United States Department of Labor 

Employees’ Compensation Appeals Board 

__________________________________________ 

R.H., Appellant 

and 

TENNESSEE VALLEY AUTHORITY, 

PARADISE FOSSIL PLANT, Drakesboro, KY, 

Employer 

__________________________________________ 

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Docket No. 13-2039 

Issued: March 5, 2014 

Appearances: Case Submitted on the Record

Ronald K. Bruce, Esq., for the appellant 

Office of Solicitor, for the Director 

DECISION AND ORDER 

Before: 

COLLEEN DUFFY KIKO, Judge 

ALEC J. KOROMILAS, Alternate Judge 

JAMES A. HAYNES, Alternate Judge 

JURISDICTION 

On September 6, 2013 appellant, through counsel, timely appealed the August 2, 2013 

merit decision of the Office of Workers’ Compensation Programs (OWCP). Pursuant to the 

Federal Employees’ Compensation Act1

 (FECA) and 20 C.F.R. §§ 501.2(c) and 501.3, the Board 

has jurisdiction over the merits of the claim. 

ISSUE 

The issue is whether appellant sustained an injury in the performance of duty on or about 

June 14, 2012. 

FACTUAL HISTORY 

Appellant, a 61-year-old retired maintenance mechanic/steamfitter, filed a claim (Form 

CA-2) for pneumoconiosis, asbestosis and bronchitis. He attributed his claimed condition to 

 1

 5 U.S.C. §§ 8101-8193. 
2

industrial exposure to coal dust and asbestos.2

 Appellant claimed that he first became aware of 

his condition on June 14, 2012. 

Dr. Glen R. Baker, Jr. interpreted a May 2, 2012 chest x-ray as positive for 

pneumoconiosis.3

 He examined appellant on July 6, 2012 and diagnosed, inter alia, mild 

bronchitis and occupational pneumoconiosis with pulmonary asbestosis, category 1/0.4

 

Dr. Baker noted that appellant had been employed for 141⁄2 years as a pipefitter and was exposed 

to coal dust and asbestos. Many of the pipes he worked on were reportedly wrapped in asbestos. 

Appellant also had a 41-year smoking history.5 He complained of shortness of breath, wheezing 

and a daily cough with variable sputum production. Exertion and exposure to hot and humid 

weather reportedly aggravated appellant’s breathing. He could walk 125 to 150 yards on level 

ground before having to stop and catch his breath. Dr. Baker commented on appellant’s May 2, 

2012 positive x-ray findings and also noted that his July 6, 2012 pulmonary function study (PFS) 

was within normal limits. He attributed appellant’s bronchitis and occupational pneumoconiosis 

to asbestos exposure, as well as other dusts, odors and fumes encountered during his 

employment. Cigarette smoking was also a contributing factor. 

OWCP referred appellant to Dr. H. Dale Haller, Jr., a pulmonary specialist Boardcertified in pulmonary disease, who examined appellant on December 13, 2012. He reviewed 

appellant’s more than 30-year employment history as a pipefitter, which included work as a 

federal civilian employee and as a private-sector contractor. Dr. Haller noted that appellant 

worked around asbestos-insulated piping, but he was not responsible for removing the insulation. 

Appellant also reported using asbestos fire blankets which produced some dust. Additionally, he 

was exposed to flue gas. However, appellant was primarily exposed to coal dust which was 

reportedly everywhere. He indicated there were days when he was covered in coal dust. 

Appellant would cough up dust and blow it out of his nose. His industrial exposure was similar 

during a 15-year stint as a private contract employee at the Paradise facility, which ended in 

2010. Dr. Haller also noted a 41-year smoking history of one and a half to two packs of 

cigarettes per day, with a recent decrease to one pack per day. Appellant reportedly retired two 

years ago. 

On physical examination, Dr. Haller noted dyspnea with exertion. Appellant had fairly 

minimal exertion at 100 yards on level ground and after 8 to 10 steps he had to stop and catch his 

breath. Dr. Haller reported no significant cough or wheezing. There was no chest pain or 

 2

 Appellant was a federal employee from 1977 until October 1994. OWCP accepted that he had been exposed to 

coal dust, asbestos and flue gas during his federal civilian service. Appellant continued to work as a pipefitter at the 

Paradise facility from 1995 through October 2010, but as a private contractor/employee. In addition to his industrial 

exposure, appellant reported a 41-year smoking history of at least one pack of cigarettes per day. 

3

 Dr. Baker is a certified B reader (National Institute for Occupational Safety and Health - NIOSH) with a 

demonstrated proficiency in classifying chest x-rays for pneumoconiosis. He is also Board-certified in both internal 

medicine and pulmonary disease. 

4

 Dr. Baker also diagnosed essential hypertension and ischemic heart disease, and noted a history of cardiac 

arrhythmia. 

5

 Appellant previously smoked one and a half to two packs of cigarettes per day, but for the past year he cut back 

to one pack per day. 
3

pressure and appellant’s lungs were clear. Dr. Haller characterized the examination as fairly 

unremarkable. He also indicated that appellant’s chest x-ray was essentially unremarkable. An 

electrocardiogram showed sinus rhythm with some premature ventricular complexes. Dr. Haller 

also administered a PFS which revealed a diffusion deficit, but was otherwise normal. However, 

the PFS results were questionable given appellant’s suboptimal and inconsistent effort. 

Dr. Haller also reviewed Dr. Baker’s July 6, 2012 findings. He noted that appellant’s 

physician did not find significant pulmonary function abnormalities. Dr. Haller explained that 

the basis for Dr. Baker’s finding was his chest x-ray interpretation of 1/0, which was a very 

subtle finding and open to interpretation. He recommended a high resolution computerized 

tomography (CT) scan for a more definitive answer regarding evidence of early interstitial 

disease. Based on his current examination, Dr. Haller did not find “any significant pulmonary 

disease, i.e., evidence for asbestosis or pneumoconiosis.” 

A January 2, 2013 chest CT scan revealed extensive emphysematous changes and no 

evidence of interstitial lung disease.6

 Small calcified granulomas were observed and there was 

no evidence of calcification along the pleural surface. 

In a January 10, 2013 supplemental report, Dr. Haller noted that he had reviewed the 

January 2, 2013 CT scan report. He reiterated the radiologist’s findings and indicated that this 

certainly would explain appellant’s diffusion deficit noted on PFS. Dr. Haller further indicated 

that there was no evidence of asbestosis or other occupational lung disease or any interstitial lung 

disease aside from the emphysema. He thought it very unlikely that appellant’s occupational 

exposures accounted for his disease. Dr. Haller stated that appellant did not have evidence of 

asbestosis or other pneumoconiosis, and it was very likely his disease was primarily due to heavy 

cigarette abuse. 

By decision dated January 18, 2013, OWCP denied the claim on the basis that appellant’s 

diagnosed pulmonary condition was not work related. It accorded determinative weight to 

Dr. Haller’s opinion in finding that appellant had not established causal relationship. 

Appellant timely requested an oral hearing. 

On April 25, 2013 appellant’s counsel contacted Dr. Haller and asked that he address 

whether the documented employment exposure contributed to appellant’s development of 

emphysema. In a May 1, 2013 response, Dr. Haller indicated that appellant’s chronic obstructive 

pulmonary disease (COPD) was principally due to his tobacco abuse. He further explained that 

heavy dust exposure had been shown to cause COPD, and in the presence of tobacco abuse, dust 

exposure accelerated decline. Dr. Haller indicated that it was possible that some of appellant’s 

work-related dust exposure contributed to his emphysema, but given his extensive smoking 

history, tobacco abuse clearly was the principle cause. 

In a May 16, 2013 report, Dr. Baker indicated that he had reviewed Dr. Haller’s findings. 

He noted that the reported reduced diffusion capacity would imply an abnormality in lung tissue 

 6

 Dr. Haller ordered the CT scan, which was interpreted by Dr. Abdelrahman M. Abdalla, a Board-certified 

diagnostic radiologist with a subspecialty in neuroradiology. 
4

such as emphysema. Dr. Baker further stated that the emphysematous changes noted on 

appellant’s CT scan could be due to his dust exposure as well as his cigarette smoking history, or 

more likely a combination of both. In conclusion, he stated that any respiratory impairment 

appellant had would be due, at least in part, to his dust exposure. 

In an August 2, 2013 decision, the hearing representative affirmed OWCP’ January 18, 

2013 denial of benefits. 

LEGAL PRECEDENT 

A claimant seeking benefits under FECA has the burden of establishing the essential 

elements of his or her claim by the weight of the reliable, probative and substantial evidence, 

including that an injury was sustained in the performance of duty as alleged and that any specific 

condition or disability claimed is causally related to the employment injury.7

To establish that an injury was sustained in the performance of duty, a claimant must 

submit: (1) medical evidence establishing the presence or existence of the disease or condition 

for which compensation is claimed; (2) a factual statement identifying employment factors 

alleged to have caused or contributed to the presence or occurrence of the disease or condition; 

and (3) medical evidence establishing that the diagnosed condition is causally related to the 

identified employment factors.8

ANALYSIS 

The Board finds that the case is not in posture for decision. 

Appellant’s physician, Dr. Baker, initially diagnosed mild bronchitis and occupational 

pneumoconiosis with pulmonary asbestosis, category 1/0. The latter diagnoses were based in 

part on Dr. Baker’s interpretation of appellant’s May 2, 2012 chest x-ray. Dr. Baker identified 

parenchymal abnormalities consistent with pneumoconiosis, but no pleural or other 

abnormalities. Small opacities were noted in the middle and lower zones of both lungs. 

Dr. Baker rated the film quality as grade 2, which is less than optimal.9

 He attributed appellant’s 

bronchitis and occupational pneumoconiosis to asbestos exposure, as well as other employmentrelated dusts, odors and fumes. Dr. Baker also identified cigarette smoking as a contributing 

factor. 

 7

 20 C.F.R. § 10.115(e), (f)(2012); see Jacquelyn L. Oliver, 48 ECAB 232, 235-36 (1996). Causal relationship is 

a medical question, which generally requires rationalized medical opinion evidence to resolve the issue. See 

Robert G. Morris, 48 ECAB 238 (1996). The fact that the etiology of a disease or condition is unknown or obscure 

does not relieve an employee of the burden of establishing a causal relationship by the weight of the medical 

evidence nor does it shift the burden of proof to OWCP to disprove an employment relationship. Judith J. Montage, 

48 ECAB 292, 294-95 (1997). 

8 Victor J. Woodhams, 41 ECAB 345, 352 (1989). 

9

 Dr. Baker’s reason for not rating the film grade 1 is not entirely legible. 
5

Appellant’s January 2, 2013 CT scan, which was interpreted by a Board-certified 

radiologist, revealed extensive emphysematous changes and no evidence of interstitial lung 

disease. The absence of interstitial lung disease on the CT scan undermines Dr. Baker’s positive 

interpretation of appellant’s May 2, 2012 chest x-ray. 

In his May 16, 2013 report, Dr. Baker indicated that the emphysematous changes noted 

on appellant’s CT scan could be due to dust exposure as well as cigarette smoking history, or 

more likely a combination of both. Based on this latest report, Dr. Baker appears to have 

abandoned his previous diagnosis of occupational pneumoconiosis with pulmonary asbestosis. 

Dr. Haller, who examined appellant at OWCP’s request, found no evidence of asbestosis 

or pneumoconiosis based on his December 13, 2012 evaluation. When he subsequently 

reviewed appellant’s CT scan, Dr. Haller indicated that appellant did not have evidence of 

asbestosis or other pneumoconiosis. He also noted that it was very likely that appellant’s 

emphysema was primarily due to heavy cigarette abuse. 

The Board finds that the evidence of record does not support a diagnosis of 

pneumoconiosis and/or asbestosis. However, there is ample evidence to support a diagnosis of 

emphysema. Appellant has a lengthy smoking history, which Dr. Haller identified as the 

primary or principle cause of his emphysema. The question remains as to whether appellant’s 

accepted employment exposure also contributed to his emphysema. Dr. Baker indicated that 

appellant’s emphysema was more likely due to a combination of his occupational dust exposure 

and cigarette smoking. When questioned by counsel, Dr. Haller indicated that appellant’s COPD 

was principally due to his tobacco abuse, and it was possible that some of his work-related dust 

exposure contributed to his emphysema. 

Appellant need not demonstrate that his occupational exposure was the sole or primary 

cause of his emphysema. The FECA Procedure Manual recognizes the following types of causal 

relationship: (1) direct causation; (2) aggravation (temporary or permanent); (3) acceleration; 

and (4) precipitation.10 As noted, Dr. Haller stated that it was possible that some of appellant’s 

work-related dust exposure contributed to his emphysema. While he did not definitively identify 

appellant’s employment exposure as a contributing factor, Dr. Haller also did not rule it out. 

Once OWCP undertakes development of the record, it must do a complete job in 

procuring medical evidence that will resolve the relevant issues in the case.11 Under the 

circumstances, it should seek further information and clarification from Dr. Haller.12 

Consequently, the case shall be remanded for further development. After OWCP has developed 

the record to the extent that it deems necessary, a de novo decision shall be issued. 

 10 Federal (FECA) Procedure Manual, Part 2 -- Claims, Causal Relationship, Chapter 2.805.2 (January 2013). 

11 Richard F. Williams, 55 ECAB 343, 346 (2004). 

12 See Federal (FECA) Procedure Manual, Part 3 -- Medical, OWCP Directed Medical Examinations, Chapter 

3.500.3f(2)(a) (July 2011). 
6

CONCLUSION 

The case is not in posture for decision. 

ORDER 

IT IS HEREBY ORDERED THAT the August 2, 2013 decision of the Office of 

Workers’ Compensation Programs is set aside and the case is remanded for further action 

consistent with this decision of the Board. 

Issued: March 5, 2014 

Washington, DC 

 

 Colleen Duffy Kiko, Judge 

 Employees’ Compensation Appeals Board 

 

 Alec J. Koromilas, Alternate Judge 

 Employees’ Compensation Appeals Board 

 

 James A. Haynes, Alternate Judge 

 Employees’ Compensation Appeals Board