 years. The amount of exposure that would be necessary to result in disease in a given individual, in their opinion, is an unknown. The doctors concluded:
[O]ur joint opinion is that there is not a better explanation for this gentleman’s original kidney failure, and we feel it is more likely than not that Mr. Vandenberg originally suffered kidney failure as a result of occupational exposure. It is also not surprising that there may be some uncertainty in establishing a specific culprit agent given the complexity of the exposures.
(Pet. Ex. E.)
In a response dated October 26, 2011, Dr. Baker disagreed, stating, “ATN implies there is a new acute injury that causes tubular damage. It is often due to decreased renal perfusion or ischemia, medical illnesses or medication. It is not due to long term or chronic exposure nor is it due to an allergy or sensitization that develops over years. ATN, if due to toxin exposure, is typically due to acute or recent exposure just before the necrosis develops. The employee did not appear to have a high level exposure to the same chemicals in December 2009 and April 2010.”
The matter came to a hearing before a compensation judge on October 5, 2011. In a Findings and Order issued on December 13, 2011, the compensation judge found (1) the employee had been exposed, throughout his working career as a painter, to fumes, solvents and substances, including those contained in Exhibits B and 9, that culminated in a personal injury to the employee’s kidneys on December 8, 2009; (2) the employee suffered an acute personal injury to his kidneys on April 30, 2010, that was causally related to his workplace exposure to chemical agents contained in the epoxy products and solvents he was using in carrying out his work duties; and (3) that the employee also suffered a personal injury in the nature of an occupational disease to his kidneys resulting in disability as of April 30, 2010, arising out of and in the course of the employee’s employment as a commercial and industrial painter. The self-insured employer appeals.
STANDARD OF REVIEW
In reviewing cases on appeal, the Workers’ Compensation Court of Appeals must determine whether “the findings of fact and order [are] clearly erroneous and unsupported by substantial evidence in view of the entire record as submitted.” Minn. Stat. § 176.421, subd. 1. Substantial evidence supports the findings if, in the context of the entire record, “they are supported by evidence that a reasonable mind might accept as adequate.” Hengmuhle v. Long Prairie Jaycees, 358 N.W.2d 54, 59, 37 W.C.D. 235, 239 (Minn. 1984). Where evidence conflicts or more than one inference may reasonably be drawn from the evidence, the findings are to be affirmed. Id. at 60, 37 W.C.D. at 240. Similarly, “[f]actfindings are clearly erroneous only if the reviewing court on the entire evidence is left with a definite and firm conviction that a mistake has been committed.” Northern States Power Co. v. Lyon Food Prods., Inc., 304 Minn. 196, 201, 229 N.W.2d 521, 524 (1975). Findings of fact should not be disturbed, even though the reviewing court might disagreed with them, “unless they are clearly erroneous in the sense that they are manifestly contrary to the weight of the evidence or not reasonably supported by the evidence as a whole.” Id.
The self-insured employer contends there is insufficient evidence to establish the employee suffered either a personal injury or an occupational disease to the kidneys arising out of and in the course of his employment. We disagree.
The employee testified that during his 34 years as a commercial and industrial painter he worked with various paints and specialty coatings, including epoxies and urethanes. Solvents, including xylene, were used to thin specialty coatings, and for cleaning painting equipment and stain from his hands. The employee testified he noticed shortness of breath in the past when working with epoxies and solvents.
For most of the summer and fall of 2009, the employee worked at BendTec applying epoxy and urethane coatings, including xylene for thinning and cleaning. Thereafter, prior to December 8, 2009, the employee worked primarily at the Mountain Iron Clinic and the Wieland Building. An index of material safety data sheets for the Mountain Iron and Wieland Building additions lists various epoxies, urethanes, latex paints, oil-based paints, paint thinner, and xylene. (Resp. Ex. 9.) The employee testified that he used similar products throughout his career as a painter.
During the week of December 8, 2009, the employee worked at a residence applying Diamond Vogel Satinenamel to an outside deck, exterior handrails, and stairs. The material safety data sheet for Satinenamel White Base states that “[c]hronic exposure may cause damage to the . . . kidneys.” Ingredients include aliphatic hydrocarbons and ethylbenzene. (Pet. Ex. B). During the week of April 27, 2010, the employee was applying epoxy coating to floors and baseboards at the border patrol station in International Falls. As was the norm when using epoxies, xylene was used as a thinner and cleaner. The material safety data sheet for Epoxy Cove Paste states that “[p]rolonged overexposure to hazardous ingredients in Section 2 may cause adverse chronic effects to the following organs or systems: . . . the urinary system.” Section 2 ingredients include ethylbenzene and xylene. The material safety data sheet for xylene similarly states that “prolonged overexposure to hazardous ingredients in Section 2 may cause adverse chronic effects to the following organs or systems: . . . the urinary system.” Ingredients include ethylbenzene and xylene. (Pet. Ex. B.)
The self-insured employer’s expert, Dr. Baker, asserted that all of the medical experts agreed the employee’s diagnosis was acute tubular necrosis. According to Dr. Baker, ATN is not due to long-term or chronic exposure or sensitization that develops over years. Rather, she maintained, ATN, if due to toxin exposure, is typically due to acute, high-level exposure just before the necrosis develops, and she opined there was no evidence to support a high level exposure to toxic chemicals in December 2009 or in April 2010.
The employee’s physicians, Drs. Maddy and Raja, following the December 8, 2009, episode, suspected a possible causal relationship between the employee’s exposure to solvents and epoxies and his loss of kidney function based on the exclusion of other possible diagnoses and causes of ATN. The employee’s kidney function improved, but between April 27 and 30, 2010, the employee was re-exposed to epoxy resins and xylene and experienced a return of his symptoms along with a substantial increase in his creatinine levels. Given the proximity in time of the recurrence of acute renal failure following re-exposure to suspected toxins, and the elimination of other possible etiologies, such as the use of certain medications or episodes of shock or infection, Dr Maddy was convinced that the cause of the employee’s acute kidney failure was his exposure to chemicals in the workplace. Drs. Connaire and Sahadevan maintained that both glomerulonephritis and ATN have been associated with solvent exposure, including xylene, and asserted that kidney toxicity from solvents is supported by medical literature stretching back almost 40 years. In their opinion, the employee’s kidney failure was a result of occupational exposures.
The compensation judge accepted the opinions of the treating physicians over the opinions of Dr. Baker. It is the compensation judge’s responsibility, as the trier of fact, to resolve conflicts in expert testimony. See Nord v. City of Cook, 360 N.W.2d 337, 342, 37 W.C.D. 364, 372 (Minn. 1985). The employer contends, however, that there is inadequate foundation for the opinions of the experts relied upon by the judge. The employee’s physicians are nephrologists, that is, experts in kidney disease. They examined and treated the employee, took extensive histories from the employee, and reviewed literature related to the relationship between the materials and products to which the employee was exposed and kidney disease. The employee provided material safety data sheets for products he used during the week of December 8, 2009, and April 30, 2010. He testified he discussed what he did for a living with Dr. Maddy, told him what kind of materials he worked with, and how long he had been working as a painter. He also stated that he discussed what he did for a living with Dr. Connaire, and that he believed Dr. Maddy had sent copies of the material safety data sheets to HCMC. As such, the doctors had adequate foundation for their opinions. See Grunst v. Immanuel-St. Joseph Hosp., 424 N.W.2d 66, 40 W.C.D. 1130 (Minn. 1988).
The self-insured employer further argues that the employee’s physicians did not express their opinions to the degree of reasonable medical certainty required by law, couching their conclusions in terms of possibilities and probabilities. Further, they assert, all of their opinions are based, in part, on the fact that they could find no other reasonable explanation for the employee’s condition. “It is well established that the truth of the opinion need not be capable of demonstration, that an expert is not required to express absolute certainty in the matter which is its subject, and it is sufficient if it is probably true.” Boldt v. Jostens, Inc., 261, N.W.2d 92, 94, 30 W.C.D. 178, 182 (Minn. 1977). Additionally, as noted in Boldt, disability resulting from diseases of uncertain or unclear etiology “have often been held compensable.” Id. at 93, 30 W.C.D. at 180.
Questions of medical causation fall within the province of the compensation judge. Felton v. Anton Chevrolet, 513 N.W.2d 457, 50 W.C.D. 181 (Minn. 1994); Foster v. Metro Produce Distrib., Dec. 13, 2002. While other inferences could be drawn from the evidence in this case, there is substantial evidence, in the record as a whole, to support the compensation judge’s findings. Hengmuhle v. Long Prairie Jaycees, 358 N.W.2d 54,59, 37 W.C.D. 235, 239 (Minn. 1984). We, accordingly, affirm.
 The self-insured employer placed the employee on layoff status effective December 4, 2009, by notice dated December 14, 2009. Although the employer denied the employee worked the week of December 7, 2009, the employer’s division manager acknowledged it was possible the employee worked at the residence and, being sick, never turned in a time card for that pay period. (T. 75.) The compensation judge found the employee continued to work for the employer the week following the layoff date of December 4, 2009. (Finding 6.) There is substantial evidence to support this finding.
 Nephrology is the study of the kidney, its anatomy, physiology, pathology, and pathophysiology. Dorland’s Illustrated Medical Dictionary 1186 (29th ed. 2000). A nephrologist is a doctor who specializes in nephrology.
 Glomerulonephritis refers to inflammation of the capillary loops in the glomeruli of the kidney and may be secondary to systemic disease, infection or possible immune or autoimmune mechanisms. Dorland’s, supra at 752. Vasculitis refers to inflammation of a blood vessel. Dorland’s, supra at 1935. Pauci-immune crescentic glomerulonephritis is characterized by the presence of epithelial crescents and antineutrophil cytoplasmic antibodies (ANCA). Dorland’s, supra at 753.
 Acute tubular necrosis is acute kidney failure with mild to severe damage or necrosis of tubule cells, usually occurring secondary to ischemia or the effects of a nephrotoxin. Dorland’s, supra at 1180.
 The employee in Boldt was diagnosed with Goodpasture’s Syndrome, a form of glomerulonephritis. The medical experts agreed the etiology of Goodpasture’s Syndrome is unknown. The employee’s physician stated it was thought to be an immunologic disease in which the patient develops antibodies to some antigen and the antibodies react against the kidneys and the lungs. The doctor also stated the antigen can probably be many different things and different for different people and the number of exposures required is unknown, but he concluded that the employee’s exposure to glue fumes “had a great deal to do with her illness.” The compensation judge, based on Dr. Dine’s opinion, found this exposure had produced the employee’s illness.