Searching over 5,500,000 cases.

Buy This Entire Record For $7.95

Download the entire decision to receive the complete text, official citation,
docket number, dissents and concurrences, and footnotes for this case.

Learn more about what you receive with purchase of this case.

Polk v. Planet Insurance Co.

Court of Workers Compensation of Montana

February 26, 1997




         Summary: Mill worker appealed decision of Department of Labor Hearing Examiner that he was not suffering from an occupational disease. Hearing Examiner found conclusions of medical panel entitled to a presumption of correctness and that the analysis of physicians finding him not suffering from an occupational disease was the better analysis.

         Held: The WCC affirmed the DOL decision. The WCC found the medical panel failed to follow statutory provisions by failing to meet as a whole to make a final determination, but found that error both harmless and not properly considered on appeal when not raised below. The WCC declined to find the presumption in favor of the panel report unconstitutional. Finally, the WCC found the decision below not clearly erroneous and supported by substantial evidence. [Note: the WCC decision was reversed by the Supreme Court in William Polk v. Planet Insurance Co., 287 Mont. 79, 951 P.2d 1015 (1997), on the ground that physicians rendering an opinion on occupational disease causation misunderstood the appropriate standard.]


         Occupational Disease: Proximate Cause. WCC affirmed DOL hearing officer's decision that medical panel correctly determined claimant was not entitled to compensation for occupational exposure. [Note: the WCC decision was reversed by the Supreme Court in William Polk v. Planet Insurance Co., 287 Mont. 79, 951 P.2d 1015 (1997), on the ground that physicians rendering an opinion on occupational disease causation misunderstood the appropriate standard.]

         This is an appeal from a finding by the Department of Labor and Industry (Department) that appellant, William Polk (claimant), is not suffering from an occupational disease.

         Procedural Background

         Claimant alleges he is suffering from a totally disabling lung disease caused by his exposure to dust and oil while employed at a mill which manufactures flour and vegetable oil from rape, flax and mustard seeds. The mill is owned by Koch Agriculture, Inc. (Koch).

         In December 1993 the claimant advised his employer that he had a respiratory infection or disease and wished to file a claim for compensation under the Occupational Disease Act (ODA). (DLI File.[1]On December 7, 1993, Koch filled out an Employer's First Report, which it forwarded to the adjuster for its workers' compensation insurer. (Id.) In that report Koch questioned the claim and specifically noted that claimant was a chain-smoker. (Id.)

         On January 6, 1994, claimant filled out, signed and submitted a formal Claim for Compensation. He wrote that he was suffering from a lung infection caused by the dust he had inhaled at work.

         On January 7, 1994, following receipt of the Employer's First Report but prior to receiving the claim itself, the adjuster for Koch's insurer wrote to claimant and requested that he submit a formal written claim for compensation and an authorization for release of medical records. (Id.) The letter also notified claimant that the insurer was "formally denying your claim for occupational disease benefits so that the panel evaluation will be scheduled by the Employment Relations Division [of the Department of Labor and Industry]." (Id.)

         Thereafter, the Department invoked the medical panel procedures specified in section 39-72-602, MCA. Initially, it designated Dr. David Anderson to examine claimant. (Id.) Dr. Anderson examined claimant on February 17, 1994. On February 24, 1994, he reported that claimant was suffering from "severe obstructive airway disease with reversible airway obstruction consistent with asthma as well as emphysema and possible pulmonary fibrosis." (Ex. 6 at 280.) Dr. Anderson wrote that "[a]lthough some of . . . [claimant's] obstructive airway disease is likely related to his history of smoking 1½ packs a day of cigarettes for 20 years, I believe the asthmatic component is more likely related to his exposure to toxic organic dusts that he was exposed to [at work]." (Id.)

         Based on Dr. Anderson's report, on March 15, 1994, the Department issued an Order Referring Copy of Medical Reports to Parties. The Order determined that claimant was suffering from an occupational disease.

Based on the attached report of the first examining physician, the Department concludes the claimant is suffering from SEVERE OBSTRUCTIVE AIRWAY DISEASE WITH REVERSIBLE AIRWAY OBSTRUCTION CONSISTENT WITH ASTHMA AS WELL AS EMPHYSEMA & POSSIBLE PULMONARY FIBROSIS which in fact arose out of and was contracted from their [sic] employment.

(DLI File; capitalization in original.) It further notified the parties of their right to a second panel examination pursuant to section 39-72-602, MCA. (Id.)

         The insurer thereafter requested a second examination and on April 12, 1994, the Department designated Dr. Michael Sadaj to conduct the examination. (Id.) On June 10, 1994, Dr. Sadaj reported:

In my opinion, Mr. Polk has chronic obstructive pulmonary disease and chronic respiratory insufficiency as a result of long term heavy smoking. In my opinion, he has no occupational lung disease.

(Ex. B at 1.)

         On June 20, 1994, the Department designated Dr. Thomas Thigpen the chair of the medical panel and sent him copies of the reports of both Drs. Anderson and Sadaj. (DLI File.) In its cover letter to Dr. Thigpen, it instructed him

to review the information provided and contact the first and second examining physicians to arrive at a consensus regarding claimant's problems and the relationship of those problems to their [sic] employment, without seeing the claimant.

(Id.) The letter requested Dr. Thigpen to submit a written report.

         On September 6, 1994, Dr. Thigpen submitted his written report. (Ex. C.) He concluded that claimant was not suffering from an occupational disease, rather he was suffering from emphysema attributable to his cigarette smoking. (Id.)

         On October 5, 1994, the Department issued another Order Referring Copy of Medical Panel Reports to Parties. (DLI File.) This time the Department determined that the claim for occupational disease benefits should be denied. It notified the parties that if they disagreed with that determination they could request a hearing. On October 20, 1994, the claimant, through his attorney, filed a request for hearing. (Id.)

         A hearing was held in Great Falls, Montana, on October 19 and 20, 1995. Claimant testified on his own behalf. Drs. Holly Strong, Dana Headapohl, David Anderson, Jeffrey Kessler and Stephen Demeter all testified concerning claimant's medical condition. Dr. Robert K. Merchant was not present at the hearing but his testimony was presented through his deposition. Margot Hart and Bruce Carmichael, who are certified rehabilitation counselors, testified concerning claimant's employability. Finally, Gordon Mattern, the plant manager of Koch, testified concerning conditions at the plant.

         The hearing officer issued his Findings of Fact; Conclusions of Law; and Final Order on March 1, 1996. He found that the law favors the final panel determination and that claimant had "not provided sufficient medical information to overcome the presumption in favor of the panel." (Findings at 8.) He further concluded:

Additionally the analysis and conclusion reached by the group of doctors who agree with the panel is found to be the better analysis. The doctors in this group are more highly qualified in pulmonary medicine and their analysis of the medical records including both radiologic and physiologic records is found more credible.

(Id.) He affirmed the Department's decision denying the claim. This appeal followed.

         Record on Appeal

         The record on appeal consists of the Department's file, the exhibits admitted at hearing, the deposition of Dr. Merchant, and a partial transcript of the hearing. The parties stipulated to the portions of the transcript which are included in the appeal. (Stipulation filed March 29, 1996.) Those portions include the transcribed testimony of Drs. Dana Headapohl, David Anderson, Jeffrey Kessler, and Stephen Demeter, the claimant, Gordon Mattern, Margot Hart, and Bruce Carmichael.

         Medical Terms

         The alleged occupational disease involves the claimant's respiratory system. To assist the reader in understanding the medical testimony and reports referenced in this decision, I provide the following explanations of key medical terms used in this decision.

         Trachea: "The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi." Dorland's Illustrated Medical Dictionary 1738 (27th ed. 1988).

         Bronchus (bronchi, pl.): "One of the two large tubes, branches of the trachea or windpipe, which conduct air to and from the lungs or one of their principal branches. The bronchi begin at the lower end of the windpipe, and end in the substance of the lungs where they divide into smaller branches." Schmidt's Attorneys' Dictionary of Medicine, Vol. 1, B-141-42 (1990).

         Bronchiole (bronchioles, pl.): "One of the finer subdivisions of the branched bronchial tree, differing from the bronchi in having no cartilage plates and having cuboidal epithelial cells." Dorland's Illustrated Medical Dictionary 236 (27th ed. 1988).

         Alveolus (alveoli, pl.): "One of the tiny air sacs of the lungs, formed by a dilatation at the end of a bronchiole (more precisely, an alveolar duct). The bronchioles are the slenderest of the many tubes which carry air into and out of the lungs. Through the thin walls of the alveoli or air sacs, the blood takes in oxygen and gives up its carbon dioxide in the process of respiration." Schmidt's Attorneys' Dictionary of Medicine, Vol. 1, A-158 (1990).

         Chronic Obstructive Pulmonary Disease (COPD): A "[g]eneralized airways obstruction, particularly of small airways, associated with varying combinations of chronic bronchitis, asthma and emphysema. The term COPD was introduced because these conditions often coexist, and it may be difficult in an individual case to decide which is the major one producing the obstruction." The Merck Manual, § 4, ch. 36, p.636 (15th ed. 1987). Dr. Anderson characterized "obstructive lung disease" as:

anything that causes airway obstruction, such as chronic bronchitis associated with smoking, bronchial asthma, and eventually will lead to a kind of chronic dilatation of the air spaces which we term 'emphysema'.

(Tr. at 52.) Dr. Merchant described the condition as "reduced airflows in the lungs . . . sort of like...breath[ing] through a small straw." (Merchant Dep. at 13.)

         Chronic bronchitis: A "long-continued form of inflammation of one or more bronchi,, often with a more or less marked tendency to recurrence after stages of quiescence. It is due to repeated attacks of acute bronchitis or to chronic general diseases; characterized by attacks of coughing, by expectoration, either scanty or profuse, and by secondary changes in the lung tissue." Dorland's Illustrated Medical Dictionary 237 (27th ed. 1988). Dr. Merchant described chronic bronchitis as a "condition where you have a lot of inflammation chronically in the airways and continually they have a lot of sputum production on a daily basis." (Merchant Dep. at 13.) He testified that chronic bronchitis is most frequently due to tobacco use but can be due to other things. (Id.)

         Asthma: A "condition marked by recurrent attacks of paroxysmal dyspnea [difficult or labored breathing], with wheezing due to spasmodic contraction of the bronchi." Dorland's Illustrated Medical Dictionary 158 (27th ed. 1988). Dr. Anderson testified that a diagnosis of occupational asthma requires a history of exposure to an occupational irritant. (Tr. at 53.) Dr. Stephen Demeter simplified the definition of asthma as "a disorder characterized by an increased response by the airways to irritants." (Id. at 134.) Grain dust and mold associated with the milling of seeds can act as an irritant. (Id. at 135.)

         Emphysema: A "condition of the lung characterized by increase beyond normal in the size of air spaces distal to the terminal bronchioles, either from dilatation of the alveoli, or from destruction of their walls." Dorland's Illustrated Medical Dictionary 547 (27th ed. 1988). Dr. Anderson concurred with the National Heart, Lung and Blood Institute's definition of emphysema as "a condition of the lung characterized by abnormal prominent enlargement of the air spaces distal to the terminal bronchials and accompanied by the destruction of their walls and without obvious fibrosis." (Tr. at 57.) Dr. Merchant explained that emphysema is a condition where large portions of lung tissue may be destroyed, which in turn may cause the airways to collapse. (Merchant Dep. at 13.) He testified that emphysema can cause an appearance of increased interstitial markings. (Id. at 19, 26.) Interstitial refers to the spaces in lung tissue, Dorland's Illustrated Medical Dictionary 546-47 (27th ed. 1988), for example the spaces between alveoli.

         Restrictive lung disease: A "ventilation disorder of the lungs (insufficient exchange of gases) due to a reduction in the volume of the lung tissue or a disorder of the chest wall, pleura, or diaphragm." Schmidt's Attorneys' Dictionary of Medicine, Vol. 3, R-83 (1990). Dr. Dana Headapohl contrasted the condition to obstructive lung disease, as follows:

Obstructive lung disease is any process that decreases the flow of air into or out of the lungs. This would include things like asthma, bronchospasm, those kinds of things. Restrictive disease, on the other hand, involves essentially the restriction of lung movement; so the lung, which is normally very elastic and compliant becomes fibrotic [characterized by scar tissue] and is unable to work as a bellows well.

(Tr. at 13.) She testified that interstitial lung disease involves fibrosis of lung tissue in the spaces between the alveoli and is a form of restrictive lung disease. (Id. at 48, 52.) In discussing the three conditions she said:

Obstructive lung disease refers to anything that causes airway obstruction, such as chronic bronchitis associated with smoking, bronchial asthma, and eventually will lead to a kind of chronic dilatation of the air spaces which we term 'emphysema'. Interstitial lung disease refers to a process that usually starts as an acute inflammation involving the alveoli, leading to inflammation within the interstitial spaces and eventually fibrosis and leads to more of what we call ventilation profusion mismatch (?) than strictly an obstructive disease. That's why one sees a drop in oxygen saturation with exercise. Restrictive lung disease can be due to pulmonary fibrosis, but it could also be due to anything that restricts the movement of the chest, such as somebody has severe arthritis and has had compression fractures.

(Id. at 52; (?) in original transcript.)

         Hypersensitivity pneumonitis: A restrictive lung disease. (Id. at 49.) It is "[a] diffuse interstitial granulomatous lung disease caused by an allergic response after inhalation of one of a variety of organic dusts or, less commonly, simple chemicals." The Merck Manual, § 4, ch. 43, p. 687 (15th ed. 1987). Granulomatous means "composed of granulomas." A granuloma is "(1) any small nodular delimited aggregation of mononuclear inflammatory cells, or (2) such a collection of modified macrophages resembling epithelial cells" and is "a chronic inflammatory response initiated by various infectious and noninfectious agents." Dorland's Illustrated Medical Dictionary 716 (27th ed. 1988). Dr. Merchant defined this disease as "an unusual condition that's actually an allergic reaction deep in the airways. And it's a different allergic reaction than you get with asthma or hay fever, and it actually causes what's called 'granulomatous inflammation' in the air sacs." (Merchant Dep. at 17.) The condition can be caused by a variety of exposures, including grain dust and molds of the type that claimant was exposed to in the workplace. (Tr. at 13.)

         Hypersensitivity pneumonitis may be either acute or chronic.

In the acute phase, there is irritation, inflammation, there may be accumu-lation of fluid in the small airways and in the alveoli . . . . [I]t's not uncommon to have fever, chills, shortness of breath, which in many cases resolves within a week or two, if you take a person away from the exposure. On x-ray, the x-ray may be normal or it can also show some patchy infiltrates; and these are generally seen in the lower lungs.
If the person continues to be exposed to the same offending agent, you can have overlapping courses; so you can have acute changes where the person might have resolved the problem, but then there's another exposure, so you have a more chronic picture developing. In the chronic form, what happens is that the lung tissue which has been inflamed and irritated scars and becomes fibrotic, which is just another term for scarring. And in this phase, the fibrotic changes are often times seen in the upper lung.

(Dr. Headapohl; Tr. at 12.) Dr. Merchant explained that the chronic form of the disease may be difficult to diagnose but "radiographically you see scar tissue development." (Merchant Dep. at 18.)

         Bronchiectasis: A "chronic dilatation of the bronchi marked by fetid breath and paroxysmal coughing, with the expectoration of mucopurulent matter. It may affect the tube uniformly, or occur in irregular pockets, or the dilated tubes may have terminal bulbous enlargements." Dorland's Illustrated Medical Dictionary 236 (27th ed. 1988). Dr. Merchant described it as "a condition where you actually have destruction not of the air sacs that you have in emphysema, but of the peripheral airways. And these airways get very dilated up, . . . the major problem is that you can't clear out secretions out of them." (Merchant Dep. at 35.) Dr. Merchant explained that there are various causes of bronchiectasis, for example, a severe pneumonia, particularly one that is not treated promptly. (Id. at 35.) Dr. Anderson described bronchiectasis as "kind of a chronic dilatation of the air space" often associated with "excessive mucus production." (Tr. at 57.) He identified aspergillosis, a fungus commonly found in grain dust, as one possible causative agent. (Tr. at 58, 61.)


         1.Claimant's employment history and occupational exposure.

         Claimant is 51 years old. After graduating from high school, he spent eight years in the United States Air Force. For ten years thereafter he worked for the Great Falls Gas Company as a meter reader and a laborer. He then worked at Holman Aviation as a janitor for three years. Finally, he worked for Evans Grain & Elevator Company and its successor company, Koch Agriculture, Inc., from 1985 until November 1993. It was during his employment with Koch that claimant allegedly contracted an occupational lung disease. (Tr. at 257-59.)

         Koch processes rape, flax and mustard seeds into flour and vegetable oil. During his employment with Koch, claimant sacked flour in 100-pound bags and cleaned machinery. He was regularly exposed to dust and oil mist. In addition, he was exposed to moldy grain. In 1992 he began wearing a mask at work to reduce his inhalation of dust and mist. (Tr. at 266-71, 281-82.)

         2.Onset of respiratory troubles.

         Prior to 1991, claimant's only history of respiratory problems was a bout with a respiratory infection and pneumonia in 1976. However, he was heavy a smoker. Between 1962 and 1993, inclusive, he smoked one and one-half packs of cigarettes a day. (Tr. at 267.) Since 1993 he has smoked only intermittently, and now limits his smoking to four cigarettes a day at most.

         In April 1991 claimant experienced fever, chills, and diarrhea for approximately ten days. (Tr. at 285.) Thereafter, in February of 1992, he was admitted to Columbus Hospital in Great Falls with primary complaints of fever, chills, and diarrhea, symptoms which were similar to those he had experienced the previous April. (Ex. 5 at 147.) He also had a "slight cough." (Id.) The admitting physician noted in his history that "the patient had an almost identical illness approximately 9 months ago." (Id.) A chest x-ray disclosed "reticular nodular infiltrate in both lung fields which was faint." (Id. at 146.) Dr. Addison, who treated claimant during this hospitalization, diagnosed claimant as suffering from infectious diarrhea, dehydration and reticular nodular infiltrate of the lungs. (Id.)

         In July 1993 the claimant sought medical care at the Great Falls Immediate Care Center for respiratory and cold-like symptoms, including a cough with productive green phlegm, fever, and nasal congestion. (Ex. G at 1.) The examining physician diagnosed "[b]acterial respiratory upper infection." (Id.)

         Thereafter, the claimant continued to experience periodic coughing and congestion. (Id. at 2.) In October he experienced an "increasing cough." (Id. at 3.) On October 12, 1993, he again sought medical care. (Id.) At that time he was diagnosed as having bronchitis and "[p]robable early chronic obstructive pulmonary disease." (Id.) The treating physician prescribed medication, rest and fluids, and encouraged claimant to stop smoking. (Id.)

         On November 9, 1993, claimant was hospitalized at the Columbus Hospital with fever, cough, shortness of breath, hypoxia, [2] and respiratory distress. (Ex. 5 at 141.) His blood oxygen saturation level at the time of admission was 87%. (Id.) According to Dr. Strong, a saturation level of less than 90% warrants the use of supplemental oxygen . (Tr. at 75.)

         Dr. Holly Strong, who specializes in pulmonary and critical care, treated claimant during his November 1993 hospitalization. She concluded that claimant suffers from hypersensitivity pneumonitis, occupational asthma, bronchiectasis, and emphysema. (Tr. at 74-77.) She indicated that the various conditions were the result of a combination of claimant's inhalation of grain dust and smoking. (Ex. 6 at 292.)

         Following claimant's November 1993 hospitalization, Dr. Strong concluded that claimant should not return to his job at Koch. (Id.) Claimant has not worked since then and continues to experience shortness of breath, becoming winded even with light activity. (Tr. at 291, 294.)

         3. The medical evidence.

         This case involves conflicting expert medical opinions. Of the doctors testifying at hearing and by deposition, Drs. Strong, Anderson, and Headapohl opined that claimant's lung condition is occupationally related, while Drs. Merchant and Demeter concluded that his condition is not occupationally related. Dr. Kessler was also unable to relate claimant's lung condition to occupational factors. Three other doctors who examined claimant, but who did not testify, provided written opinions that claimant does not suffer from an occupational disease. Finally, Dr. Patterson, who did a biopsy of lung tissue, found "minimal alveolar fibrosis of undetermined etiology" and "inflammatory infiltrate" of the bronchus which he characterized as "suggestive of possibly a hypersensitivity." (Ex. D at 1.)

         Dr. Holly Strong

         Dr. Holly Strong practices pulmonary medicine. She received her M.D. degree from the University of Guadalajara and completed residencies in internal medicine (three years), pulmonary medicine (two years), and critical care (one year). (Tr. 71.) At the time of hearing, she had been practicing pulmonary and critical care medicine for three years, was board certified in internal medicine, and was board eligible but not certified in pulmonary medicine. (Id. 71, 79.)

         Dr. Strong treated claimant during his November 1993 hospitalization and has been his treating physician since that time. In her opinion claimant is suffering from (1) hypersensitivity pneumonitis; (2) bronchiectasis, which she characterized as "a type of chronic bronchitis, which is much more severe"; (3) a small element of emphysema; and (4) asthma. (Id. at 74-76.) She testified that the hypersensitivity pneumonitis is related to claimant's exposure to grain dust while working at the Koch mill. (Id. at 74.) She said the bronchiectasis could have been caused by prior pneumonia, early hypersensitivity pneumonitis, or some sort of syndrome:[3] she was unable to specifically attribute any of it to occupational factors. (Id. at 75, 80.) She attributed claimant's emphysema to smoking. (Id. at 75.) Finally, she attributed claimant's asthma to his exposure to organic grain dust. (Id. at 77.)

         Dr. Strong noted that hypersensitivity pneumonitis is often called "farmers' lung" because of its incidence among persons who "work in grains, granaries and millers." (Id.) She said that organisms occurring in grain are thought to cause the condition, however, not all persons working with grain or exposed to the organisms contract the disease. (Id.) According to Dr. Strong, smokers appear to be more susceptible to the disease. (Id. at 77, 82.)

         According to Dr. Strong, claimant's most debilitating symptom is hypoxia, which is a lack of sufficient oxygen in his blood.[4](Id. at 75.) Because his blood is insufficiently oxygenated, "[h]e is unable to walk across a room without getting very short of breath." (Id.) After brief exercise claimant's oxygen saturation drops to between 70% and 80%. (Id.) Dr. Strong noted that claimant "cannot walk across a room without probably needing more oxygen -- supplemental oxygen." (Id. at 76.) Claimant obviously cannot return to his work at the mill, however, Dr. Strong indicated that he could work in a sedentary position. (Id. at 80.)

         Dr. Strong attributed claimant's hypoxia primarily to hypersensitivity pneumonitis. (Id. at 75.) She agreed that emphysema can cause desaturation of blood oxygen (id. at 81) but felt that claimant's emphysema was neither advanced nor severe (id. at 75, 83). Her opinion concerning the "small" degree of emphysema (id. at 75) was based on a high-resolution CT scan performed on June 20, 1995 (id. at 82-83, 89), which she interpreted as "rather diagnostic of hypersensitivity pneumonitis" and as showing "a small amount of emphysema" (id. at 83). She indicated, however, that a radiologist is more qualified than she is to read and interpret the CT scan. (Id. at 82-83.)

         Dr. David Anderson

         Dr. David Anderson is a member of the occupational disease panel designated by the Department pursuant to section 39-72-601, MCA. He completed a residency in internal medicine and a fellowship in pulmonary diseases at the Mayo Clinic. (Tr. at 42.) He has practiced medicine in the State of Montana since 1979. (Id.) He is board certified in internal medicine but not in pulmonary medicine.[5](Id. at 43.) Approximately 80% of his outpatient practice involves the treatment of pulmonary diseases and a "good percentage" of his hospital practice involves critical care of patients suffering from pulmonary diseases or conditions. (Id.) In the course of his practice he often treats people who work in the grain industry. (Id.)

         Dr. Anderson performed an occupational disease evaluation of claimant in February 1994. He reported his findings to the Department in a letter of February 24, 1994:

My impression is that William does have severe obstructive airway disease with reversible airway obstruction consistent with asthma as well as emphysema and possible pulmonary fibrosis. To me it appears that this came on when he was working for the Montana Vegetable Oil Company probably as a result of exposure to toxic organic dust in his work that involved unloading grain and often having to clean out the inside of grain bins, shoveling grain into an auger. He also assisted other people in welding during his employment and this might have also have been a contributing factor to his lung disease.
Although some of his obstructive airway disease is likely related to his history of smoking 1½ packs a day of cigarettes for 20 years, I believe the asthmatic component is more likely related to his exposure to toxic organic dusts that he was exposed to.

(Ex. 6 at 280.)

         Dr. Anderson testified at the hearing that claimant suffers from asthmatic bronchitis, emphysema, and hypersensitivity pneumonitis. (Tr. at 58.) In his opinion the asthma and the hypersensitivity pneumonitis were caused by claimant's exposure to grain dust and mold at the Koch mill. (Id. at 58-59). He explained the role of mold found in grain and grain dust.

People can become hypersensitized to the mold, and they can develop several things. They can develop asthma from exposure to the same, they can develop a syndrome that's called toxic organic dust syndrome; or they can develop a syndrome that's called hypersensitivity pneumonitis, where they actually develop what looks like pneumonia on chest x-ray, but is actually a hypersensitivity reaction to the pneumonia. So they can develop several different syndromes associated with that exposures [sic] to mold, especially mold that's growing with grain.

(Id. at 45.)

         Dr. Anderson testified that claimant's history of smoking contributed to his asthma (id. at 58-59) and apportioned claimant's overall disability at 60% to occupational factors and 40% to smoking and other factors. (Id. at 59.) He apportioned the hypersensitivity pneumonitis at 100% to occupational factors. (Id.)

         Dr. Anderson's diagnosis of asthma was based on claimant's response to bronchodilators[6]during pulmonary function testing. (Id. at 53-54.) After administration of bronchodilators claimant's lung function tests increased significantly. (Id.) Dr. Anderson said that the increase was diagnostic for asthma. (Id.)

         Dr. Anderson identified several facts supporting his diagnosis of hypersensitivity pneumonitis. First, claimant's blood oxygen saturation did not remarkably improve with the administration of bronchodilators. (Id. at 53-54.) Significant improvement would be expected if claimant's hypoxia was primarily due to asthma. (Id.) Thus, the lack of significant improvement suggested another cause for the hypoxia. Second, claimant's defusion capacity, which "measures the disappearance of carbon monoxide from air that you breathe," was significantly reduced, indicating the possible "presence of interstitial lung disease or the presence of emphysema." (Id. at 54.) Third, an enhanced CT scan of the lungs, taken June 29, 1995, revealed (1) "some evidence of emphysema, but not a very severe emphysema"; (2) evidence of interstitial lung disease or fibrosis "predominantly in the upper lobes and . . . kind of towards the periphery of the lung"; and (3) "evidence of bronchiectases in the lower lobes." [7](Id. at 56-57.) In Dr. Anderson's opinion, the degree of emphysema identified by the scan was insufficient to explain claimant's hypoxia. (Id. at 57, 67.)

         Dr. Anderson concluded that the primary condition disabling claimant is "pulmonary fibrosis related to the hypersensitivity pneumonia." (Id. at 59.) He pointed out that asthma is treatable and that if asthma were claimant's only problem he could still perform a number of other occupations. (Id.) Considering claimant's overall condition, Dr. ...

Buy This Entire Record For $7.95

Download the entire decision to receive the complete text, official citation,
docket number, dissents and concurrences, and footnotes for this case.

Learn more about what you receive with purchase of this case.