Citation NR: 9801399 Decision Date: 01/20/98 Archive Date: 01/28/98 DOCKET NO. 95-42 190 ) DATE ) ) On appeal from the Department of Veterans Affairs Regional Office in Atlanta, Georgia THE ISSUE Entitlement to service connection for lung disease, claimed as asbestosis. REPRESENTATION Appellant represented by: Veterans of Foreign Wars of the United States WITNESS AT HEARINGS ON APPEAL Appellant ATTORNEY FOR THE BOARD M. L. Kane, Associate Counsel INTRODUCTION The veteran had active military service from October 1942 to February 1947. This matter comes before the Board of Veterans’ Appeals (Board) on appeal from an August 1995 rating decision of the Department of Veterans Affairs (VA) Regional Office (RO) in Atlanta, Georgia, which, in pertinent part, denied service connection for a pulmonary disorder due to exposure to asbestos. In July 1997, a hearing was held before the undersigned, who is the Board member making this decision and who was designated by the Acting Chairman to conduct that hearing pursuant to 38 U.S.C.A. § 7107(c) (West Supp. 1997). At the hearing, the veteran submitted additional evidence. As he has waived the RO’s consideration of this evidence, the case need not be remanded to the RO for consideration and the issuance of a supplemental statement of the case. See 38 C.F.R. § 20.1304(c) (1997). CONTENTIONS OF APPELLANT ON APPEAL The veteran contends that he has asbestosis as a result of exposure to asbestos during service while working in engine rooms. DECISION OF THE BOARD The Board, in accordance with the provisions of 38 U.S.C.A. § 7104 (West 1991 & Supp. 1997), has reviewed and considered all of the evidence and material of record in the veteran's claims file. Based on its review of the relevant evidence in this matter, and for the following reasons and bases, it is the decision of the Board that the preponderance of the evidence is against the claim of entitlement to service connection for asbestosis. FINDINGS OF FACT 1. The veteran’s claim that he has asbestosis as a result of exposure to asbestos during military service is plausible, and the RO has obtained sufficient evidence for an equitable disposition of this claim. 2. The balance of the medical evidence does not establish that the veteran has asbestosis. 3. Lung disease, claimed as asbestosis, was not incurred in or aggravated by service. CONCLUSIONS OF LAW 1. The veteran has presented a well-grounded claim for service connection for asbestosis, and VA has satisfied its statutory duty to assist him in developing facts pertinent to this claim. 38 U.S.C.A. § 5107(a) (West 1991); 38 C.F.R. §§ 3.103 and 3.326(a) (1997). 2. The veteran is not entitled to service connection for lung disease, claimed as asbestosis. 38 U.S.C.A. § 1110 (West 1991); 38 C.F.R. §§ 3.102, 3.303, and 3.304 (1997). REASONS AND BASES FOR FINDINGS AND CONCLUSIONS I. Factual Background In December 1994, the veteran filed a claim for service connection for asbestosis. His service medical records were already associated with the claims file. These records showed no objective findings regarding a pulmonary disorder. The report of his separation examination conducted in January 1947 indicated that a chest x-ray was negative. His notice of separation showed that his occupation during service was chief motor machinist mate. He had served on four different ships and had been stationed at the San Francisco, California, Naval Shipyard. The veteran submitted medical evidence in support of his claim. The report of a chest x-ray performed in June 1991 indicated that there were extensive hilar lymph node calcifications and scattered calcified granulomata throughout both lungs. Bilateral apical pleural thickening was also noted. There was no acute infiltrate or effusion. The report indicated that there had been no change from a study of July 1989. The report of a chest x-ray performed in June 1993 at Robert Wood Johnson University Hospital indicated that there were extensive calcific granulomata, consistent with old healed granulomatous disease. There was mild bilateral apical pleural thickening. An irregular one- centimeter nodular density with trailing margins was seen in the left apex posteriorly, probably in the apical posterior segment of the left upper lobe. It was not certain whether this was due to fibrosis or a possible solitary pulmonary lesion. The lungs were otherwise clear of acute disease. It was noted that underlying chronic obstructive pulmonary disease was suspected. The veteran also submitted a report by Andrew R. Freedman, M.D., of Pulmonary and Critical Care Associates dated August 1993. The report indicated that the veteran had an asymptomatic abnormal chest x-ray. He related a history of tuberculosis (TB) since he was a child. He also related a history of rather intense exposure to asbestos both during his many years as a maintenance mechanic, as well as during his years in the Navy from 1942 to 1947 where he worked in the engine room. He indicated that he had had a positive PPD (purified protein derivative of tuberculin) since he was a child. In 1962, he was assessed as having had TB and had received one year of isoniazid (INH) at Roosevelt Hospital. He indicated that he took a second course of anti- tuberculosis medication in 1983 during hospitalization at Newark Beth Israel Center. The veteran was asymptomatic with respect to his lungs. He had minimal cough or dyspnea. There was no sputum production. He had no wheezing. He indicated that he had smoked 1 1/2 packs of cigarettes per day for 35 years, but he stopped smoking in 1982. Examination of his lungs was unremarkable with no rales, wheezes, or use of accessory muscles. Dr. Freedman reviewed the chest x-ray from June 1993, as discussed above. He also reviewed the veteran’s chest x-rays from 1989 through 1991 and indicated that there had been no progression. Dr. Freedman stated that the abnormalities throughout the veteran’s x-rays would be consistent with his prior histories of TB as well as asbestos. Pulmonary function tests (PFTs) conducted in August 1993 showed a normal forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and forced expiratory volume in one second as percent of forced vital capacity (FEV1%). Flow rates at low lung volumes were mildly reduced. No evidence was encountered post-bronchodilator. Lung volumes were normal, and diffusing capacity was at the lower limits of normal. Dr. Freedman stated the study was consistent with very mild small airways dysfunction. Dr. Freedman indicated that the veteran had evidence of old TB, asbestosis, and perhaps mild allergic rhinitis and mild bronchitis. The veteran also submitted a letter from Robert J. Ollins, M.D., an internist, dated December 1994. Dr. Ollins stated that the veteran had, inter alia, asbestosis. It was noted that the veteran’s chest x-ray showed evidence of previous granulomatous disease with extensive hilar lymph calcification and calcified granulomata throughout both lungs. In February 1995, the veteran submitted a statement regarding his asbestos exposure. He indicated that prior to entry into service, he worked on a farm and at logging companies, and he had no knowledge of any asbestos exposure during this time. He stated that during service he worked in the engine rooms of various ships where the pipes were covered with asbestos and the pipe joints were bolted together with an asbestos sheet packing between the joints. He indicated that the pipe joints frequently leaked requiring that a section of the asbestos be removed and replaced. He also stated that the mufflers of the engines were covered with asbestos, and the asbestos had to be removed in order to replace the electrolysis rods every 60-90 days. He stated that the pipes in the living and dining areas were also covered with asbestos. He indicated that after May 1946, he worked at Hunters Point Naval Shipyard where he removed asbestos from pipes on ships that were being retired. After his separation from service, he was employed at a manufacturer of heavy machinery from 1947 until 1965. He stated that although there was some asbestos used in the factory for brakes and clutches, he did not work directly on building any of this equipment. He stated that he was told in 1960 that he had scarring of his lungs. He stated that the company he worked for from 1965 until 1983 probably used asbestos in some valves and pipes, but he did not have contact with it. He also indicated that he had smoked 1 1/2 packs of cigarettes per day from 1936 until 1982. With his statement, the veteran submitted additional medical evidence duplicative of the evidence he submitted with his claim in December 1994. In January 1995, the veteran underwent a VA physical examination. He related a history of pulmonary tuberculosis in 1964 due to pulmonary scarring. Examination of his lungs showed breath sounds were decreased at the right base. There were no wheezes on auscultation. There were no E to A changes (say E, E, E, comes out as A, A, A, upon auscultation of lung showing consolidation). The diagnosis was historical pulmonary fibrosis. Chest x-rays showed multiple calcified lymph nodes bilaterally. There were also multiple calcific densities in both lung parenchyma. There was an oval density with irregular margins at the head of the right clavicle. The radiologist indicated that this might represent overlapping shadows; however, an abnormality in this region could not be excluded. There were no pleural effusions. A rating decision of August 1995 denied service connection for asbestosis. In his substantive appeal, the veteran indicated that there were inaccuracies in the medical evidence. He stated that he did not have an active TB infection when he took medication in 1962, and he only took INH for 2-3 days in 1983. He stated that he had radiology reports from Roosevelt Hospital showing that he had scars on his lungs in 1960. He indicated that these were the first x- rays done after his separation from service. Associated with the claims file is the report of PFTs conducted in February 1996. It is not indicated where this test was conducted, however, the patient ID number on the report is the same as that used by the examiner who did the VA pulmonary examination in January 1995. The report showed that FVC was 97 percent of predicted, FEV1 was 83 percent of predicted, and FEV1% was 85 percent of predicted. The interpretation was borderline obstruction. In October 1996, the RO received a copy of a letter from Dr. Freedman to the veteran dated September 1993. Dr. Freedman indicated that the veteran had evidence of old TB and asbestosis. The abnormalities on his chest x-rays were stable. Breathing tests demonstrated some very mild bronchitis. It was recommended that the veteran have chest x-rays performed every six months for two years. In November 1996, the veteran had a hearing before a local Hearing Officer. He testified that he was positive for the tine test indicating TB as a child. He stated that a radiology report from 1972 stated “presumably tuberculosis,” and that was when he was placed on medication. In 1983, while hospitalized for another condition, he was told that he was having a relapse of TB and again placed on medication. He testified that he had never actually been diagnosed with TB. He stated that he first had problems with his lungs in 1960. After discovering scarring on his lungs, he was monitored until 1970 to see if anything developed. He indicated that he had had two diagnoses of asbestosis - from Dr. Freedman in 1993 and from Dr. Ollins in 1995. He stated that he had recently had a CT scan. He testified that since his separation from service, he had worked as a maintenance mechanic and an erector of heavy machinery, but he was not aware of any asbestos exposure. At the hearing, the veteran submitted additional evidence. He submitted a copy of a definition of silicosis. The veteran also submitted medical records from Newark Beth Israel Medical Center covering a period of hospitalization from January 1983 through February 1983. He was hospitalized for an unrelated condition, although a discharge diagnosis of chronic obstructive pulmonary disease was also rendered. He was transferred to Beth Israel from another medical facility where a lung scan was strongly suggestive of pulmonary emboli. The discharge summary indicated that the veteran was a known smoker of one pack per day for the past 45 years. A pulmonary angiogram was normal. A pulmonary arteriogram showed no evidence of overt thrombosis or embolization. He continued to have a low grade fever during hospitalization, and he was placed on INH for a one-week period. A Gallium scan was abnormal, and it showed multiple uptake areas in the bilateral lung base, greater on the right. A lung scan conducted on January 17, 1983, showed a matched ventilation and perfusion abnormality and low probability of pulmonary emboli. A lung scan conducted on February 10, 1983, showed multiple segmental perfusion defects compatible with pulmonary emboli, which were new since the prior study. The discharge summary indicated that a lung biopsy had showed chronic inflammatory cells. A pathology report indicated that bronchial washings were negative for malignant cells, but many bronchial epithelial cells and few histiocytes were present. Several chest x-rays were performed during the veteran’s period of hospitalization. X-rays conducted on January 14, 1983, showed extensive bilateral perihilar and parenchymal calcifications, probably due to previous granulomatous disease. There was no evidence of active infiltrate, pleural effusion, or pneumothorax. There was bilateral apical pleural thickening. X-rays conducted on January 17, 1983, showed extensive calcifications throughout the lungs, the hilar, and the periphery of the lungs suggesting an old granulomatous infection. There was widening of both apical pleura of indeterminate significance. X-rays conducted on January 18, 1983, also showed hilar and perihilar calcifications. There were also multiple small parenchymal calcifications bilaterally which could be due to old granulomatous disease. No pneumonic consolidation, pneumothorax, or pleural effusion was noted. X-rays conducted on January 21, 1983, showed extensive bilateral hilar calcifications and scattered calcifications in both lungs. There was evidence of bilateral apical pleural thickening. Both costophrenic sulci appeared to be clear. X-rays conducted on January 28, 1983, showed multiple calcifications in the hilar regions and scattered throughout the lungs, probably a residual of an old infection such as tuberculosis or other granulomatous disease. There was an abnormality in the left lung in the periphery which was not apparent in the study of January 21st. It was noted that this could be a new lesion developing, but the decubitus films were not optimum for further evaluating this point. Additional x-rays were conducted on January 29, 1983, and it was noted that there were developing pulmonary changes in the left base. It was noted on January 30, 1983, that the changes might represent areas of pneumonia or possibly infarction superimposed upon a residual of old pulmonary disease with calcifications in the lung and both hila. X-rays conducted on January 31, 1983, showed further progression of right basilar changes. A linear and trispiral tomography of the chest showed multiple peripheral pulmonary densities raising the question of septic emboli or organized infarcts or secondarily infected infarcts. X-rays conducted on February 1, 1983, showed no marked interval change. X- rays conducted on February 2, 1983, showed small calcified granulomata in the lungs bilaterally. There was extensive calcification of hilar nodes bilaterally. There was no evidence of acute inflammatory disease. X-rays conducted on February 8, 1983, showed an infiltrate at the left base which was not present on January 17th and was slightly more prominent than shown on February 1st. It was noted that opacifications in the posterior sulci suggested fluid or the residual of old pleural disease. The new change at the left base probably represented an area of pneumonia or infarction. The cause of the chronic pulmonary changes was emphysema, possibly associated with fibrotic disease and a residual of old granulomatous infection. The radiologist’s conclusion was that there was a background of chronic pulmonary disease with calcifications due to old granulomatous infection and suspected emphysematous changes and fibrotic pulmonary disease. X-rays done on February 10, 1983, showed a small effusion on the right with no evidence of effusion on the left. There was pulmonary emphysema and extensive calcification of the hilar nodes, as well as calcified granuloma in the lung. There was pleural reaction in the right costophrenic sulcus as well as increased markings at the right base posteriorly. X-rays conducted on February 16, 1983, showed ill-defined densities at the left base and along the lower right chest wall region. Both costophrenic sulci were clear. There were multiple calcific densities throughout both lungs, predominately in the hilar regions, rule-out tuberculosis or histosardosis [sic]. There was no definite evidence of pneumothorax. X-rays conducted on February 17, 1983, showed peripheral opacification in the left base and left apex with a cavity in the left apical region. There was also a small fixed pneumothorax in the left apex. Right-side apical pleural thickening was noted. There were bilateral marked calcifications in both hilar regions and the perihilar region. The findings were suggestive of multiple peripheral pulmonary densities raising the question of septic emboli, organized infarct, or secondary infected infarct. The veteran also submitted medical records from Roosevelt Hospital covering the period October 1960 through May 1974. X-rays conducted in October 1960 showed scattered, different- sized calcified densities throughout the lung fields bilaterally with conglomeration of calcified densities at the hilar regions bilaterally. The radiologist’s opinion was bilateral pulmonary calcifications, etiology to be determined. After these findings, chest x-rays were periodically performed. X-rays conducted in July 1961 showed no essential change since October 1960 in the disseminated small nodular calcifications throughout both lung fields and extensive calcifications in both hilar areas. No infiltrations were seen. Both costophrenic and diaphragms were irregular. The radiologist’s opinion was pulmonary calcifications. X-rays conducted in June 1962 showed scattered bilateral calcified densities, mostly at the hilar regions. The findings were unchanged. The radiologist’s opinion was bilateral pulmonary calcifications. X-rays conducted in January 1963 showed scattered calcified densities on both sides, with conglomerated calcified stippling at the hilar regions bilaterally. The findings were unchanged. The radiologist’s opinion was bilateral pulmonary calcifications. X-rays conducted in March 1964 showed scattered bilateral calcified densities, mainly in the hilar regions bilaterally. The radiologist’s opinion was bilateral pulmonary calcifications. X-rays conducted in May 1969 showed slight emphysema and numerous calcifications in both lungs and both hila. The appearance was unchanged since August 1965. No new infiltrate or effusion was present on x-rays in July 1970. X-rays conducted in July 1971 showed scattered calcifications predominately in the hilar regions and some emphysematous changes of the lungs. There was no infiltration. The radiologist’s opinion was evidence of previous inflammatory disease with no changes since July 1970. In August 1971, a diagnosis of old primary pulmonary tuberculosis was rendered, and the veteran was started on prophylactic INH. X-rays conducted in September 1972 showed mild to moderate bilateral emphysematous changes. There was apical pleural scarring and a moderate amount of perihilar, globular calcifications. There were also some calcifications throughout the lungs. The radiologist’s opinion was pulmonary emphysema with evidence of previous inflammatory disease, presumably tuberculosis. X-rays conducted in April 1973 showed numerous calcifications adjacent to the hilar regions which were coarse and globular. There were also several smaller calcifications scattered throughout the lungs, and there was apical pleural scarring. Emphysematous changes were also seen. X-rays conducted in May 1974 showed no changes. The veteran also submitted copies of his service medical records which were duplicative of evidence already associated with the claims file. The veteran also submitted a report by Mark Schlosberg, M.D., dated November 1995. He was referred to Dr. Schlosberg for a pulmonary evaluation regarding asbestos exposure. He denied any shortness of breath, coughing, wheezing, or dyspnea. He related a past medical history significant for a positive PPD test and prior INH therapy. He also related a history of asbestos exposure during service and a history of cigarette smoking approximately one-half pack per day for 35 years. Dr. Schlosberg reviewed a chest x-ray conducted in November 1995. The x-ray showed bilateral apical pleural thickening and left upper lobe irregular nodular calcifications. There were also calcifications in the right upper lobe, in the region of the right medial clavicular head. There were extensive calcifications of the hilar nodes, as well as some calcification in the region of the subcarinal nodes. Granuloma was noted in the left lower and right lower zones. There was a suggestion of some pleural thickening bilaterally laterally. No obvious calcified plaques were noted along the hemidiaphragm. The costophrenic angle was not as sharp on the right. The x-ray was compared to a prior study of January 1995, and the findings were essentially unchanged. Dr. Schlosberg also reviewed prior chest x-rays from June 1993, June 1991, and July 1989. It was noted that the findings were not noted on the x-ray reports from the 1960’s and 1970’s. Dr. Schlosberg’s impression was that the veteran had bilateral pulmonary granulomata, calcified with bilateral hilar calcification and apical pleural thickening, all suggestive of old tuberculosis. In addition, the finding of the blunted left costophrenic angle would support previous tuberculosis. There was a suggestion of bilateral pleural thickening laterally, as well as in the left costophrenic angle, which was not noted on old films. This may represent previous asbestos exposure, although no other pleural plaques were noted, especially along the hemidiaphragm. It was recommended that the veteran obtain a CT scan of the chest to look for pleural based plaques and interstitial changes which would suggest asbestosis. The veteran also submitted the report of a CT scan of the chest conducted in November 1996. There were numerous mediastinal and hilar calcified nodes consistent with healed granulomatous disease. There were no pleural effusions. There were scattered small calcified granulomata throughout both lungs. A 5 millimeter nodule was present in the left lung base which was not calcified and which could represent a granuloma, although specific etiology could not be determined. There were scattered foci of interstitial fibrosis with some of these foci associated with small areas of pleural thickening. The findings were typical for post- inflammatory scarring, possibly related to the veteran’s prior history of tuberculosis. Findings typical of asbestosis were not observed. The examiner’s impressions included: (1) multiple pulmonary calcified granulomata and multiple calcified hilar and mediastinal nodes, consistent with healed granulomatous disease; and (2) several small areas of interstitial disease with adjacent pleural thickening in both lungs, predominately in the upper lung zones, and most likely on the basis of previous granulomatous disease, definite findings of asbestosis not observed. The veteran also submitted medical literature in support of his claim. An article from the British Journal of Industrial Medicine entitled “Asbestotic radiological abnormalities among United States merchant marine seamen” indicated that one-third of chest x-rays reviewed of long-term (most had been at sea for more than 20 years) United States seamen showed parenchymal or pleural abnormalities. He submitted lists of articles regarding pulmonary diseases as a result of asbestos exposure from the National Institute for Occupational Safety and Health. An article from the American Journal of Industrial Medicine entitled “Asbestos-Related Chest X-Ray Changes Among Greek Merchant Marine Seamen” indicated that mariners may have asbestos-related disease many years from onset of exposure on ships. In December 1996, the RO received a statement from the veteran and medical reports from Roosevelt Hospital. This evidence was duplicative of evidence already associated with the claims file. The veteran indicated that he was seeking a second opinion from the Emory Pulmonary Clinic. Associated with the claims file is a report from Jeffrey Pine, M.D., of Pulmonary Medicine at the Emory Clinic dated January 1997. It was noted that the veteran wanted to know whether he had evidence of asbestos exposure and wanted an opinion regarding a pulmonary nodule. It was indicated that the veteran was being followed by Dr. Ollins, his primary physician, and Dr. Schlosberg, his pulmonologist. The veteran brought extensive records concerning prior hospitalizations, evaluations, a CT scan, and old x-rays. He related a history of asbestos exposure during service. Dr. Pine reviewed the x-rays from the 1960’s and 1970’s, as described above. Dr. Pine also reviewed x-rays from 1989, 1991, 1993, and November 1995. He also reviewed the CT scan from November 1996, as described above. Dr. Pine indicated that the CT scan showed some areas of focal linear fibrosis, but not what one would expect to see with asbestos exposure (i.e., diffuse interstitial fibrosis of the lung bases). Dr. Pine stated that this was not seen, and no significant pleural plaques were seen either. Clinically, the veteran did not complain of shortness of breath, coughing, wheezing, or significant dyspnea. There was no history of histoplasmosis (i.e., obvious exposure to the Ohio- Mississippi Valley area), but he did have a history of having a positive PPD as a young child in 1933. Dr. Pine’s impression was history of asbestos exposure while in the service. However, there was nothing to suggest obvious asbestosis or complications (i.e., CT scan did not show any pleural plaques or diffuse interstitial fibrosis). He did not have any rales or clubbing. He did have a pulmonary nodule that was non-calcified that might represent a neoplasm, but this could also be part of the diffuse granulomatis disease noted on his x-ray that had been present in the past. However, there was no old CT scan beyond November 1996 to see if the nodule was present previously. In July 1997, the veteran had a hearing before a Member of the Board. He stated that he was not exposed to asbestos after his separation from service. He indicated that he believed the scarring in his lungs was caused by exposure to asbestos and that it took a number of years after exposure for it to manifest itself in scarring. He indicated that Dr. Freedman found that the veteran had evidence of asbestos, and he was a pulmonary doctor. Dr. Ollins was the veteran’s primary care doctor. He stated that Doctors Schlosberg and Pine were basing their opinions that the veteran did not have asbestosis on CT reports and studies. He contended that readings he had done indicated that CT scans were useful, but should not be used as a final decision. He stated that he was aware that the doctors stated that he did not have asbestosis, but that he contended that the scarring was directly related to asbestos exposure. At his hearing before the Board, the veteran submitted additional evidence and signed a statement waiving the RO’s consideration of that evidence. The veteran’s statement dated May 1997 indicated that Doctors Freedman, Schlosberg, and Pine had not taken into account the fact that the scarring in his lungs occurred somewhere between his separation from service in 1947 and the first x-ray taken after separation from service in 1960. He contended that the scarring in his lungs was a manifestation of exposure to asbestos. He submitted the report of PFTs conducted in April 1997 which showed mild obstruction, no restriction, and decreased diffusion. He also submitted an article which indicated that tuberculosis commonly occurred in association with other disease processes, such as silicosis. The veteran also submitted the report of a CT scan of the chest conducted in May 1997. This study was compared with a prior one conducted in February 1997. There was no definite evidence for adenopathy. It was again noted that there were small areas of chronic interstitial process involving both apices, the posterior aspect of the left upper lobe, the peripheral aspect of the left mid-lung field, the anterior aspect of the right middle lobe, and the anterior aspect of the left lower lobe. There were a few small nodular densities demonstrated and focal areas of very localized pleural thickening, but they all had an identical anatomic appearance. There was evidence of prior granulomatous disease. There was no change in the tiny calcified granuloma as well as very tiny nodule of soft tissue density. There had been no interval change since February 1997, and it was noted that the February 1997 study had shown no interval change since the November 1996 study. II. Legal Analysis A. Well-Grounded Claim Service connection means that the facts, shown by evidence, establish that a particular injury or disease resulting in disability was incurred coincident with active military service or, if pre-existing such service, was aggravated during service. 38 U.S.C.A. § 1110 (West 1991); 38 C.F.R. § 3.303(a) (1997). A person seeking benefits under a program administered by the Secretary must submit a claim that is well grounded. 38 U.S.C.A. § 5107(a) (West 1991). A claim for direct service connection requires three elements to be well grounded. First, there must be competent (medical) evidence of a current disability. Second, there must be competent (lay or medical) evidence of incurrence or aggravation of disease or injury during active service. Third, there must be competent (medical) evidence of a nexus between the inservice disease or injury and the current disability. Caluza v. Brown, 7 Vet. App. 498, 506 (1995), aff’d 78 F.3d 604 (Fed.Cir. 1996) (table). The veteran has presented credible evidence of exposure to asbestos during service. He has presented medical evidence containing a diagnosis of asbestosis, and that diagnosis was based, at least in part, on the history of exposure to asbestos during service, although it also apparently relied upon what the doctor represented as “intense” exposure to asbestos post-service. Assuming the credibility of this evidence, the claim must be said to be plausible, and therefore well grounded. The veteran having stated a well-grounded claim, the Department has a duty to assist in the development of facts relating to the claim. 38 U.S.C.A. § 5107(a) (West 1991). In this case, medical records have been obtained, examinations provided, and hearings held. There is no indication of additional relevant evidence that would be needed to evaluate the claim fairly. There is no statute specifically dealing with asbestos and service-connection for asbestos-related diseases, nor has the Secretary promulgated any specific regulations. However, in 1988, VA issued a circular on asbestos-related diseases which provided guidelines for considering asbestos compensation claims. See Department of Veterans Benefits, Veterans' Administration, DVB Circular 21-88-8, Asbestos-Related Diseases (May 11, 1988). The information and instructions contained in the DVB Circular have since been included in VA Adjudication Procedure Manual, M21-1, part VI, para. 7.21 (January 31, 1997) (hereinafter M21-1). VA must analyze the veteran’s claim of entitlement to service connection for asbestosis under these administrative protocols using the following criteria. Ennis v. Brown, 4 Vet. App. 523, 527 (1993); McGinty v. Brown, 4 Vet. App. 428, 432 (1993). The latency period for asbestos-related diseases varies from 10 to 45 or more years between first exposure and development of disease. M21-1, Part VI, 7.21(b)(2), p. 7-IV- 3 (January 31, 1997). An asbestos-related disease can develop from brief exposure to asbestos. Id. Some of the major occupations involving asbestos exposure include work in shipyards. M21-1, Part VI, 7.21(b)(1), p. 7-IV-3 (January 31, 1997). There is a prevalence of asbestos-related disease among shipyard workers since asbestos was used extensively in military ship construction. M21-1, Part VI, 7.21(b)(2), p. 7-IV-3 (January 31, 1997). It is a fact that many U.S. Navy veterans during World War II were exposed to chrysotile products, as well as amosite and crocidolite, since these varieties of African asbestos were used extensively in military ship construction. Id. With asbestos-related claims, the Board must also determine whether the claim-development procedures applicable to such claims have been followed. Ashford v. Brown, 10 Vet. App. 120, 124-125 (1997) (while holding that the veteran’s claim had been properly developed and adjudicated, the Court indicated that the Board should have specifically referenced the DVB Circular and discussed the RO’s compliance with the Circular’s claim-development procedures). With these claims, the RO must determine whether or not military records demonstrate evidence of asbestos exposure during service, develop whether or not there was pre-service and/or post- service occupational or other asbestos exposure, and determine whether there is a relationship between asbestos exposure and the claimed disease, keeping in mind the latency and exposure information discussed above. M21-1, Part VI, 7.21(d)(1), p. 7-IV-3 and 7-IV-4 (January 31, 1997). In this case, the record shows that the RO complied with these procedures. The Department has satisfied its duty to assist. B. Application of the Law to the Facts The veteran’s contentions regarding exposure to asbestos during service are plausible. Furthermore, his service records indicate that he was stationed at a naval shipyard, that he served on board a number of vessels, and that his main occupation was chief motor machinist mate. There is no evidence contradicting the veteran’s assertions of exposure, and his assertions are consistent with his service occupation and duty. Based on this evidence, exposure to asbestos during service is established. See McGinty v. Brown, 4 Vet. App. 428 (1993) (held that the veteran’s testimony as to the cause of his disease was not competent evidence of causation because the determination of the cause of a disease is a medical matter; however, the veteran was competent to testify as to the facts of his asbestos exposure, i.e., wearing asbestos gloves while performing his duties as a “hot caseman” in the Navy). As to the remainder of the elements of the veteran’s claim, the record includes some medical evidence supporting a diagnosis of asbestosis. It also includes medical evidence that is not favorable to his claim. Therefore, the Board must assess this evidence in rendering a decision, including an analysis of the credibility and probative value of the evidence, accounting for evidence which it finds to be persuasive or unpersuasive, and providing reasons for rejecting any evidence favorable to the veteran. See Masors v. Derwinski, 2 Vet. App. 181 (1992); Hatlestad v. Derwinski, 1 Vet. App. 164 (1991); Gilbert v. Derwinski, 1 Vet. App. 49 (1990). Moreover, the Board may not base a decision on its own unsubstantiated medical conclusions, but, rather, may reach a medical conclusion only on the basis of independent medical evidence in the record or adequate quotation from recognized medical treatises. See Colvin v. Derwinski, 1 Vet. App. 171 (1991). Evidence in support of the veteran’s claim includes Dr. Freedman’s report from August 1993 and Dr. Ollins’ letter of December 1994. Evidence not favorable to his claim includes Dr. Pine’s report from January 1997 and Dr. Schlosberg’s report from November 1995. In this case, the preponderance of the evidence is against the claim for service connection for asbestosis because the medical evidence unfavorable to his claim is more persuasive and of greater weight than the favorable medical evidence. First, Dr. Freedman’s assessment was not phrased in terms of a definitive diagnosis of asbestosis. Rather, it was phrased as an assessment of “evidence of” asbestosis, as well as old TB. Next, Dr. Ollins did not apparently diagnose asbestosis, but listed it as one of ten conditions for which he was following the veteran. The veteran has indicated that Dr. Ollins is his primary care physician and not a pulmonary specialist. Dr. Ollins may have simply listed Dr. Freedman’s assessment of asbestosis. It does not appear that he conducted any medical tests of his own sufficient to diagnose or rule out asbestosis. The medical evidence from Dr. Pine indicating that the veteran does not have asbestosis is more probative than Dr. Freedman’s assessment for the following reasons. First, Dr. Pine conducted an extensive review of the veteran’s prior medical history, including the chest x-rays from the 1960’s and 1970’s, prior to rendering an opinion. Contrary to the veteran’s contention that Dr. Pine only based his opinion on the results of a CT scan, Dr. Pine’s report showed that he considered several other reports and studies. In support of his opinion, Dr. Pine delineated the specific findings of asbestosis that the veteran did not have (i.e., diffuse interstitial fibrosis of the lung bases, pleural plaques, rales, or clubbing). His opinion was based on review of the veteran’s medical history with consideration of the findings of other health professionals, unlike Dr. Freedman’s assessment in August 1993. Furthermore, Dr. Pine’s opinion was based on the more recent medical evidence, including the results of a CT scan in 1996. Second, Dr. Freedman indicated that the abnormalities on the veteran’s chest x-rays would be consistent with tuberculosis as well as asbestosis. No effort was made to differentiate between the two conditions, and Dr. Freedman did not discuss the specific objective findings that would support a diagnosis of asbestosis. Additional support for Dr. Pine’s opinion that the veteran does not have asbestosis can be found in the rest of the medical evidence. A lung biopsy performed in 1983 only showed chronic inflammatory cells, and there was no indication that there was evidence of asbestosis. Dr. Schlosberg stated that the findings of bilateral pulmonary granulomata, calcified with bilateral hilar calcification and apical pleural thickening, all suggested old tuberculosis. The only possible finding indicative of asbestos-related disease was a suggestion of bilateral pleural thickening laterally as well as in the left costophrenic angle. Dr. Schlosberg stated this “may” represent previous asbestos exposure, but it was also noted that no other pleural plaques were found. The radiographic changes that would be indicative of asbestos exposure include interstitial pulmonary fibrosis (asbestosis), pleural effusions and fibrosis, pleural plaques, mesotheliomas of pleura and peritoneum. M21-1, Part VI, 7.21(a)(1), p. 7-IV-3 (January 31, 1997). Granulomatous disease or calcific changes are not included in this list of representative changes. Despite the abnormal chest x-ray findings from 1960 through 1983, as detailed above, none of the medical examiners during this time period stated that the veteran had findings indicative of asbestosis. Rather, the abnormal findings, including the scarring of his lungs, were consistently related to old healed granulomatous disease such as tuberculosis. A diagnosis of old primary pulmonary tuberculosis was rendered in 1971, and the veteran was treated with INH. The veteran’s contention that the abnormal x-ray findings beginning in 1960, including the scarring of his lungs, were due to asbestos exposure is not competent evidence. There is no evidence that he possesses the requisite medical knowledge to render a probative opinion that any lung condition is in any manner related to his period of service. Grottveit v. Brown, 5 Vet. App. 91, 93 (1993) (citing Espiritu v. Derwinski, 2 Vet. App. 492 (1992)). The article submitted by the veteran referring to a relationship between tuberculosis and silicosis is irrelevant. This evidence does not relate the veteran’s tuberculosis to his alleged asbestos exposure during service. Likewise, the various articles regarding the incidence of asbestosis in seamen also have no bearing on the veteran’s particular situation. For these reasons, the Board concludes that the evidence against the veteran’s claim is more probative and of greater weight and, based on this evidence, finds as fact that the veteran does not have asbestosis as a result of his military service. Accordingly, for the reasons and bases given above, the preponderance of the evidence is against the claim for service connection for asbestosis, and he is not entitled to the application of the benefit of the doubt. See 38 U.S.C.A. § 5107(b) (1996). ORDER Entitlement to service connection for asbestosis is denied. J. SHERMAN ROBERTS Member, Board of Veterans' Appeals NOTICE OF APPELLATE RIGHTS: Under 38 U.S.C.A. § 7266 (West 1991 & Supp. 1997), a decision of the Board of Veterans' Appeals granting less than the complete benefit, or benefits, sought on appeal is appealable to the United States Court of Veterans Appeals within 120 days from the date of mailing of notice of the decision, provided that a Notice of Disagreement concerning an issue which was before the Board was filed with the agency of original jurisdiction on or after November 18, 1988. Veterans' Judicial Review Act, Pub. L. No. 100-687, § 402, 102 Stat. 4105, 4122 (1988). The date which appears on the face of this decision constitutes the date of mailing and the copy of this decision which you have received is your notice of the action taken on your appeal by the Board of Veterans' Appeals. - 2 -