Citation Nr: 0917372 Decision Date: 05/08/09 Archive Date: 05/19/09 DOCKET NO. 07-39 858 ) DATE ) ) On appeal from the Department of Veterans Affairs Regional Office in St. Petersburg, Florida THE ISSUES 1. Entitlement to service connection for the cause of the Veteran's death. 2. Entitlement to service connection for tinnitus for accrued benefits purposes. 3. Entitlement to an initial compensable rating for bilateral hearing loss for accrued benefits purposes. REPRESENTATION Appellant represented by: Veterans of Foreign Wars of the United States WITNESSES AT HEARING ON APPEAL Appellant and friend ATTORNEY FOR THE BOARD Nancy S. Kettelle, Counsel INTRODUCTION The Veteran served on active duty from October 1967 to October 1969; his decorations and awards included the Combat Infantryman's Badge and the Bronze Star Medal. This matter comes to the Board of Veterans' Appeals (Board) on appeal from a November 2006 rating decision of the Department of Veterans Affairs (VA) Regional Office (RO) in St. Petersburg, Florida. The appellant and a friend testified at a Board hearing held at the RO in January 2009. The issues of entitlement to service connection for tinnitus for accrued benefits purposes and entitlement to an initial compensable rating for bilateral hearing loss for accrued benefits purposes are addressed in the REMAND portion of the decision below and are REMANDED to the RO via the Appeals Management Center (AMC), in Washington, DC. Other matters In May 2005, the Veteran filed his claim for service connection for progressive supranuclear palsy, Parkinson's like syndrome. In an August 2005 rating decision, the RO denied the service connection claim. The record shows that the RO received the Veteran's notice of disagreement with its decision in January 2006. The Veteran died in May 2006, and the appellant filed her VA Form 21-534, Application for Dependency and Indemnity Compensation, Death Pension and Accrued Benefits by a Surviving Spouse or Child, in June 2006. Although the Veteran's claim for service connection for progressive supranuclear palsy, Parkinson's like syndrome, was pending at the time of his death and the appellant filed a claim for accrued benefits shortly after his death, there is no indication that the RO has adjudicated that claim, that is, entitlement to service connection for progressive supranuclear palsy, Parkinson's like syndrome, for accrued benefits purposes. The Board refers that issue to the RO for adjudication. FINDINGS OF FACT 1. The Veteran had active military service in the Republic of Vietnam from March 1968 to March 1969, which entitles him to the presumption of exposure to herbicide agents in service; in addition, there is credible evidence that he was personally exposed to herbicide agents and other toxins during that time. 2. Competent medical evidence relates the Veteran's atypical Parkinsonism plus with signs and symptoms of progressive supranuclear palsy to his in-service exposure to herbicide agents and other toxins. 3. The Veteran died in May 2006, and the Certificate of Death lists aspiration pneumonia as the immediate cause of his death with severe Parkinson's plus, supranuclear palsy, as the underlying cause. CONCLUSION OF LAW A service-connected disability caused the Veteran's death, and service connection for the cause of the Veteran's death is established. 38 U.S.C.A. §§ 1310, 5107 (West 2002); 38 C.F.R. §3.312 (2008). REASONS AND BASES FOR FINDINGS AND CONCLUSION The Board acknowledges that VA has duties related to notice and assistance to a claimant in the development of a claim as mandated under the provisions of 38 U.S.C.A. §§ 5103, 5103A (West 2002 & Supp. 2008) and 38 C.F.R. § 3.159 (2008). In this case, the Board concludes that no further notice or assistance is required as the outcome of the Board's decision is favorable to the appellant, and no prejudice to the appellant could result from this adjudication. See Bernard v. Brown, 4 Vet. App. 384. 393 (1993). As noted in the Introduction, the appellant provided testimony at a Board hearing in January 2009. In addition, she has submitted evidence to the Board for which she has waived initial review by the RO. The appellant is seeking service connection for the cause of the Veteran's death due to aspiration pneumonia for which the underlying cause was his Parkinsonism and supranuclear palsy. The appellant contends this disability was related to the Veteran's exposure to herbicides and other toxins during his service in Vietnam. To establish service connection for the cause of death, the evidence must show that disability incurred in or aggravated by service either caused or contributed substantially or materially to the cause of death. 38 U.S.C.A. § 1310; 38 C.F.R. § 3.312. For a service connected disability to be the cause of death, it must singly or with some other condition be the immediate or underlying cause, or be etiologically related. 38 C.F.R. § 3.312(b). For a service-connected disability to constitute a contributory cause, it is not sufficient to show that it causally shared in producing death; rather, it must be shown that there was a causal connection. 38 C.F.R. § 3.312(c). In general, service connection may be granted for disability resulting from disease or injury incurred in or aggravated during active military service. 38 U.S.C.A. § 1110; 38 C.F.R. § 3.303. Service connection may be granted on a presumptive basis for certain chronic diseases, including organic diseases of the nervous system, if manifested to a degree of 10 percent or more within one year of separation from active service. 38 U.S.C.A. §§ 1101, 1112 (West 2002); 38 C.F.R. §§ 3.307(a)(3), 3.309(a) (2008). Service connection may also be established for disease diagnosed after discharge from service when all the evidence establishes that the disease was incurred in service. 38 U.S.C.A. § 1113(b); 38 C.F.R. § 3.303(d). A veteran who had active service in the Republic of Vietnam at any time from January 9, 1962, to May 7, 1975, will be presumed to have been exposed to an herbicide agent during that service. 38 U.S.C.A. § 1116(f); 38 C.F.R. § 3.307(a)(6)(iii). For the purposes of 38 C.F.R. § 3.307, the term herbicide agent means a chemical in an herbicide used in support of the United States and allied military operations in the Republic of Vietnam during the period beginning on January 9, 1962, and ending on May 7, 1975, specifically: 2,4-D, 2,4,5-T and its contaminant TCDD; cacodylic acid; and picloram. 38 C.F.R. § 3.307(a)(6)(i). When such a veteran develops a disorder listed in 38 C.F.R. § 3.309(e), which disorders have been shown to be caused by exposure to Agent Orange, to a degree of 10 percent or more within the specified period, the disorder shall be presumed to have been incurred during service. 38 U.S.C.A. § 1116; 38 C.F.R. §§ 3.307(a)(6), 3.309(e). Diseases to which the presumption applies are: chloracne or other acneform diseases consistent with chloracne, Type 2 diabetes (also known as Type II diabetes mellitus or adult- onset diabetes), Hodgkin's disease, chronic lymphocytic leukemia, multiple myeloma, non-Hodgkin's lymphoma, acute and subacute peripheral neuropathy, porphyria cutanea tarda, prostate cancer, respiratory cancers (cancer of the lung, bronchus, larynx, or trachea) and soft-tissue sarcomas (other than osteosarcoma, chondrosarcoma, Kaposi's sarcoma, or mesothelioma). 38 U.S.C.A. § 1116; 38 C.F.R. § 3.309(e). The above-listed diseases shall have become manifest to a degree of 10 percent or more at any time after service, except that chloracne or other acneform disease consistent with chloracne, porphyria cutanea tarda, and acute and subacute peripheral neuropathy shall have become manifest to a degree of 10 percent or more within a year after the last date on which the veteran was exposed to an herbicide agent during active military, naval, or air service. 38 U.S.C.A. § 1116; 38 C.F.R. §§ 3.307(a)(6)(ii). VA has determined that a presumption of service connection based on exposure to herbicides used in the Republic of Vietnam during the Vietnam era is not warranted for any condition for which VA has not specifically determined a presumption of service connection is warranted. See 59 Fed. Reg. 341-46 (1994); 61 Fed. Reg. 414421 (1996); 64 Fed. Reg. 59232 (1999); 67 Fed. Reg. 42600-08 (2002); 68 Fed. Reg. 27,630-41 (2003). More recently, VA clarified that a presumption of service connection based on exposure to herbicides used in the Republic of Vietnam during the Vietnam era is not warranted for the following conditions: hepatobiliary cancers; oral, nasal, and pharyngeal cancer; bone and joint cancer; leukemia (other than chronic lymphocytic leukemia (CLL); skin cancers (melanoma, basal, and squamous cell); breast cancer; cancers of the female reproductive system (cervix, uterus, ovary); testicular cancer; urinary bladder cancer; renal cancer; abnormal sperm characteristics and infertility; spontaneous abortion; neonatal or infant death and stillbirth in offspring of exposed individuals; low birthweight in offspring of exposed individuals; neurobehavioral disorders (cognitive and neuropsychiatric); movement disorders including Parkinson's disease and amyotrophic lateral sclerosis (ALS); chronic peripheral nervous system disorders; respiratory disorders (other than certain respiratory cancers); gastrointestinal, metabolic, and digestive disorders (changes in liver enzymes, lipid abnormalities, ulcers); immune system disorders (immune suppression, autoimmunity); circulatory disorders; amyloid light-chain (AL) amyloidosis; endometriosis; effects on thyroid homeostasis; gastrointestinal tumors (esophagus, stomach, pancreas, colon, rectum); brain tumors; and any other condition for which the Secretary has not specifically determined a presumption of service connection is warranted. See 72 Fed. Reg. 32395-407 (2007). Notwithstanding the foregoing, the United States Court of Appeals for the Federal Circuit has determined that the Veterans' Dioxin and Radiation Exposure Compensation Standards (Radiation Compensation) Act, Pub. L. No. 98-542, § 5, 98 Stat. 2724, 2727- 29 (1984), does not preclude a veteran from establishing service connection with proof of actual direct causation. Combee v. Brown, 34 F.3d 1039 (Fed. Cir. 1994). The United States Court of Appeals for Veterans Claims (Court) has specifically held that the provisions of Combee are applicable in cases involving Agent Orange exposure. McCartt v. West, 12 Vet. App. 164, 167 (1999). Direct service connection can be established by "showing that the disease or malady was incurred during or aggravated by service, "a task which "includes the difficult burden of tracing causation to a condition or event during service." Combee 34 F.3d at 1043. In order to prevail on direct service connection there must be medical evidence of a current disability; medical evidence, or in certain circumstances, lay evidence of in-service occurrence or aggravation of a disease or injury; and medical evidence of a nexus between an in-service injury or disease and the current disability. See Hickson v. West, 12 Vet. App. 247, 253 (1999); see also Pond v. West, 12 Vet App. 341, 346 (1999). The standard of proof to be applied in decisions on claims for veterans' benefits is set forth in 38 U.S.C.A. § 5107. A claimant is entitled to the benefit of the doubt when there is an approximate balance of positive and negative evidence. See 38 C.F.R. § 3.102. When a claimant seeks benefits and the evidence is in relative equipoise, the claimant prevails. See Gilbert v. Derwinski, 1 Vet. App. 49 (1990). The preponderance of the evidence must be against the claim for benefits to be denied. See Alemany v. Brown, 9 Vet. App. 518 (1996). In this case, as of the time of his death, the only disability for which service connection had been granted was bilateral hearing loss, rated as noncompensably disability. The veteran died in May 2006, and the Certificate of Death lists aspiration pneumonia as the immediate cause of death and severe Parkinson's plus, supranuclear palsy, as the underlying cause. The Veteran's service treatment records do not include any complaint or finding that has been related to Parkinson's disease, Parkinsonism, or supranuclear palsy, and there is no medical evidence of such within the first post-service year. Records from the University of South Florida, College of Medicine Medical Clinics show that the Veteran was first seen in the neurology clinic in November 2003. At that time, the appellant reported that the Veteran had a history of having developed a cough about a year earlier that had been treated as a respiratory problem, but it had never cleared up. She reported that in August 2003, the Veteran's right eye appeared to be bulging and his left eye appeared to be more sunken. His speech was noted to be slurred at that time. She also reported that the Veteran appeared more rigid in his normal gait and was somewhat unsteady, especially on a ladder. The Veteran reported vision changes had occurred, with blurring and double vision. The appellant noted that the Veteran had been gritting his teeth and had broken two teeth in the past three months. She also remarked on memory changes and a silly laugh. The medical records from the University of South Florida Medical Clinics document extensive laboratory studies and tests. On a long term disability insurance form dated in July 2004, the Veteran reported he had been unable to work since January 2004, and a neurologist, Theresa A. Zesiewicz, M.D., Assistant Director, Parkinson's Disease and Movement Disorders Center at the University of South Florida, stated the Veteran was unable to work and that his diagnoses were progressive supranuclear palsy and Parkinson-like syndrome. In a letter dated in March 2005, Dr. Zesiewicz noted that the Veteran had been exposed to Agent Orange in service, and that his wife, the appellant here, was concerned about dioxin. Dr. Zesiewicz referred the Veteran to a VA neurologist, J.S, M.D. She also stated that an input would be appreciated from Dr. Leon Prockop, whom she described as a world-renowned neurotoxicologist. VA medical records show the Veteran saw the VA neurologist, J.S, M.D., in May 2005. The neurologist noted it was reported that the Veteran's first symptoms began in 2003, that the Veteran fell in March 2003 requiring stitches to the left brow, and that in September 2003 he had gone to an emergency room with stroke-like symptoms, blurred and double vision, slurred speech, inappropriate laugh, unsteady gait, coughing, and problems swallowing, but that no stroke was found. The physician further noted that a MRI (magnetic resonance imagining) study had shown hyperintensity in the periventricular white mater and that the Veteran's neurologist had noted extrapyramidal syndrome. Sinemet had been started in August 2004. On examination, Dr. J.S. noted that Veteran's mental status was grossly normal but that he could not perform sequential movement of the hand-Luria test, which was said to be indicative of marked executive function deficit. There was limited excursion and range of voluntary gaze, speech was dysarthric, but understandable. All movement of the tongue and mouth were slow. There was marked axial rigidity of muscles with rigidity in limbs less that in the axial muscles. There was mild to moderate slowness of hand movements and finger taps. Rapid alternating movements were clumsy. There were no resting, postural, or action tremors. The Veteran was slow to rise; he had good stride, but poor arm swing and poor postural reflexes. Deep tendon reflexes showed hyper-reflexia with spread. The impression was atypical Parkinsonism partially responsive to dopamine replacement. Dr. J.S. said that the marked deficit in voluntary gaze, axial rigidity, and Parkinsonism suggest the diagnosis of progressive supranuclear palsy. He said the etiology was not clear. He noted that the Veteran had a history of exposure to toxicants used in Vietnam but that as far as he knew there was no clustering of progressive supranuclear palsy in veterans, but this might become evident with time. On referral for a second opinion, Dr. Prockop of the University of South Florida Physicians Group examined the Veteran in May 2005. He noted the Veteran had been referred by Dr. Zesiewicz for a second opinion with respect to his progressive supranuclear palsy and possible connection to Agent Orange during his Vietnam experience. After review of the Veteran's medical records and physical examination, Dr. Prockop said he knew of no significant database to link the Agent Orange exposure to the Veteran's neurodegenerative process. He suggested an additional MRI of the brain to exclude progressive ischemic disease as a potential etiology. The physician said he would review the literature base to see if there was any further data on this potential connection. After a July 2005 visit, Dr. Prockop said he was continuing to review data concerning dioxin and its potential relationship to the Veteran's condition. Dr. Prockop said that at the present, he could say it is possible that there is a connection between the Veteran's dioxin exposure and his Parkinson plus syndrome but that at the present time, probability could not be established. He said that with further investigation that perhaps a probable statement could be made. In addition, in a letter dated in August 2005, Dr. Zesiewicz said the Veteran's opthalmoplegia and masked facies as well as cogwheel rigidity and extra paramedical dysfunction fit the picture of a Parkinson plus syndrome, possibly progressive supranuclear palsy. She said it was possible that there is a connection between the Veteran's exposure to Agent Orange and his development of Parkinsonism but the exact etiology was unclear. In a VA neurology clinic follow-up note dated in August 2005, it was noted that in 2003 the Veteran has been diagnosed as having progressive supranuclear palsy by Dr. Zesiewicz and that he had initially presented with slurred speech, swallowing difficulties and poor coordination. In August 2005, the Veteran complained continued fatigue, drooling, and swallowing difficulties with choking on liquids and saliva. In addition, he complained of memory difficulties, gait problems, stiff posture, and stiffness of the neck. The assessment after examination was questionable progressive supranuclear palsy. The plan included obtaining a swallow evaluation via speech therapy with the possibility for percutaneous endoscopic gastrostomy (PEG) tube placement in the near future. After testing in the speech pathology clinic in September 2005, the speech pathology section chief said that although there was no aspiration observed on the study of that date, the Veteran should be considered at risk for aspiration on all consistencies and required careful feed and modified diet consistency. It was further noted that the Veteran had had previously documented aspiration of both thin and nectar-thick liquid. In a November 2005 statement, prepared with the assistance of the appellant and received at the RO in January 2006, the Veteran reported that after completing advanced training, he was assigned to Co. A, 2nd Battalion, 508th Infantry 3rd Brigade 82nd Airborne Division and in late February 1968, his brigade was deployed to Vietnam. In this regard, the Board notes that the National Personnel Records Center (NPRC) has reported the Veteran was in Vietnam from March 1968 to March 1969. In his narrative, the Veteran reported that in April 1968 he was transferred to Co. A, 2nd Battalion, 505th Infantry, 82nd Airborne Division. He said that for the first several days after his transfer, his MOS (military operational specialty) was 11C10, ammo bearer and handler. He said his MOS was then changed to 36K20, forward radio operator and in that capacity he relayed combat operational information and information pertaining to battle coordination. He said that after the Citadel had been retaken during the battle of Hue, the 505th moved south to the III Corps military region where Bien Hoa was the base of operations. The Veteran pointed out that the adjacent Bien Hoa Air force Base was the primary location for chemical storage and point of deployment for chemical defoliation operations in Vietnam, Cambodia, and Laos. He named areas of operations to which operations were deployed from Bien Hoa as including Saigon, Hoc Mon Bridge, Cu-Chi, Hobo Woods, the Iron Triangle, the Michelin Rubber Plantation, Song Be River, and the Cambodian border. In his November 2005 statement, the Veteran said the areas of operations where he served were regularly sprayed with Agent Orange and other chemical defoliants. He said that while in the field, his fatigues were wet or saturated with chemicals as a result of either direct spray or spray drift. He also said that while in the field it was common practice to scavenge for edible jungle vegetation and to drink water from streams, rivers, and any other available source. He also recalled that empty 55 gallon drums in which chemicals had been stored were often converted into latrines, shower cisterns, storage containers for gasoline and diesel fuel, and even for barbeques. He pointed out that it was not until October 1969 that a message was sent from Fort Detrick Maryland, to MACV concerning cleaning drums that contained herbicides with instructions on how to clean the drums and warning that it was particularly important to clean Agent Orange drums. The Veteran said it was common practice for empty drums to be sold to the Vietnamese who used them for fuel storage. He pointed out that although Saigon was never sprayed with defoliants, the trees along Saigon's streets were denuded of leaves and it had been discovered that when chemically contaminated fuel is used in an internal combustion engine, the contaminants are concentrated and aerosolized in the engine exhaust resulting in a highly toxic mixture. In his November 2005 statement, the Veteran reported quantities of Agents Orange, White, and Blue that had been used in various areas in Vietnam where he had participated in operations, including in and around Bien Hoa. With his statement, the Veteran submitted copies of articles to which he referred and from which he obtained quantitative data. In January 2006, the Veteran submitted an extensive array of journal articles and other literature pertaining to research studies of various environmental toxins, including herbicides and their neurological effects, as well as literature regarding the dates, locations, and quantities of herbicides used by the United States in Vietnam, encompassing the dates and locations of his service in Vietnam. Among the materials submitted by the Veteran and received at the RO in January 2006 was a report by Kenneth Rudo, Ph.D., State Toxicologist, North Carolina, dated in January 2004. In that report, Dr. Rudo, with reference to a specific veteran with Parkinson-like symptoms, concluded there was a more likely than not association between that veteran's Parkinsonism and exposure to Agent Orange during his service in Vietnam. In his extensive report, which contains references to numerous scientific studies and literature discussing potential neurological health effects of dioxin exposure, he in essence found an environmental link to Parkinson-like symptoms. He further noted that the National Academy of Sciences, in their report "Veterans and Agent Orange - Update 2002," were in general agreement with information presented in his report. He concluded that because the evidence showed the veteran with respect to whom he wrote was directly exposed to Agent Orange and because of the peer-reviewed evidence to which he referred and the strength of various epidemiological studies, it was more likely than not that the Vietnam exposure to Agent Orange was responsible for that veteran's neurological problems, described as Parkinson-like symptoms. In December 2005, the VA neurologist, Dr. J.S., saw the Veteran at a follow-up visit. In the report, he noted that he Veteran and his wife had brought documents that associated atypical Parkinsonism with exposure to Agent Orange. Dr. J.S. noted that a report by Dr. Kenneth Rudo suggested that the atypical Parkinsonism suffered by a particular veteran was related to exposure to Agent Orange while in Vietnam. Dr. J.S. said that as he had noted earlier, atypical Parkinsonism has been associated with ingestion of toxicants. He said that the documents submitted by the Veteran and his wife provide evidence that dioxins (and other pesticides and herbicide agents found in Agent Orange) can produce a neurodegenerative syndrome after a long latency. Dr. J.S. said that given the fact that the Veteran suffers from atypical Parkinsonism (similar to progressive supranuclear palsy) and that his exposure to toxicants was well documented, he could state that most likely his condition is a consequence of the exposure (i.e., service-connected disability). Dr. J.S. said that of course not everyone exposed had developed this condition, but certainly it appeared that a cluster of individuals had developed this syndrome. He said very likely genetic predisposition and cumulative dose would determine who develops the syndrome. In a letter dated in January 2006, which was received at the RO in February 2006, Dr. Prockop stated that he had seen the Veteran in follow-up on that date in January 2006 with continued severe symptoms and signs of progressive supranuclear palsy and a Parkinson-like illness. He noted that he came accompanied by his wife and further documents concerning his exposure to Agent Orange during the Vietnam War. Dr. Prockop said that according to the medical records now available, the exposure was complicated by the use of a variety of other chemicals, mainly insecticides and rodenticides in storage capacities. He said that as a result, the chemicals probably had a cumulative effect such that the Veteran developed the Parkinson-like syndrome. Dr. Prockop said that therefore, in his opinion, the Veteran merits compensation or benefits from the Federal government because this information shows clearly that it is more likely than not that his exposure to Agent Orange (dioxin) and other chemicals while serving his country in Vietnam is significantly associated with his symptoms and medical/neurological condition. The Certificate of Death for the Veteran shows he died in May 2006. It lists aspiration pneumonia as the immediate cause of his death with severe Parkinson's plus supranuclear palsy as the underlying cause. In its November 2006 rating decision, the RO denied entitlement to service connection for the cause of the Veteran's death. The RO noted that severe Parkinson's and supranuclear palsy are not among the conditions VA considers presumptive conditions for service connection based on exposure to herbicides used in Vietnam, and the RO said service connection for the cause of the Veteran's death was denied because evidence failed to show it was related to military service. The appellant disagreed with the denial of her cause of death claim. In its statement of the case, dated in December 2007, the RO stated that the medical evidence and opinions of records had been carefully considered. The RO said the most persuasive opinion of record was from Dr. J.S., but the RO said the physician did not provide reasoning or rationale for his opinion. In the statement of the case, the RO referred to a report of the National Academy of Sciences titled "Veterans and Agent Orange 2000 - Update 2004" and said it stated that after review of the cumulative scientific data, the National Academy of Sciences had determined there is no positive association between herbicide exposure and Parkinson's disease. The RO said that based on the National Academy of Sciences findings in Update 2004 and other pertinent information, VA had determined that presumption of service connection is not warranted for Parkinson's disease based on exposure to herbicides used during the Vietnam war or to dioxin. The RO said it had carefully reviewed and considered the evidence of record and stated that the findings from the National Academy of Sciences had greater probative value and more evidentiary weight due to the deficiencies noted in Dr. J.S's opinion. The RO concluded that service connection for the cause of the Veteran's death was denied because evidence failed to show it was related to military service. At the January 2009 hearing, the appellant, who is a registered nurse, presented testimony that repeated information concerning the Veteran's exposure to herbicides in Vietnam that had been presented in the Veteran's November 2005 statement that was received by the RO in January 2006. The appellant presented resumes for physicians who had provided opinions regarding the etiology of the Veteran's neurological symptoms, which had been described as not exactly fitting a regular diagnosis of Parkinson's. In particular, she pointed out that Dr. Zesiewicz, Assistant Director, Parkinson's Disease and Movement Disorders Center at the University of South Florida, is board-certified in neurology and is a fellow of the American Academy of Neurology with authorship of more than 50 papers and co- authorship of five books on movement disorders. The appellant also presented biographical information concerning Dr. J.S., pointing out that he has a Ph.D. degree in pharmacology and physiology as well as a medical degree with training in neurology at the University of Chicago and as a fellow in movement disorders at the University of Miami. He is a professor of neurology at the University of South Florida, a VA staff physician, and directs a basic research laboratory with projects in neurodegeneration, neurotoxicology, and adult stem cell biology. In addition, the appellant presented information concerning Dr. Prockop and submitted his resume showing he is Founding Chair, Emeritus and Professor, Department of Neurology, University of South Florida. His is full-time faculty participating in teaching, patient care, research and writing. He has authored scores of journal articles and his research interests include the blood-brain and blood-cerebral spinal fluid barriers, increased intracranial pressure, neuroimaging, and neurotoxicology. He has been the president of the American Society of Neuroimaging, editor in chief of the Journal of Neuroimaging, a member of the Practice Committee and Legislative Affairs Committee of the American Academy of Neurology, and Chair of the Environmental Neurology Research Group of the World Federation of Neurology. At the hearing, the appellant testified as to the Veteran's symptoms and the course of his disease. In addition, she presented testimony along with documentary evidence pertaining to questions of whether and to what extent, if any, there is a relationship between exposure to herbicides and dioxins in Vietnam and Parkinson's. She referred to a Mayo Clinic Website June 2006 description of study results planned for publication in the June 2006 issue of the journal Movement Disorders. It states that Mayo Clinic researchers have found that using pesticides for farming or other purposes increases the risk of developing Parkinson's disease for men. If further states that overall, the study found that men with Parkinson's were 2.4 times more likely to have had exposure to pesticides than those who did not have Parkinson's. Among the documents submitted by the appellant in January 2009 are copies of journal articles published on the Internet and excerpts from such. It includes a print-out of an e-Pub ahead of print at www.neurology.org in March 2008 by L. Brighina, M.D. of the Mayo Clinic, et al., and titled "?- Synuclein, pesticides, and Parkinson disease." The authors stated their objective was to test possible joint effects of Petersburg, Florida THE ISSUES 1. Entitlement to service connection for the cause of the Veteran's death. 2. Entitlement to service connection for tinnitus for accrued benefits purposes. 3. Entitlement to an initial compensable rating for bilateral hearing loss for accrued benefits purposes. REPRESENTATION Appellant represented by: Veterans of Foreign Wars of the United States WITNESSES AT HEARING ON APPEAL Appellant and friend ATTORNEY FOR THE BOARD Nancy S. Kettelle, Counsel INTRODUCTION The Veteran served on active duty from October 1967 to October 1969; his decorations and awards included the Combat Infantryman's Badge and the Bronze Star Medal. This matter comes to the Board of Veterans' Appeals (Board) on appeal from a November 2006 rating decision of the Department of Veterans Affairs (VA) Regional Office (RO) in St. Petersburg, Florida. The appellant and a friend testified at a Board hearing held at the RO in January 2009. The issues of entitlement to service connection for tinnitus for accrued benefits purposes and entitlement to an initial compensable rating for bilateral hearing loss for accrued benefits purposes are addressed in the REMAND portion of the decision below and are REMANDED to the RO via the Appeals Management Center (AMC), in Washington, DC. Other matters In May 2005, the Veteran filed his claim for service connection for progressive supranuclear palsy, Parkinson's like syndrome. In an August 2005 rating decision, the RO denied the service connection claim. The record shows that the RO received the Veteran's notice of disagreement with its decision in January 2006. The Veteran died in May 2006, and the appellant filed her VA Form 21-534, Application for Dependency and Indemnity Compensation, Death Pension and Accrued Benefits by a Surviving Spouse or Child, in June 2006. Although the Veteran's claim for service connection for progressive supranuclear palsy, Parkinson's like syndrome, was pending at the time of his death and the appellant filed a claim for accrued benefits shortly after his death, there is no indication that the RO has adjudicated that claim, that is, entitlement to service connection for progressive supranuclear palsy, Parkinson's like syndrome, for accrued benefits purposes. The Board refers that issue to the RO for adjudication. FINDINGS OF FACT 1. The Veteran had active military service in the Republic of Vietnam from March 1968 to March 1969, which entitles him to the presumption of exposure to herbicide agents in service; in addition, there is credible evidence that he was personally exposed to herbicide agents and other toxins during that time. 2. Competent medical evidence relates the Veteran's atypical Parkinsonism plus with signs and symptoms of progressive supranuclear palsy to his in-service exposure to herbicide agents and other toxins. 3. The Veteran died in May 2006, and the Certificate of Death lists aspiration pneumonia as the immediate cause of his death with severe Parkinson's plus, supranuclear palsy, as the underlying cause. CONCLUSION OF LAW A service-connected disability caused the Veteran's death, and service connection for the cause of the Veteran's death is established. 38 U.S.C.A. §§ 1310, 5107 (West 2002); 38 C.F.R. §3.312 (2008). REASONS AND BASES FOR FINDINGS AND CONCLUSION The Board acknowledges that VA has duties related to notice and assistance to a claimant in the development of a claim as mandated under the provisions of 38 U.S.C.A. §§ 5103, 5103A (West 2002 & Supp. 2008) and 38 C.F.R. § 3.159 (2008). In this case, the Board concludes that no further notice or assistance is required as the outcome of the Board's decision is favorable to the appellant, and no prejudice to the appellant could result from this adjudication. See Bernard v. Brown, 4 Vet. App. 384. 393 (1993). As noted in the Introduction, the appellant provided testimony at a Board hearing in January 2009. In addition, she has submitted evidence to the Board for which she has waived initial review by the RO. The appellant is seeking service connection for the cause of the Veteran's death due to aspiration pneumonia for which the underlying cause was his Parkinsonism and supranuclear palsy. The appellant contends this disability was related to the Veteran's exposure to herbicides and other toxins during his service in Vietnam. To establish service connection for the cause of death, the evidence must show that disability incurred in or aggravated by service either caused or contributed substantially or materially to the cause of death. 38 U.S.C.A. § 1310; 38 C.F.R. § 3.312. For a service connected disability to be the cause of death, it must singly or with some other condition be the immediate or underlying cause, or be etiologically related. 38 C.F.R. § 3.312(b). For a service-connected disability to constitute a contributory cause, it is not sufficient to show that it causally shared in producing death; rather, it must be shown that there was a causal connection. 38 C.F.R. § 3.312(c). In general, service connection may be granted for disability resulting from disease or injury incurred in or aggravated during active military service. 38 U.S.C.A. § 1110; 38 C.F.R. § 3.303. Service connection may be granted on a presumptive basis for certain chronic diseases, including organic diseases of the nervous system, if manifested to a degree of 10 percent or more within one year of separation from active service. 38 U.S.C.A. §§ 1101, 1112 (West 2002); 38 C.F.R. §§ 3.307(a)(3), 3.309(a) (2008). Service connection may also be established for disease diagnosed after discharge from service when all the evidence establishes that the disease was incurred in service. 38 U.S.C.A. § 1113(b); 38 C.F.R. § 3.303(d). A veteran who had active service in the Republic of Vietnam at any time from January 9, 1962, to May 7, 1975, will be presumed to have been exposed to an herbicide agent during that service. 38 U.S.C.A. § 1116(f); 38 C.F.R. § 3.307(a)(6)(iii). For the purposes of 38 C.F.R. § 3.307, the term herbicide agent means a chemical in an herbicide used in support of the United States and allied military operations in the Republic of Vietnam during the period beginning on January 9, 1962, and ending on May 7, 1975, specifically: 2,4-D, 2,4,5-T and its contaminant TCDD; cacodylic acid; and picloram. 38 C.F.R. § 3.307(a)(6)(i). When such a veteran develops a disorder listed in 38 C.F.R. § 3.309(e), which disorders have been shown to be caused by exposure to Agent Orange, to a degree of 10 percent or more within the specified period, the disorder shall be presumed to have been incurred during service. 38 U.S.C.A. § 1116; 38 C.F.R. §§ 3.307(a)(6), 3.309(e). Diseases to which the presumption applies are: chloracne or other acneform diseases consistent with chloracne, Type 2 diabetes (also known as Type II diabetes mellitus or adult- onset diabetes), Hodgkin's disease, chronic lymphocytic leukemia, multiple myeloma, non-Hodgkin's lymphoma, acute and subacute peripheral neuropathy, porphyria cutanea tarda, prostate cancer, respiratory cancers (cancer of the lung, bronchus, larynx, or trachea) and soft-tissue sarcomas (other than osteosarcoma, chondrosarcoma, Kaposi's sarcoma, or mesothelioma). 38 U.S.C.A. § 1116; 38 C.F.R. § 3.309(e). The above-listed diseases shall have become manifest to a degree of 10 percent or more at any time after service, except that chloracne or other acneform disease consistent with chloracne, porphyria cutanea tarda, and acute and subacute peripheral neuropathy shall have become manifest to a degree of 10 percent or more within a year after the last date on which the veteran was exposed to an herbicide agent during active military, naval, or air service. 38 U.S.C.A. § 1116; 38 C.F.R. §§ 3.307(a)(6)(ii). VA has determined that a presumption of service connection based on exposure to herbicides used in the Republic of Vietnam during the Vietnam era is not warranted for any condition for which VA has not specifically determined a presumption of service connection is warranted. See 59 Fed. Reg. 341-46 (1994); 61 Fed. Reg. 414421 (1996); 64 Fed. Reg. 59232 (1999); 67 Fed. Reg. 42600-08 (2002); 68 Fed. Reg. 27,630-41 (2003). More recently, VA clarified that a presumption of service connection based on exposure to herbicides used in the Republic of Vietnam during the Vietnam era is not warranted for the following conditions: hepatobiliary cancers; oral, nasal, and pharyngeal cancer; bone and joint cancer; leukemia (other than chronic lymphocytic leukemia (CLL); skin cancers (melanoma, basal, and squamous cell); breast cancer; cancers of the female reproductive system (cervix, uterus, ovary); testicular cancer; urinary bladder cancer; renal cancer; abnormal sperm characteristics and infertility; spontaneous abortion; neonatal or infant death and stillbirth in offspring of exposed individuals; low birthweight in offspring of exposed individuals; neurobehavioral disorders (cognitive and neuropsychiatric); movement disorders including Parkinson's disease and amyotrophic lateral sclerosis (ALS); chronic peripheral nervous system disorders; respiratory disorders (other than certain respiratory cancers); gastrointestinal, metabolic, and digestive disorders (changes in liver enzymes, lipid abnormalities, ulcers); immune system disorders (immune suppression, autoimmunity); circulatory disorders; amyloid light-chain (AL) amyloidosis; endometriosis; effects on thyroid homeostasis; gastrointestinal tumors (esophagus, stomach, pancreas, colon, rectum); brain tumors; and any other condition for which the Secretary has not specifically determined a presumption of service connection is warranted. See 72 Fed. Reg. 32395-407 (2007). Notwithstanding the foregoing, the United States Court of Appeals for the Federal Circuit has determined that the Veterans' Dioxin and Radiation Exposure Compensation Standards (Radiation Compensation) Act, Pub. L. No. 98-542, § 5, 98 Stat. 2724, 2727- 29 (1984), does not preclude a veteran from establishing service connection with proof of actual direct causation. Combee v. Brown, 34 F.3d 1039 (Fed. Cir. 1994). The United States Court of Appeals for Veterans Claims (Court) has specifically held that the provisions of Combee are applicable in cases involving Agent Orange exposure. McCartt v. West, 12 Vet. App. 164, 167 (1999). Direct service connection can be established by "showing that the disease or malady was incurred during or aggravated by service, "a task which "includes the difficult burden of tracing causation to a condition or event during service." Combee 34 F.3d at 1043. In order to prevail on direct service connection there must be medical evidence of a current disability; medical evidence, or in certain circumstances, lay evidence of in-service occurrence or aggravation of a disease or injury; and medical evidence of a nexus between an in-service injury or disease and the current disability. See Hickson v. West, 12 Vet. App. 247, 253 (1999); see also Pond v. West, 12 Vet App. 341, 346 (1999). The standard of proof to be applied in decisions on claims for veterans' benefits is set forth in 38 U.S.C.A. § 5107. A claimant is entitled to the benefit of the doubt when there is an approximate balance of positive and negative evidence. See 38 C.F.R. § 3.102. When a claimant seeks benefits and the evidence is in relative equipoise, the claimant prevails. See Gilbert v. Derwinski, 1 Vet. App. 49 (1990). The preponderance of the evidence must be against the claim for benefits to be denied. See Alemany v. Brown, 9 Vet. App. 518 (1996). In this case, as of the time of his death, the only disability for which service connection had been granted was bilateral hearing loss, rated as noncompensably disability. The veteran died in May 2006, and the Certificate of Death lists aspiration pneumonia as the immediate cause of death and severe Parkinson's plus, supranuclear palsy, as the underlying cause. The Veteran's service treatment records do not include any complaint or finding that has been related to Parkinson's disease, Parkinsonism, or supranuclear palsy, and there is no medical evidence of such within the first post-service year. Records from the University of South Florida, College of Medicine Medical Clinics show that the Veteran was first seen in the neurology clinic in November 2003. At that time, the appellant reported that the Veteran had a history of having developed a cough about a year earlier that had been treated as a respiratory problem, but it had never cleared up. She reported that in August 2003, the Veteran's right eye appeared to be bulging and his left eye appeared to be more sunken. His speech was noted to be slurred at that time. She also reported that the Veteran appeared more rigid in his normal gait and was somewhat unsteady, especially on a ladder. The Veteran reported vision changes had occurred, with blurring and double vision. The appellant noted that the Veteran had been gritting his teeth and had broken two teeth in the past three months. She also remarked on memory changes and a silly laugh. The medical records from the University of South Florida Medical Clinics document extensive laboratory studies and tests. On a long term disability insurance form dated in July 2004, the Veteran reported he had been unable to work since January 2004, and a neurologist, Theresa A. Zesiewicz, M.D., Assistant Director, Parkinson's Disease and Movement Disorders Center at the University of South Florida, stated the Veteran was unable to work and that his diagnoses were progressive supranuclear palsy and Parkinson-like syndrome. In a letter dated in March 2005, Dr. Zesiewicz noted that the Veteran had been exposed to Agent Orange in service, and that his wife, the appellant here, was concerned about dioxin. Dr. Zesiewicz referred the Veteran to a VA neurologist, J.S, M.D. She also stated that an input would be appreciated from Dr. Leon Prockop, whom she described as a world-renowned neurotoxicologist. VA medical records show the Veteran saw the VA neurologist, J.S, M.D., in May 2005. The neurologist noted it was reported that the Veteran's first symptoms began in 2003, that the Veteran fell in March 2003 requiring stitches to the left brow, and that in September 2003 he had gone to an emergency room with stroke-like symptoms, blurred and double vision, slurred speech, inappropriate laugh, unsteady gait, coughing, and problems swallowing, but that no stroke was found. The physician further noted that a MRI (magnetic resonance imagining) study had shown hyperintensity in the periventricular white mater and that the Veteran's neurologist had noted extrapyramidal syndrome. Sinemet had been started in August 2004. On examination, Dr. J.S. noted that Veteran's mental status was grossly normal but that he could not perform sequential movement of the hand-Luria test, which was said to be indicative of marked executive function deficit. There was limited excursion and range of voluntary gaze, speech was dysarthric, but understandable. All movement of the tongue and mouth were slow. There was marked axial rigidity of muscles with rigidity in limbs less that in the axial muscles. There was mild to moderate slowness of hand movements and finger taps. Rapid alternating movements were clumsy. There were no resting, postural, or action tremors. The Veteran was slow to rise; he had good stride, but poor arm swing and poor postural reflexes. Deep tendon reflexes showed hyper-reflexia with spread. The impression was atypical Parkinsonism partially responsive to dopamine replacement. Dr. J.S. said that the marked deficit in voluntary gaze, axial rigidity, and Parkinsonism suggest the diagnosis of progressive supranuclear palsy. He said the etiology was not clear. He noted that the Veteran had a history of exposure to toxicants used in Vietnam but that as far as he knew there was no clustering of progressive supranuclear palsy in veterans, but this might become evident with time. On referral for a second opinion, Dr. Prockop of the University of South Florida Physicians Group examined the Veteran in May 2005. He noted the Veteran had been referred by Dr. Zesiewicz for a second opinion with respect to his progressive supranuclear palsy and possible connection to Agent Orange during his Vietnam experience. After review of the Veteran's medical records and physical examination, Dr. Prockop said he knew of no significant database to link the Agent Orange exposure to the Veteran's neurodegenerative process. He suggested an additional MRI of the brain to exclude progressive ischemic disease as a potential etiology. The physician said he would review the literature base to see if there was any further data on this potential connection. After a July 2005 visit, Dr. Prockop said he was continuing to review data concerning dioxin and its potential relationship to the Veteran's condition. Dr. Prockop said that at the present, he could say it is possible that there is a connection between the Veteran's dioxin exposure and his Parkinson plus syndrome but that at the present time, probability could not be established. He said that with further investigation that perhaps a probable statement could be made. In addition, in a letter dated in August 2005, Dr. Zesiewicz said the Veteran's opthalmoplegia and masked facies as well as cogwheel rigidity and extra paramedical dysfunction fit the picture of a Parkinson plus syndrome, possibly progressive supranuclear palsy. She said it was possible that there is a connection between the Veteran's exposure to Agent Orange and his development of Parkinsonism but the exact etiology was unclear. In a VA neurology clinic follow-up note dated in August 2005, it was noted that in 2003 the Veteran has been diagnosed as having progressive supranuclear palsy by Dr. Zesiewicz and that he had initially presented with slurred speech, swallowing difficulties and poor coordination. In August 2005, the Veteran complained continued fatigue, drooling, and swallowing difficulties with choking on liquids and saliva. In addition, he complained of memory difficulties, gait problems, stiff posture, and stiffness of the neck. The assessment after examination was questionable progressive supranuclear palsy. The plan included obtaining a swallow evaluation via speech therapy with the possibility for percutaneous endoscopic gastrostomy (PEG) tube placement in the near future. After testing in the speech pathology clinic in September 2005, the speech pathology section chief said that although there was no aspiration observed on the study of that date, the Veteran should be considered at risk for aspiration on all consistencies and required careful feed and modified diet consistency. It was further noted that the Veteran had had previously documented aspiration of both thin and nectar-thick liquid. In a November 2005 statement, prepared with the assistance of the appellant and received at the RO in January 2006, the Veteran reported that after completing advanced training, he was assigned to Co. A, 2nd Battalion, 508th Infantry 3rd Brigade 82nd Airborne Division and in late February 1968, his brigade was deployed to Vietnam. In this regard, the Board notes that the National Personnel Records Center (NPRC) has reported the Veteran was in Vietnam from March 1968 to March 1969. In his narrative, the Veteran reported that in April 1968 he was transferred to Co. A, 2nd Battalion, 505th Infantry, 82nd Airborne Division. He said that for the first several days after his transfer, his MOS (military operational specialty) was 11C10, ammo bearer and handler. He said his MOS was then changed to 36K20, forward radio operator and in that capacity he relayed combat operational information and information pertaining to battle coordination. He said that after the Citadel had been retaken during the battle of Hue, the 505th moved south to the III Corps military region where Bien Hoa was the base of operations. The Veteran pointed out that the adjacent Bien Hoa Air force Base was the primary location for chemical storage and point of deployment for chemical defoliation operations in Vietnam, Cambodia, and Laos. He named areas of operations to which operations were deployed from Bien Hoa as including Saigon, Hoc Mon Bridge, Cu-Chi, Hobo Woods, the Iron Triangle, the Michelin Rubber Plantation, Song Be River, and the Cambodian border. In his November 2005 statement, the Veteran said the areas of operations where he served were regularly sprayed with Agent Orange and other chemical defoliants. He said that while in the field, his fatigues were wet or saturated with chemicals as a result of either direct spray or spray drift. He also said that while in the field it was common practice to scavenge for edible jungle vegetation and to drink water from streams, rivers, and any other available source. He also recalled that empty 55 gallon drums in which chemicals had been stored were often converted into latrines, shower cisterns, storage containers for gasoline and diesel fuel, and even for barbeques. He pointed out that it was not until October 1969 that a message was sent from Fort Detrick Maryland, to MACV concerning cleaning drums that contained herbicides with instructions on how to clean the drums and warning that it was particularly important to clean Agent Orange drums. The Veteran said it was common practice for empty drums to be sold to the Vietnamese who used them for fuel storage. He pointed out that although Saigon was never sprayed with defoliants, the trees along Saigon's streets were denuded of leaves and it had been discovered that when chemically contaminated fuel is used in an internal combustion engine, the contaminants are concentrated and aerosolized in the engine exhaust resulting in a highly toxic mixture. In his November 2005 statement, the Veteran reported quantities of Agents Orange, White, and Blue that had been used in various areas in Vietnam where he had participated in operations, including in and around Bien Hoa. With his statement, the Veteran submitted copies of articles to which he referred and from which he obtained quantitative data. In January 2006, the Veteran submitted an extensive array of journal articles and other literature pertaining to research studies of various environmental toxins, including herbicides and their neurological effects, as well as literature regarding the dates, locations, and quantities of herbicides used by the United States in Vietnam, encompassing the dates and locations of his service in Vietnam. Among the materials submitted by the Veteran and received at the RO in January 2006 was a report by Kenneth Rudo, Ph.D., State Toxicologist, North Carolina, dated in January 2004. In that report, Dr. Rudo, with reference to a specific veteran with Parkinson-like symptoms, concluded there was a more likely than not association between that veteran's Parkinsonism and exposure to Agent Orange during his service in Vietnam. In his extensive report, which contains references to numerous scientific studies and literature discussing potential neurological health effects of dioxin exposure, he in essence found an environmental link to Parkinson-like symptoms. He further noted that the National Academy of Sciences, in their report "Veterans and Agent Orange - Update 2002," were in general agreement with information presented in his report. He concluded that because the evidence showed the veteran with respect to whom he wrote was directly exposed to Agent Orange and because of the peer-reviewed evidence to which he referred and the strength of various epidemiological studies, it was more likely than not that the Vietnam exposure to Agent Orange was responsible for that veteran's neurological problems, described as Parkinson-like symptoms. In December 2005, the VA neurologist, Dr. J.S., saw the Veteran at a follow-up visit. In the report, he noted that he Veteran and his wife had brought documents that associated atypical Parkinsonism with exposure to Agent Orange. Dr. J.S. noted that a report by Dr. Kenneth Rudo suggested that the atypical Parkinsonism suffered by a particular veteran was related to exposure to Agent Orange while in Vietnam. Dr. J.S. said that as he had noted earlier, atypical Parkinsonism has been associated with ingestion of toxicants. He said that the documents submitted by the Veteran and his wife provide evidence that dioxins (and other pesticides and herbicide agents found in Agent Orange) can produce a neurodegenerative syndrome after a long latency. Dr. J.S. said that given the fact that the Veteran suffers from atypical Parkinsonism (similar to progressive supranuclear palsy) and that his exposure to toxicants was well documented, he could state that most likely his condition is a consequence of the exposure (i.e., service-connected disability). Dr. J.S. said that of course not everyone exposed had developed this condition, but certainly it appeared that a cluster of individuals had developed this syndrome. He said very likely genetic predisposition and cumulative dose would determine who develops the syndrome. In a letter dated in January 2006, which was received at the RO in February 2006, Dr. Prockop stated that he had seen the Veteran in follow-up on that date in January 2006 with continued severe symptoms and signs of progressive supranuclear palsy and a Parkinson-like illness. He noted that he came accompanied by his wife and further documents concerning his exposure to Agent Orange during the Vietnam War. Dr. Prockop said that according to the medical records now available, the exposure was complicated by the use of a variety of other chemicals, mainly insecticides and rodenticides in storage capacities. He said that as a result, the chemicals probably had a cumulative effect such that the Veteran developed the Parkinson-like syndrome. Dr. Prockop said that therefore, in his opinion, the Veteran merits compensation or benefits from the Federal government because this information shows clearly that it is more likely than not that his exposure to Agent Orange (dioxin) and other chemicals while serving his country in Vietnam is significantly associated with his symptoms and medical/neurological condition. The Certificate of Death for the Veteran shows he died in May 2006. It lists aspiration pneumonia as the immediate cause of his death with severe Parkinson's plus supranuclear palsy as the underlying cause. In its November 2006 rating decision, the RO denied entitlement to service connection for the cause of the Veteran's death. The RO noted that severe Parkinson's and supranuclear palsy are not among the conditions VA considers presumptive conditions for service connection based on exposure to herbicides used in Vietnam, and the RO said service connection for the cause of the Veteran's death was denied because evidence failed to show it was related to military service. The appellant disagreed with the denial of her cause of death claim. In its statement of the case, dated in December 2007, the RO stated that the medical evidence and opinions of records had been carefully considered. The RO said the most persuasive opinion of record was from Dr. J.S., but the RO said the physician did not provide reasoning or rationale for his opinion. In the statement of the case, the RO referred to a report of the National Academy of Sciences titled "Veterans and Agent Orange 2000 - Update 2004" and said it stated that after review of the cumulative scientific data, the National Academy of Sciences had determined there is no positive association between herbicide exposure and Parkinson's disease. The RO said that based on the National Academy of Sciences findings in Update 2004 and other pertinent information, VA had determined that presumption of service connection is not warranted for Parkinson's disease based on exposure to herbicides used during the Vietnam war or to dioxin. The RO said it had carefully reviewed and considered the evidence of record and stated that the findings from the National Academy of Sciences had greater probative value and more evidentiary weight due to the deficiencies noted in Dr. J.S's opinion. The RO concluded that service connection for the cause of the Veteran's death was denied because evidence failed to show it was related to military service. At the January 2009 hearing, the appellant, who is a registered nurse, presented testimony that repeated information concerning the Veteran's exposure to herbicides in Vietnam that had been presented in the Veteran's November 2005 statement that was received by the RO in January 2006. The appellant presented resumes for physicians who had provided opinions regarding the etiology of the Veteran's neurological symptoms, which had been described as not exactly fitting a regular diagnosis of Parkinson's. In particular, she pointed out that Dr. Zesiewicz, Assistant Director, Parkinson's Disease and Movement Disorders Center at the University of South Florida, is board-certified in neurology and is a fellow of the American Academy of Neurology with authorship of more than 50 papers and co- authorship of five books on movement disorders. The appellant also presented biographical information concerning Dr. J.S., pointing out that he has a Ph.D. degree in pharmacology and physiology as well as a medical degree with training in neurology at the University of Chicago and as a fellow in movement disorders at the University of Miami. He is a professor of neurology at the University of South Florida, a VA staff physician, and directs a basic research laboratory with projects in neurodegeneration, neurotoxicology, and adult stem cell biology. In addition, the appellant presented information concerning Dr. Prockop and submitted his resume showing he is Founding Chair, Emeritus and Professor, Department of Neurology, University of South Florida. His is full-time faculty participating in teaching, patient care, research and writing. He has authored scores of journal articles and his research interests include the blood-brain and blood-cerebral spinal fluid barriers, increased intracranial pressure, neuroimaging, and neurotoxicology. He has been the president of the American Society of Neuroimaging, editor in chief of the Journal of Neuroimaging, a member of the Practice Committee and Legislative Affairs Committee of the American Academy of Neurology, and Chair of the Environmental Neurology Research Group of the World Federation of Neurology. At the hearing, the appellant testified as to the Veteran's symptoms and the course of his disease. In addition, she presented testimony along with documentary evidence pertaining to questions of whether and to what extent, if any, there is a relationship between exposure to herbicides and dioxins in Vietnam and Parkinson's. She referred to a Mayo Clinic Website June 2006 description of study results planned for publication in the June 2006 issue of the journal Movement Disorders. It states that Mayo Clinic researchers have found that using pesticides for farming or other purposes increases the risk of developing Parkinson's disease for men. If further states that overall, the study found that men with Parkinson's were 2.4 times more likely to have had exposure to pesticides than those who did not have Parkinson's. Among the documents submitted by the appellant in January 2009 are copies of journal articles published on the Internet and excerpts from such. It includes a print-out of an e-Pub ahead of print at www.neurology.org in March 2008 by L. Brighina, M.D. of the Mayo Clinic, et al., and titled "?- Synuclein, pesticides, and Parkinson disease." The authors stated their objective was to test possible joint effects of SNCA REP1 genotypes (that is, the ?-synuclein gene (SNCA) with variability in the length of a dinucleotid repeat sequence (REP1)) and pesticides exposures on the risk of Parkinson's disease. This was a case-control study, and odds ratios and 95 percent confidence limits were determined using conditional logistic regression models. The results included the finding that in the lowest quartile of age of diagnosis in the study (less than or equal to 59.8 years) an increased risk of Parkinson's disease was associated with the use of herbicides, with an odds ratio of 2.46, with a 95 percent confidence limit of 1.34 - 4.52. The study authors stated their overall conclusion was that their findings suggest that SNCA REP1 genotype and herbicides have independent effects on risk of Parkinson's disease, primarily in younger subjects. She also submitted a journal article from Toxicology by Donggun Sul, et. al., and titled "2,3,7,8-TCDD neurotoxicity in neuroblastoma cells is caused by increased oxidative stress, intracellular calcium levels, and tau phosphorylation" at www.10.1016/j.tox.2008.10.006. In their study, the authors evaluated the neurotoxic effects of TCDD on neuronal cells using mouse neuroblastoma cells (clone N2a) and explored the underlying mechanisms of the toxicity. The authors stated that study results revealed that treatment with increasing doses of 2,3,7,8-tetrachlorodibenzo-?-dioxin (TCDD) decreased the viability of mouse neuroblastoma cells (clone N2a) and increased DNA damage in a dose-dependent manner compared to controls. They also said that a malondialdehyde assay revealed dose-dependent TCDD-induced lipid peroxidation. In addition, they noted that TCDD neurotoxicity in N2a cells was accompanied by elevated intracellular calcium levels, which in turn increased the phosphorylation of tau via up-regulation of phospho-glycogen synthase kinase-3ß. The authors said that taken together, these results indicate that TCDD exposure induces neurotoxicity in N2a cells by increasing DNA damage, oxidative stress, and intracellular calcium levels. They said the TCDD-mediated increase of tau phosphorylation in particular indicates an important role for tau hyperphosphorylation in TCDD-induced neurotoxicity. The appellant submitted a synopsis of a study titled "Military Deployment and the Risk of Parkinson's Disease" by L.M. Nelson, et al, and the appellant refers to this study as being from Stanford University. She did not refer to the study date, and has stated it is an unpublished study. She argues that it should be given weight in adjudication of her claim just as the National Academy of Sciences has reviewed unpublished material in preparation of its reports to VA concerning Agent Orange and health outcomes. In the abstract of the unpublished study submitted by the appellant, it was reported that newly diagnosed patients with Parkinson's disease were identified within the Kaiser Permanente Northern California health maintenance organization during the years 1994-1995. Investigation of military employment was restricted to male patients, and men without Parkinson's disease from the same population were randomly selected and frequency matched by age and respondent type to the Parkinson's disease cases. Odds ratios for the association between military deployment and Parkinson's disease were estimated using logistic regression with adjustment for age and cigarette smoking. Among the results was the finding that the risk of Parkinson's disease was increased among men who were deployed during the Vietnam war (odds ratio 2.6, confidence interval 0.9 - 7.13) but not among men who served at the time of the Vietnam war but were not deployed (odds ratio 0.9, confidence interval 0.4 - 1.7). The appellant also submitted a copy of the Iowa Study Update 2007 of the Agricultural Health Study. It stated that using information collected from the entire Agricultural Health Study, its findings included the finding that individuals who used paraquat, cyanazine, trifluralin, or 2,4,5-T had an increased risk of Parkinson's disease. The appellant submitted a copy of the abstract of a journal article titled "Park3 Influences Age at Onset in Parkinson Disease: A Genome Scan in the GenePD Study" by Anita L. DeStefano of Boston University, et. al. Am J Hum Genet. 2002 May; 70(5): 1089-1095. In the abstract, the authors state that Parkinson's disease is a late-onset neurodegenerative disorder. They further state that the mean age at onset is 61 years, but the disease can range from juvenile cases to cases in the 8th or 9th decade of life. The authors state that they performed geomewide linkage analysis using variance-component methodology to identify genes influencing age of onset of Parkinson's disease in a population of affected relatives (mainly affected sibling pairs) participation in the GenePD study. They state that association between Parkinson's disease age at onset and a particular allele of marker D2S1394 located at particular chromosomal loci was observed in the GenePD sample. They said study results suggested this allele may be in linkage disequilibrium with a mutation influencing Parkinson's disease susceptibility or age at on onset of Parkinson's disease. The appellant also submitted an abstract of an article titled "Herbicide exposure modifies GSTP1 haplotype association to Parkinson onset age" by J.B. Wilk, of Boston University, et. al., from NEUROLOGY 2006, 67:2206-2210. In the abstract, the authors stated as background that polymorphisms in the glutathione S-transferase pi gene (GSTP1), encoding GSTP1-1, a detoxification enzyme, may increase the risk of Parkinson's disease with exposure to pesticides. The authors said that using a sample of familial Parkinson's disease cases, they explored whether GSTP1 polymorphisms were associated with the age at onset of Parkinson's disease symptoms and whether that relation was modified by exposure to herbicides. They stated that seven single-nucleotide polymorphisms (SNPs) were genotyped and tested for association with Parkinson's disease onset age in men in three strata: no exposure to herbicides; residential exposure to herbicides; and occupational exposure to herbicide. The results were that three SNPs were associated with Parkinson's disease onset age in the group of men occupationally exposed to herbicides. Three additional SNPs had significant trends for the association of Parkinson's disease onset age across the herbicide exposure groups. The authors said that haplotype results also provided evidence that the relation between GSTP1 and onset age was modified by herbicide exposure. They reported one haplotype was associated with an approximately 8-years- earlier onset in the occupationally exposed group and a 2.8- years-later onset in the nonexposed group. The appellant argues that the above study provides support for the fact that in even those cases involving a predisposition to Parkinson's disease that herbicides impact on onset age. She asserts that this is relevant to her claim as the Veteran was diagnosed was Parkinson's disease in 2003 at age 56. She asserts that the average onset age of Parkinson's disease in the general population is 61 years and that the average of diagnosis is 66 to 68 years of age. She further states that Parkinson's disease has an onset of usually six to eight years before diagnosis. She reasons this indicates the Veteran's age at onset was around 49 years of age, approximately 12 years before the general population, and that this would closely match what she calculates as the 10.8-year difference (what she says is 8 years later plus 2.8 years earlier) between the occupationally exposed to no exposure group in the study described in the preceding paragraph. The appellant has argued that the Veteran was exposed to malathion in service in Vietnam and that malathion has been scientifically significantly associated with Parkinson's disease. In this regard, she submitted a commentary cited as Cecil P.F. Sr., Young A.L. (2007): Operation FLYSWATTER: A War Within a War. Env SCi Pollut Res 15(1) 3-7. The commentary discusses fixed-wing aerial spraying of insecticides for mosquito control in Vietnam from October 1966 to December 1971. It was known as Operation FLYSWATTER and used modified UC-123 transport planes to spray malathion insecticide. Locations for Malathion storage and servicing included the Bien Hoa Air Base in Vietnam. In 1968, there were 230 insecticide sorties, and by 1969 a total of 14 bases and adjacent cities were sprayed every 9 days weather permitting. Malathion was applied at the rate of 0.59 liters/hectare of a 57 percent concentrate; one insecticide sortie covered about 6,000 hectares. Operation FLYSWATTER required over 1,300 individual missions and dispensed approximately 1.76 million liters of malathion concentrate. It was stated that unlike herbicide missions, it was not required that insecticide target areas be clear of friendly forces and that this was among the reasons for veterans in the future to believe they had been sprayed with dioxin-contaminated Agent Orange during combat field operations. With the Operation FLYSWATTER commentary, the appellant submitted a research article titled "Pesticide exposure and risk of Parkinson's disease: A family-based case-control study" by Dana B. Hancock of Duke University, et. al. BMC Neurology 2008, 8:6 doi:10/1186/1471-2388/8/6. The authors stated that using 319 cases and 296 relative and other controls, they examined associations of direct pesticide application, well-water consumption, and farming residences/occupations with Parkinson's disease using generalized estimating equations while controlling for age at examination, sex, cigarette smoking, and caffeine consumption. The authors said that overall, individuals with Parkinson's disease were significantly more likely to report direct pesticide application than their unaffected relatives (odds ratio 1.61, 95 percent confidence interval 1.13 - 2.29). They said that two specific insecticide classes, organochlorines (including chlordane and dichloro-diphenyl- trichloroethane (DDT)) and organophosphorous chemicals (including chlorpyrifos, diazinon, and malathion) were found to be significantly associated with Parkinson's disease. They further said that two less common classes in their sample, the botanical class (including rotenone) and the chlorophenoxy acid/ester class (including 2,4- dichlorophenoxyactic acid (2,4-D) and Agent Orange) showed strong odds ratio estimates, which they said were possibly indicative of a positive association with Parkinson's disease but that these associations were not [statistically] significant. In January 2009, the appellant also submitted an electronic media 86-slide power point presentation prepared by Mr. Alan Oates, Director of Special Projects, U.S. Military Veterans with Parkinson's (USMVP). The presentation is titled "Vietnam Veterans' Chemical Exposures & Links To Parkinson's Disease." The presentation is in three parts. Part One, titled Exposure, pertains to chemical exposures in Vietnam including Agent Orange, other herbicides, organophosphates (including malathion and malaoxon), and other chemicals. Mr. Oates includes slides on what he calls the Stanford Deployment Study, what he describes as the Mayo Clinic Study on Alpha Synuclein Pesticides and Parkinson's Disease (2008), the Iowa Agriculture Health Study Update 2007, and Operation FLYSWATTER, copies of which were submitted by the appellant and were outlined above, along with the BMC Neurology Study. What Mr. Oates refers to as the BMC Neurology Study appears to be the same as the earlier-described article submitted by the appellant and titled "Pesticide exposure and risk of Parkinson's disease: A family-based case-control study" by Dana B. Hancock of Duke University, et al. BMC Neurology 2008, 8:6 doi:10/1186/1471-2388/8/6. In Part Two of his power point presentation, which is titled "TCDD A Neurotoxin," Mr. Oates discusses the journal article from Toxicology by Donggun Sul, et. al., and titled "2,3,7,8-TCDD neurotoxicity in neuroblastoma cells is caused by increased oxidative stress, intracellular calcium levels, and tau phosphorylation" at www.10.1016/j.tox.2008.10.006. As outlined earlier, the appellant submitted a copy of this article. In his presentation, Mr. Oates states that this article shows that TCDD reduces viability of neuron cells, causes oxidative stress, damages DNA in the cells, increases lipid peroxidation, and increases intracellular calcium levels, which causes hyperphosphorylation of tau. Mr. Oates discusses how the study findings are associated with Parkinson's disease. In Part Three of his power point presentation, titled "Exposure and Neuroprotective Impacts," Mr. Oates presents slides stating that melatonin is a hormone that is protective of dopamine cells, the loss of which is a hallmark of Parkinson's disease. He further states that studies have shown TCDD reduces melatonin serum levels in rat models. In addition, he refers to studies suggesting that malathion interferes with the production of serotonin, which is required for production and secretion of melatonin. From this, he concludes that TCDD and malathion reduce melatonin, critical for protection of dopamine cells, the death of which results in Parkinson's disease. He argues that this shows that chemical exposure in Vietnam leads to Parkinson's disease. In addition, Mr. Oates presents argument in support of his contention that Parkinson's disease should be placed on the VA list of diseases that may be presumed to be due to exposure to herbicides. In addition, in January 2009, the appellant submitted a July 2008 memorandum from Christopher Reid, M.D., PhD., who stated he is a physician-scientist and Ph.D. in neurobiology. He stated that he had been requested to investigate the plausibility that American veterans may had developed Parkinson's disease as a result of Agent Orange exposure in Vietnam. He stated that he was writing with respect to the case of the Veteran, who was a Vietnam veteran diagnosed with Parkinson's disease in 2003, [at age 56], approximately 35 years after departing Vietnam. In his memorandum Dr. Reid said he had analyzed service data and medical data from veterans deployed to Vietnam between 1966 and 1973 and found that early-onset Parkinson's disease was common in the analyzed group of veterans. Dr. Reid stated that he found that the average reported age of Parkinson's disease diagnosis was several years lower than commonly reported in the general population (55 +/- 6 years versus 62 years) with a relatively consistent time between Vietnam service and Parkinson's diagnosis (31 +/- 7 years). Dr. Reid cited and discussed various studies and journal articles. He noted that Parkinson's disease is generally considered to develop as a consequence of genetics and/or exposure to neuronal toxins. He said that careful review of the available data on Parkinson's disease and environmental exposures indicates and increased risk of Parkinson's disease associated with the use of herbicides and specific pesticides. He further stated that pesticides with chemical structures similar to that of Agent Orange (dioxin) have a particularly strong relationship to increased risk of Parkinson's disease. In his memorandum, Dr. Reid further referred to published articles that he said demonstrated that genetics and environmental exposure to pesticides appear to combine together to define the age of Parkinson's disease onset as well as an individual's risk of developing Parkinson's disease overall. He also noted that a number of investigators had reached the conclusion that a dose-response relationship existed between environmental (pesticide) exposure and Parkinson's disease and that genetics and environment are interactive with respect to causing Parkinson's disease. He also referred to a study of male patients at Kaiser Permanente during the years 1994-1995 that showed that men deployed in World War II or Vietnam were at increased risk for Parkinson's disease compared to controls but that men who served in the military but who were not deployed were not at increased risk. In his summary, Dr. Reid said there is a growing consensus that pesticides and herbicides can cause early-onset Parkinson's disease in individuals carrying genes that increase their vulnerability to environmental toxins. Dr. Reid said that the group of 122 Vietnam veterans who self- reported Parkinson's disease in his study represents early- onset Parkinson's disease in the context of presumed Agent Orange exposure during Vietnam. He said that even those individuals in the group with later-onset Parkinson's disease appear to show a time interval between their Vietnam service and Parkinson's disease diagnosis that is commensurate with their younger counterparts, which he said is a trait consistent with a shared mechanism of causation. Dr. Reid said it is therefore his opinion that the connection between military service and Parkinson's disease is not coincidental, but more likely than not represents an example of the increased risk of Parkinson's disease, which he said is demonstrably associated with wartime deployment. The Board appreciates the extensive effort the appellant has invested in obtaining evidence and developing arguments she has submitted in conjunction with her claim. As was outlined above, the Veteran's service treatment records include no complaint or finding that has been associated with his Parkinson's plus, supranuclear palsy, and 2003 is the earliest medical evidence pertaining to neurological symptoms and the time of initial diagnosis. There is, therefore, no basis for service connection for any Parkinsonism or Parkinson's like symptoms as having been manifest in service or within the first post-service year, the latter of which would allow service connection on presumptive basis as a chronic disease under 38 C.F.R. § 3.309(a). Further, movement disorders including Parkinson's disease are not among the diseases for which service connection may be granted on a presumptive basis as associated with herbicide exposure under 38 C.F.R. § 3.309(e), precluding an award of benefits under that regulation. Nevertheless, as indicated above, the appellant is not precluded from establishing service connection on a direct basis under 38 C.F.R. § 3.303(d). See Combee v. Brown, 34 F.3d 1039 (Fed. Cir. 1994); McCartt v. West, 12 Vet. App. 164, 167 (1999). Based on the evidence outlined above, the Board finds the Veteran had active military service in the Republic of Vietnam from March 1968 to March 1969, which entitles him to the presumption of exposure to herbicide agents in service. In addition, based on the Veteran's November 2005 statement documenting his locations in Vietnam and the military use of herbicides in those locations, there is credible evidence that he was personally exposed to herbicide and toxic agents during that time. The Board recognizes, as stated earlier, that the VA Secretary has determined that a presumption of service connection is not warranted based on exposure to herbicides for movement disorders including Parkinson's disease, and further that the National Academy of Sciences, including in its Update 2004, has concluded, based on its evaluation of epidemiologic evidence that there is inadequate or insufficient information to determine whether an association exists between exposure to herbicides and Parkinson's disease. See 72 Fed. Reg. 32395-407 (2007). In the Federal Register, VA said that taking into account the available evidence and the National Academy of Sciences' analysis, the Secretary has found that the credible evidence against an association between herbicide exposure and Parkinson's disease outweighs the credible evidence for such an association and has determined that a positive association does not exist. Id. There is, however, of record competent medical evidence, namely from the Veteran's VA neurologist, Dr. J.S., who has a background in neurotoxicology and from a private neurologist, Dr. Prockop, who is a university neurology professor and practicing physician with a background in neurotoxicology, both of whom relate the Veteran's atypical Parkinsonism plus with signs and symptoms of supranuclear palsy to his in- service exposure to herbicide agents and other toxicants in service. As outlined earlier, both of these physicians considered questions of the etiology of the Veteran's neurological disorder over several months, and stated that after they reviewed material concerning the Veteran's exposure to herbicides and other toxicants along with journal articles and other documents with references to scientific studies and literature discussing potential neurologic health effects of dioxin exposure and other chemicals, they each opined that with respect to this Veteran, his exposure to herbicides and other chemicals resulted in his Parkinson's-like illness. Because the opinions provided by these physicians, who specialize in neurology and neurotoxicity, are specific to this Veteran and take into account his specific activities and exposures and in arriving at their conclusions consider extensive research papers, including those provided by the Veteran, the Board finds this evidence at least in equipoise with the National Academy of Sciences conclusion that there is inadequate or insufficient information to determine whether such an association generally exists between exposure to herbicides and Parkinson's disease. Under the benefit of the doubt rule, in order for the claimant to prevail, there need not be a preponderance of the evidence in the claimant's favor, but only an approximate balance of the positive and negative evidence, which is the case here. With reasonable doubt resolved in the appellant's favor, the Board concludes that the Veteran's atypical Parkinsonism plus with signs and symptoms of progressive supranuclear palsy was incurred in service. As the Veteran's Parkinson's plus with supranuclear palsy was the underlying cause of his death, the Board concludes that the criteria for service connection for the cause of the Veteran's death have been met. ORDER Service connection for the cause of the Veteran's death is granted. REMAND In December 2005, the Veteran filed a claim for service connection for bilateral hearing loss and in February 2006 added a claim of service connection for tinnitus. The Veteran died in May 2006, and the appellant filed her VA Form 21-534, Application for Dependency and Indemnity Compensation, Death Pension and Accrued Benefits by a Surviving Spouse or Child, in June 2006. In a rating decision dated in November 2006, the RO denied service connection for the cause of the Veteran's death, denied service connection for tinnitus for accrued benefits purposes, and granted service connection for bilateral hearing loss with a noncompensable rating for accrued benefits purposes. In a letter to the appellant dated in November 2006, the RO notified the appellant of its decision and her appellate rights. In May 2007, the appellant expressed disagreement with the denial of her dependency and indemnity compensation claim as well as the denial of accrued benefits, and she expressed her disagreement saying the denial of her claim was clear and unmistakable error. The appellant's representative, in a statement received at the RO in July 2007, requested specifically that its statement be accepted as a notice of disagreement with the rating decision dated in November 2006. The RO issued a statement of the case concerning the issue of service connection for the cause of the Veteran's death, the appellant perfected her appeal, and that issue was resolved in the above decision. The RO did not, however, issue a statement of the case that addresses the issue of entitlement to service connection for tinnitus for accrued benefits or the issue of entitlement to an initial compensable rating for bilateral hearing loss for accrued benefits purposes, and those issues must be remanded for issuance of a statement of the case. Manlincon v. West, 12 Vet. App. 238, 240-241 (1999). Accordingly, the case is REMANDED for the following action: Readjudicate the claims of entitlement to service connection for tinnitus for accrued benefits purposes and entitlement to an initial compensable rating for bilateral hearing loss for accrued benefits purposes. If any benefit sought remains denied, issue an appropriate statement of the case and notify the appellant and her representative of the action necessary to perfect an appeal. The appellant has the right to submit additional evidence and argument on the matters the Board has remanded. Kutscherousky v. West, 12 Vet. App. 369 (1999). This case must be afforded expeditious treatment. The law requires that all claims that are remanded by the Board of Veterans' Appeals or by the United States Court of Appeals for Veterans Claims for additional development or other appropriate action must be handled in an expeditious manner. See 38 U.S.C.A. §§ 5109B, 7112 (West Supp. 2008). ______________________________________________ M. SABULSKY Veterans Law Judge, Board of Veterans' Appeals Department of Veterans Affairs