Dravo Lime Co., Inc. v. Eakins, No. 2003-SC-1027-WC.
| Citation | 156 S.W.3d 283 |
| Decision Date | 17 February 2005 |
| Docket Number | No. 2003-SC-1042-WC.,No. 2003-SC-1027-WC. |
| Parties | DRAVO LIME COMPANY, INC., Appellant, v. Glenn EAKINS; Hon. Sheila C. Lowther, Chief Administrative Law Judge; and Workers' Compensation Board, Appellees, Glenn Eakins, Cross-Appellant, Dravo Lime Company, Inc; Hon. Sheila C. Lowther, Administrative Law Judge; and Workers' Compensation Board, Cross-Appellees. |
| Court | United States State Supreme Court (Kentucky) |
Relying on testimony from a witness who was not a practicing physician regarding the chemical properties of calcium oxide and its effects on the human body, an Administrative Law Judge (ALJ) determined that the claimant's exposure to the substance caused his pulmonary fibrosis and impairment. Furthermore, the ALJ refused to credit employer-funded disability benefits against the claimant's award. The Workers' Compensation Board (Board) affirmed on both issues. The Court of Appeals affirmed the finding of causation but reversed and remanded on the question of a credit, directing the ALJ to determine whether the disability policy provided an offset for workers' compensation benefits and to reconsider the matter of a credit in that light. KRS 342.730(6). The employer appeals the finding of causation, and the claimant cross-appeals regarding the credit.
Dravo Lime Company operated a limestone mine and also processed limestone rock into lime and hydrated lime. The claimant worked at the facility for 33 years, performing a number of different jobs. He had worked as a crusher operator, conveyor man, and mechanic in the mine; screening plant operator; heavy equipment operator; and foreman. He had also worked at the lime plant and been a bagger at the hydrate plant for a number of years. His latest assignment was to drive a truck that sprayed water to control dust throughout the facility, but he stated that he also did whatever else was needed.
The claimant testified at length regarding his exposure to limestone dust and also to dust from processed lime, indicating that he was exposed to the latter for about 30 years. He testified that because calcium oxide was highly caustic and was pulverized during processing, workers were provided with a barrier cream to help prevent the substance from coming in contact with their skin. Large quantities of vinegar were also kept on hand to neutralize it.
On March 10, 1998, the claimant worked at the lime plant, operating a backhoe under the kilns in which the rock was processed, filling trucks with lime. While doing so, he began to experience a burning sensation in his mouth, nose, and chest. He reported the symptoms to his foreman and was ordered to ride in the foreman's truck for the rest of the day. He awoke during that night, sweating and unable to breathe.
Dr. Schworer, the claimant's family physician, referred him to Dr. Griffin, a pulmonary specialist. Dr. Griffin noted the claimant's long exposure to "silica" at a limestone quarry and ordered pulmonary testing, which revealed a fairly severe restrictive lung disease that did not change after the administration of a bronchodilator. Dr. Griffin diagnosed restrictive lung disease of unknown etiology. In early May, 1998, he hospitalized the claimant for several days and performed a bronchoscopy, thorcotomy, and lung biopsy. An examination of the tissue revealed focal alveolar thickening and focal fibrosis as well as dense fibrous pleuritis with pleural adhesions. The pathologist's report also noted that chronic bronchitis, lung fibrosis, and pleural thickening were among the findings reported in patients exposed to wollastonite-limestone dusts and included a citation to an article in an environmental research journal. After reviewing the report, Dr. Griffin changed his diagnosis to chronic bronchitis, lung fibrosis, and pleural thickening due to wollastonite-limestone dust exposure. Although Dr. Griffin reported the pathologist's notation in a follow-up letter to Dr. Schworer, the letter also expressed uncertainty that exposure to limestone dust contributed to the claimant's lung disease and deferred judgment in that regard.
Following the claimant's release from the hospital, he developed a blood clot and was hospitalized again. Immediately after that hospitalization, he informed his employer of the injury and began to receive short-term disability benefits. As filed on May 3, 1999, the claimant's application for benefits alleged "White Lung" due to limestone exposure. As the evidence developed, however, he came to allege that his pulmonary impairment was due to burning and scarring of his lungs from his years of exposure to calcium oxide.
Dr. Grainger evaluated the claimant on March 17, 1999. Based upon pulmonary function studies that revealed an FVC of 43% of the predicted normal and an FEV1 of 72% of the predicted normal, he diagnosed severe restrictive pulmonary disease that accounted for a 70% AMA impairment. Having noted that the claimant "worked in the mines for 25 years," his opinion was that the condition was due to the claimant's many years of working in "mine dust." It caused him to be "100% disabled."
Dr. Powell evaluated the claimant on July 2, 1999. He noted a history of 33 years in mining at a limestone quarry, 20 years of which were spent underground and 13 years of which were spent outside at the hydrating plant. Dr. Powell reported an FVC value of 51% of the predicted normal value and an FEV1 value of 54% diagnosing a moderate obstructive ventilatory defect. He classified the claimant's x-rays as being category 1/1/Q/Q, consistent with occupational pneumoconiosis. He indicated, however, that results from the lung biopsy should be used to determine whether the apparent nodularity was due to silicosis, noting that the claimant's primary exposure had been to calcium carbonate, which was not known to cause nodular lung disease.
In May, 2000, Dr. Powell was asked to review a CT scan taken in April, 1998, to determine whether it evidenced pneumoconiosis "secondary to [the claimant's] exposure to limestone." Having done so, he reported finding no changes that would lead him to diagnose pneumoconiosis. When deposed on June 16, 2000, he reviewed the biopsy records. Although he agreed that the findings were abnormal and that there was some focal fibrosis, he noted that no silica was found in the tissue, making it unlikely that the changes were due to silicosis. He concluded, therefore, that the lung disease and x-ray changes were unrelated to the claimant's work.
Dr. Jarboe evaluated the claimant on July 14, 1999, and interpreted x-rays as revealing no evidence of pneumoconiosis. He obtained an FVC value of 50% and an FEV1 of 51% but reported that they were invalid due to lack of effort. When deposed on June 20, 2000, Dr. Jarboe acknowledged that the CT scan and biopsy revealed abnormalities, that there was evidence of "some nonspecific type of fibrosis," and that the claimant was suffering from restrictive lung disease. He noted, however, that the biopsy revealed no evidence of silica or the nodulation one would expect with pneumoconiosis or, more specifically, with silicosis.
The university evaluation was performed by Drs. Goldwin and Collins. Dr. Goldwin interpreted an x-ray as revealing category 1/0 scar-like opacities or atelectasis but no abnormalities that were consistent with pneumoconiosis. Dr. Collins conducted a pulmonary examination on August 11, 1999. She recorded a history of the March, 1998, incident and noted that the claimant had worked from 1960 until March 10, 1998, as a limestone miner. She obtained an FVC value of 57.3% and an FEV1 value of 58.7%, pre-bronchodilator, and an FVC value of 57.3% and an FEV1 value of 60.2%, post-bronchodilator. Based on the foregoing, she concluded that the claimant suffered from silicosis secondary to the mining and handling of limestone.
When deposed by the employer on June 30, 2000, Dr. Collins was asked to review the biopsy report. After doing so, she changed her opinion and testified that the biopsy ruled out silica dust inhalation as the cause of the fibrosis in the claimant's lungs. On cross-examination, she acknowledged that there was moisture in the lungs. She also acknowledged that the claimant had demonstrated to her what happens when lime is exposed to moisture by mixing some of it with water, probably in a specimen cup. Asked what happened, she responded that "it fumed and spewed and gassed and got hot, and almost melted the cup." The following colloquy then ensued:
Q. And that's, I think, when you discovered that there's a significant difference between lime, lime rock, and lime rock dust; did you not?
A. Yes.
Q. Does that make a difference in terms of your trying to diagnose Mr. Eakins' condition?
A. No, sir.
Q. The fact that he was inhaling lime, as opposed to rock dust, does not make a difference?
A. I'm not aware that it does, sir.
Q. The findings on the biopsy, the x-ray, and the CT scan all show fibrosis, correct?
A. Yes, sir. They did.
Q. What is fibrosis?
A. That is the deposits of fibrous tissue in response to inflammation.
Q. And Mr. Eakins described to you his inhalation of lime; correct?
A. Yes, sir.
Q. And lime, as you saw demonstrated for you by Mr. Eaklins, causes fire, or whatever you want to call it, gases, etc.; correct?
A. Well, it certainly created an exothermic reaction; I'll guarantee that.
Q. And to that extent, with your knowledge that there is liquid within the lung, and if Mr. Eakins had been inhaling this stuff, would this not then cause, as was described in your report, a blistering of his lung?
A. I honestly have no idea about the inhalation of small enough particles of that material when it interacted with the liquid lining the insides of the...
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