Citation Nr: 1602097	
Decision Date: 01/19/16    Archive Date: 01/27/16

DOCKET NO.  03-10 284	)	DATE
	)
	)

On appeal from the
Department of Veterans Affairs Regional Office in Togus, Maine



THE ISSUE

Entitlement to service connection for chronic peripheral neuropathy, to include as due to exposure to Agent Orange.



REPRESENTATION

Appellant represented by:	Neil B. Riley, Attorney



WITNESS AT HEARING ON APPEAL

The Veteran



ATTORNEY FOR THE BOARD

T. Mainelli, Counsel


INTRODUCTION

The Veteran served on active duty from November 1963 to November 1965 and on active duty for training (ACDUTRA) in the Army Reserves in July 1967. 

This matter is before the Board of Veterans' Appeals (Board) on appeal of a rating decision issued in June 2002 by the Togus, Maine, Regional Office (RO) of the Department of Veterans Affairs (VA) (hereinafter Agency of Original Jurisdiction (AOJ)).

This case has a lengthy procedural history.  In September 2005, the Veteran participated in a Board hearing before a Veterans Law Judge (VLJ), now retired, and in October 2006, the Board denied service connection for chronic peripheral neuropathy, to include as due to exposure to Agent Orange.  The Veteran appealed the Board's decision to the United States Court of Appeals for Veterans Claims (Court).  In an Order in June 2008, the Veterans Court granted a Joint Motion for Remand (JMR) of the parties to the appeal, vacated the Board's decision, and remanded the case for readjudication consistent with the JMR.

In response to his September 2009 request, the Board remanded the case in December 2009 to afford the Veteran another Board hearing, as the Veteran was unrepresented in his prior hearing and had since retained counsel.  In February 2010, the Veteran testified at a hearing conducted by the VLJ who conducted his 2005 hearing.

In June 2010, the Board again denied the claim, and the Veteran again appealed the Board's denial to the Court.  In February 2011, the Court granted the parties' second JMR, vacating the Board's decision and remanding the case for readjudication. 

Per his third hearing request, in May 2011, the Board remanded the matter to afford the Veteran the opportunity to participate in a new Board hearing, as the Veteran had changed his representation.  In August 2011, the Veteran appeared at a third hearing before the VLJ who conducted his 2005 and 2009 hearings.  Transcripts of these hearings have been associated with the Veteran's claims file. 

In October 2011, pursuant to 38 C.F.R. § 20.901, the Board requested an advisory opinion from an independent medical expert (IME) on the questions of whether the Veteran was likely to have been exposed to significant levels of Agent Orange during his training at Camp Drum (Ft. Drum) some five years after the area was sprayed, and whether such exposure would be sufficient to cause the Veteran to develop chronic peripheral neuropathy some 25 years later.  The opinion was received in December 2011, and consistent with this negative opinion, the Board again denied the Veteran's claim in March 2012.  The parties to the appeal submitted another JMR, which the Court granted in January 2013.

In June 2013, the Veteran requested to participate in a fourth Board hearing, and the VLJ who had conducted the Veteran's prior hearings informed the Veteran that this hearing request would be held in abeyance until the Board undertook the development mandated by the 2013 JMR, namely to obtain opinion from an appropriately qualified expert in speaking to the issue of the extent of residual herbicides present at Fort Drum in 1964, 1965 and 1967.  Accordingly, in July 2013, the Board requested another advisory opinion from an IME, which was rendered in August 2013.  The Board provided this opinion to the Veteran and his attorney, and in response, the Veteran's attorney submitted a private medical opinion authored in December 2013.

After the completion of the development mandated by the 2013 JMR, the Board revisited the Veteran's hearing request, previously held in abeyance, and requested that he provide good cause for participating in a fourth hearing, as under ordinary circumstances, a Veteran is entitled to no more than one such hearing.  The Veteran's attorney submitted a letter asserting such good cause in October 2014.  However, the VLJ who had conducted the Veteran's prior three hearings had since retired; therefore, in December 2014, the Board informed the Veteran of this fact, which automatically entitled him to elect to participate in a new hearing and have his case decided by the individual who received his testimony.  In January 2015, the Veteran's attorney responded that the Veteran would like to participate in a new hearing to be conducted at the AOJ, thereby necessitating a remand of this matter.

In August 2015, the Veteran testified before the undersigned Veterans Law Judge.  A copy of the hearing transcript is associated with the claims folder.

In October 2015, the Veteran's attorney submitted additional evidence in support of the appeal with a waiver of AOJ consideration of this evidence in the first instance.

This appeal was processed using the Veterans Benefits Management System (VBMS).  Accordingly, any future consideration of this case should take into consideration the existence of this electronic record.

This appeal has been advanced on the Board's docket pursuant to 38 C.F.R. § 20.900(c) (2015).  38 U.S.C.A. § 7107(a)(2) (West 2014).


FINDINGS OF FACT

1.  Resolving reasonable doubt in favor of the Veteran, the Veteran was exposed to herbicides during his active military service while stationed at Fort Drum.

2.  Resolving reasonable doubt in favor of the Veteran, the Veteran's chronic peripheral neuropathy results from his exposure to herbicides during active service.


CONCLUSION OF LAW

The criteria for service connection for chronic peripheral neuropathy, to include as due to exposure to Agent Orange, have been met.  38 U.S.C.A. §§ 101(24), 1110, 1116, 1131, 5107 (West 2014); 38 C.F.R. §§ 3.6, 3.303, 3.307 (2015).
REASONS AND BASES FOR FINDINGS AND CONCLUSION

As provided for by the Veterans Claims Assistance Act of 2000 (VCAA), VA has a duty to notify and assist claimants in substantiating a claim for VA benefits.  38 U.S.C.A. §§ 5100, 5102, 5103, 5103A, 5107, 5126 (West 2014); 38 C.F.R. §§ 3.102, 3.156(a), 3.159, 3.326(a) (2015).  As the decision below reflects a full grant of the benefit sought, no further discussion of VA's duty to notify or assist the Veteran is required.

The Veteran seeks to establish his entitlement to service connection for chronic peripheral neuropathy as due to exposure to herbicides during active military service.  He asserts that he was exposed to herbicides while stationed at Fort Drum during training exercises in 1964 (six weeks), 1965 (six weeks) and 1967 (2 weeks).  His duties included sleeping outside on the ground, eating his meals in the woods, digging foxholes, and training outdoors.  The Veteran does not contend that his chronic peripheral neuropathy manifested contemporaneous in time to his military service.  Rather, he first reports the onset of neuromuscular abnormalities in the 1980s.

Service connection is established for disability resulting from personal injury suffered or disease contracted in the line of duty, or for aggravation of a preexisting injury suffered or disease contracted in the line of duty, during periods of active service.  38 U.S.C.A. §§ 1110, 1131. 

In general, service connection requires competent evidence showing: (1) the existence of a present disability; (2) in-service incurrence or aggravation of a disease or injury; and (3) a causal relationship between the present disability and the disease or injury incurred or aggravated during service.  Shedden v. Principi, 381 F.3d 1163, 1167 (Fed. Cir. 2004). 

The law provides that diseases associated with exposure to certain herbicide agents used in support of military operations in the Republic of Vietnam (Vietnam) during the Vietnam era will be considered to have been incurred in service.  38 U.S.C.A. § 1116(a)(1); 38 C.F.R. § 3.307(a)(6).  The presumption of service connection requires exposure to an herbicide agent and manifestation of the disease to a degree of 10 percent or more within the time period specified for each disease.  38 C.F.R. § 3.307(a)(6)(ii). 

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 U.S.C.A. § 1116(a)(4); 38 C.F.R. § 3.307(a)(6)(i).  A Veteran who is not entitled to a presumption of exposure to herbicides may nonetheless show actual exposure to herbicides.  Haas v. Peake, 525 F.3d 1168, 1193-94 (Fed. Cir. 2008)

Effective September 6, 2013, VA amended its regulations regarding presumptive service connection for peripheral neuropathy associated with herbicide exposure.  See 78 Fed. Reg. 54763-54766 (September 6, 2013) (final rule) (replacing the terms "acute and subacute" and "transient" peripheral neuropathy with "early onset" peripheral neuropathy; removing the requirement under the former §§ 3.307(a)(6)(ii) and 3.309(e) that "acute and subacute" peripheral neuropathy appear within weeks or months after exposure; and removing the requirement that the condition resolve within two years of the date of onset in order for the herbicide presumption to apply).  In summary, under the regulatory amendment, to warrant service connection, "early-onset" peripheral neuropathy must 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 a herbicide agent during active military, naval, or air service.  38 C.F.R. § 3.307(a)(6)(ii).

Notably, the Secretary of VA has determined that there is no positive association between exposure to herbicides and any other condition for which the Secretary has not specifically determined that a presumption of service connection is warranted.  See 59 Fed. Reg. 341-346 (1994); see also 61 Fed. Reg. 57586-57589 (1996).  In prescribing a regulation for presumptive service connection, the Secretary relies on reports from the National Academy of Sciences (NAS) - which submits a report to the Secretary at least every two years - and all other available sound medical, scientific and analysis.  38 U.S.C.A. § 1116; Agent Orange Act of 1991, Pub. L. No. 102-4, 105 Stat. 11 (1991).  By statute, an association between the occurrence in humans and exposure to an herbicide agent shall be considered positive if the credible evidence for the association is equal to or outweighs the credible evidence against the association.  38 U.S.C.A. § 1116(b)(3).

Nonetheless, even when a Veteran is found not to be entitled to a regulatory presumption of service connection for a given disability, the claim must be reviewed to determine whether service connection can be established on a direct basis.  Combee v. Brown, 34 F.3d 1039, 1043-1044 (Fed. Cir. 1994); McCartt v. West, 12 Vet. App. 164, 167 (1999).  

When there is an approximate balance of positive and negative evidence regarding any issue material to the determination of a matter, the Secretary shall give the benefit of the doubt to the claimant.  38 U.S.C.A. § 5107; 38 C.F.R. § 3.102; see also Gilbert v. Derwinski, 1 Vet. App. 49, 53 (1990). 

The Veteran had a period of active service from November 1963 to November 1965 with ACDUTRA in the Army Reserves in July 1967.  His service treatment records (STRs) document his presence at Fort Drum in 1964.  His presence at Fort Drum in 1965 and 1967 has been conceded. 

The Veteran does not contend, and the evidence does not show, that his peripheral neuropathy manifested contemporaneous in time to his military service.  Rather, he first reports the onset of neuromuscular abnormalities in the 1980s.  This testimony is consistent with VA records in May 1982 wherein he reported the sudden onset of back pain and numbness in the right lower extremity while at work.  In May 1983, a computed tomography (CT) scan showed a protruding disc at L5-S1.  In July 1986, the Veteran complained of numbness and a prickly sensation in his right foot and a burning sensation in his left foot.  He also complained of numbness and tingling in each arm.  The pertinent diagnosis was ruptured disc at L5-S1. 

In June 1989, the Veteran was evaluated for complaints of low back pain with pain in the right leg.  He also complained of muscle spasms in the low back and leg, as well numbness in the right shoulder and arm.  On physical examination, he did not exhibit any weakness or difficulty in using any of his extremities, and his gait was normal.  The physician noted that the Veteran's original industrial injury had probably resulted in a low back strain with later myofascial restrictions. 

In April 1990, the Veteran was seen for a disability evaluation for his back and leg pain resulting from a work-related injury in May 1982.  His symptoms included low back pain and right posterior thigh and leg pain with occasional numbness in the right leg and up into the right shoulder and arm.  On physical examination, there was no obvious atrophy in the lower extremities and his muscle strength was normal.  The diagnosis was chronic low back myofascial syndrome.  It was noted that a diagnosis of fibromyalgia had been made and that the diagnosis was consistent with myofascial syndrome and referred to the same condition.

In September 1990, the Veteran was seen for a neurological examination related to persistent back and leg pain and radiating pain in the right shoulder and arm.  The pertinent diagnoses were fibromyalgia and fibromyositis in the cervical, dorsal, and lumbosacral areas, a ruptured disc at L5-S1, chronic low back pain from an initial acute sprain, and hand strain. 

In April 1999, the Veteran was evaluated for possible muscular dystrophy.  At that time, he complained of periodic or paroxysmal proximal weakness, exacerbated by cold, stress, and sitting too long. 

In July 2000, the Veteran was seen for a follow-up evaluation at VA due to an abnormal electromyography (EMG) study and a "curious waddling-type gait."  History included a back injury in 1982, cramping, and unusual muscular restrictions in movement.  He had been evaluated for muscular dystrophy and specific gene mutations with negative results.  A nerve biopsy showed rare atrophic fibers, both Type I and Type II, but no clear diagnosis of a neuromuscular syndrome had been made.  Results of repeat EMG studies were read as most typical of mild peripheral neuropathy, which was sensory motor in nature.  Based on the described symptoms, the physician expressed the opinion that the Veteran's muscle disorder was in the nature of myotonia rather than neuropathy or myopathy, but the exact diagnosis remained unclear. The physician noted the Veteran's history of exposure to ether and urethane where he worked, but no other toxic exposures were known or considered.

In February 2002, the Veteran had an Agent Orange examination at VA.  The Veteran stated that he was possibly exposed to Agent Orange in service.  He gave a medical history which included fibromatosis and a neuromuscular disorder of unknown etiology.

In March 2002, the Veteran was seen at VA for follow-up related to his abnormal gait.  EMG testing of the lower extremities was consistent with a predominantly motor peripheral neuropathy.  EMG testing also showed moderately severe right carpal tunnel syndrome, moderately progressed since May 1999.  The diagnoses were moderately severe right carpal tunnel syndrome with modest progression from 1999, motor greater than sensory axonal and demyelinating (mixed) peripheral neuropathy with significant progression by NCV and EMG criteria, and possible right L-5 radiculopathy as exemplified by the paraspinal examination. 

The physician, Dr. S.N.M., Chief of Neurology, noted that the differential diagnoses for motor or motor greater than sensory axonal loss neuropathies included arsenic poisoning, which had been excluded previously, chronic inflammation demyelinating polyneuropathy, chronic non-immune polyneuropathy (including entities such as monoclonal gammopathy of undetermined significance, multiple myeloma, SLE, or cryoglobulinemia), hereditary neuropathy, and multifocal motor neuropathy with conduction block. 

Based on the present study, the physician stated that there was no evidence of multifocal motor neuropathy or chronic inflammatory demyelinating polyneuropathy.  He noted that other differential diagnoses included Charcot-Marie-Tooth disease, type 2; Diapason neuropathy; Disulfiram associated neuropathy; the axonal form of Guillain-Barre syndrome, which it clearly was not; hyperinsulinism; Nitrofurantoin use; organophosphate poisoning; porphyria; paraneoplastic lymphoma or carcinoma; and Vincristine.  The physician noted that it was interesting that the Veteran was exposed to herbicides in the military and was being evaluated for Agent Orange exposure, but it was difficult to prove one way or the other the causal relationship. 

Dr. S.N.M. expressed the opinion that, clinically and by history and by EMG, there was a weak correlation that the Veteran probably had a neuropathy relative to exposure to some kind of toxins, including Agent Orange, but that it was extremely hard to make a correlation because according to published VA data approved by Congress, peripheral neuropathy associated with Agent Orange should have its origin within the first 12 to 18 months in order to be considered a service-connected condition.  It was noted that the Veteran's complaints had been present for a number of years, but had not been documented as having onset within 12 to 18 months of his time spent in the military in "Vietnam," but the nature of the peripheral neuropathy as suggested by the EMG was suggestive of a toxic neuropathy.

In March 2005, the Veteran was evaluated by K.D.S., DO, for a history of peripheral neuropathy of over 15 years' duration with a history of exposure to Agent Orange at Fort Drum in 1964, 1965, and 1967.  The Veteran stated that the camp had been sprayed with Agent Orange in 1959 and it had remained in the soil.  He reported that his VA physician could not exclude the possibility of peripheral neuropathy related to Agent Orange toxicity.  After neurological examination, the doctor noted that the results of electrodiagnostic testing of the lower extremities showed mixed polyneuropathy with both demyelinating and axonal features.  She noted that the neuropathic features noted on examination could be consistent with toxic neuropathy, but that laboratory studies for other potential etiologies should be done.

In May 2005, Dr. K.D.S. stated that the electrodiagnostic testing confirmed features consistent with polyneuropathy.  The doctor stated that: "I cannot determine that [the Veteran's] polyneuropathy is secondary to agent orange exposure nor can I exclude that there is a toxic neuropathy."

In October 2011, the Board sought an IME opinion.  The information then of record, obtained from the Department of Defense, showed that, in 1959, 13 drums of Agent Orange were sprayed over 4 square miles of Fort Drum.  The area selected for the defoliant was a target area for explosive ordnance, not for troop maneuvers.  www.dod.mil/pubs/foi/operation_and_plans/.../TacticalHerbicides.pdf.  (December 2006).  The IME was asked to address the following questions: 

Whether it is more likely than not, at least as likely as not, or less likely than not that the Veteran was actually exposed to an herbicide, Agent Orange, at Ft. Drum in 1964, through contact with the foliage, soil, or ground water outside of the area where the Agent Orange was applied to foliage in 1959.  In other words, what was the environmental fate of the Agent Orange five years after its use in an area not actually sprayed with Agent Orange, and, if any residue of Agent Orange was present, did it pose a health risk to the Veteran? 

If the Veteran was actually exposed to the residue of Agent Orange in 1964, in 1965, and in 1967, whether it is more likely than not, at least as likely as not, or less likely than not that the Veteran's exposure to the residue of Agent Orange actually caused chronic peripheral neuropathy, first manifested in 1990, 25 years after exposure to the herbicide?

Also, would the health risk increase with similar exposure in 1965 and in 1967?

In December 2011, a Board Certified Neurologist, who is a Professor of Neurology and Radiology at the University of Massachusetts Medical School, noted that the medical evidence showed progression of the Veteran's peripheral neuropathy between 2000 and 2002.  In the opinion of the IME, it was "extremely unlikely" that peripheral neuropathy was related to Agent Orange exposure because the Veteran's time at Ft. Drum occurred five years after the spraying was performed and it was therefore unlikely that there was sufficient residual Agent Orange in that area to cause peripheral neuropathy.  In addition, the IME expert noted that peripheral neuropathy related to Agent Orange exposure occurs within one year of exposure and the Veteran was exposed to very low levels of Agent Orange, if any at all, and the Veteran did not develop peripheral neuropathy until more than 30 years later.  The IME concluded that it was less likely than not that the Veteran was exposed to Agent Orange and, if so exposed, that the toxic exposure would have any relationship to the current peripheral neuropathy.

Thereafter, the Board sought an IME opinion from a Board Certified Specialist in Occupational Medicine, pursuant to the terms of a JMR which concluded that the IME examiner in December 2011 was not shown to possess the expertise to provide opinion as to how much residual herbicide contamination existed at Fort Drum during the Veteran's presence.

An August 2013 IME opinion, provided by a Board Certified Specialist in Occupational Medicine, first concluded that, to a reasonable degree of medical certainty, that it was not at least as likely as not that the Veteran was actually exposed to an herbicide at Fort Drum in 1964 through contact with the foliage, soil or groundwater outside of the area.  The examiner indicated that the record showed that herbicide spraying at Fort Drum occurred in a target area used for explosive ordnance and not troop maneuvers.  In order for the Veteran to have been exposed, he would have had to be stationed in the sprayed area while the area was still wet.  The Veteran, however, had been stationed in a contonement area.  

The IME explained that Agent Orange dried quickly after spraying and broke down within hours to days when exposed to sunlight (if not bound chemically to a biological surface such as soil, leaves and grass) and was no longer harmful.  The dioxin TCDD was an unwanted byproduct of herbicides.  Dioxins were pollutants which were released into the environment by burning waste, diesel exhaust, chemical manufacturing and other processes.  TCDD was the most toxic of dioxins having been classified as a human carcinogen by the Environmental Protection Agency (EPA).  The half-life of TCDD in humans was calculated between 6 to 12 years.  The examiner stated that any remaining TCDD in the area of the Veteran's presence would have been "miniscule."  As a result of continuing degradation, the Veteran's similar exposure in 1965 and 1967 would not increase his probability of developing chronic peripheral neuropathy as there was no indication that he was exposed to residual TCDD at these later dates.  It was also noted that the Veteran might have been exposed to other toxins related to peripheral neuropathy during that time period, which added to the difficulty in ascribing a possible association to herbicide exposure at Fort Drum.

The IME next opined that it was not more likely than not that the Veteran's exposure to herbicide residue actually caused his chronic peripheral neuropathy, which first manifested in 1990 (or 25 years after herbicide exposure).  In so opining, the examiner cited the potential causes of toxic neuropathy listed by Dr. S.N.M.  It was noted that the most common toxin that caused neuropathies were drug related, and that the record did not contain a full listing of all medications taken by the Veteran during the relevant time period nor other toxins to which he may have been exposed.  It was further noted that Dr. S.N.M. did not diagnose the Veteran as having a toxic neuropathy resulting from Agent Orange exposure, but rather exposure to some kind of toxin.  Overall, the IME opined that it was not more likely than not that the Veteran's peripheral neuropathy was caused by exposure to an herbicide at Fort Drum in 1964 though contact with the foliage, soil or groundwater outside of the area where the herbicide was applied to foliage in 1959.

In response, the Veteran submitted a December 2013 opinion from an orthopaedic surgeon.  This examiner, referencing the World Health Organization Fact Sheet #225, indicated that dioxin 2,3,7, 8-tetrachlorodibenzo-para-dioxin (TCDD) was present in some batches of the herbicide Agent Orange used as a defoliant during the Vietnam War.  TCDD concentrated in tissues and body cells which had high levels of fat.  It was noted that more than 90 percent of human exposure to dioxin was through the food supply but direct exposure also occurred.  It was also likely that other toxic substances or dioxin-like PCBs were present as a consequence of Agent Orange exposure.  The examiner also noted that the relationship between peripheral nervous system, peripheral neuropathy and dioxin was influenced by the high fat content of the peripheral nerve.  The examiner noted that an EPA analysis of issues related to dioxin toxicity demonstrated that dioxin exposure had long-term negative effects.  On review of the record, the examiner found that the Veteran's peripheral neuropathies were at least as likely as not due to his exposure to Agent Orange in service.

Additionally, the Veteran's attorney submitted another opinion in October 2015 by a different orthopedic surgeon.  This examiner, on review of the record and the Veteran's testimony, found that the Veteran manifested marked ataxia and a mixed motor/sensory peripheral neuropathy that was at least as likely as not secondary to Agent Orange exposure in service.

As noted in prior IME requests, the record on appeal involves two dispositive issues.  The first issue is whether the Veteran had actual herbicide exposure at Fort Drum in 1964, 1965 and 1967 and, if so, whether his peripheral neuropathy has been caused by such exposure.

The documentary evidence of record establishes that, in 1959, 13 drums of Agent Orange were sprayed over 4 square miles of Fort Drum.  The area selected for the defoliant was a target area for explosive ordnance.  The central issue in this case concerns whether the Veteran's presence at Fort Drum 5 years after this spraying involved an actual herbicide exposure.  

The Board has obtained expert opinion from a Board Certified Specialist in Occupational Medicine who, by referencing the properties of TCDD, found that it was not at least as likely as not that the Veteran was actually exposed to an herbicide at Fort Drum in 1964 through contact with the foliage, soil or groundwater outside of the area.  In essence, the examiner opined that the toxic properties of TCDD would have degraded over the 5-year period between the actual spraying (1959) and the Veteran's presence (1964) to the point where the Veteran's exposure would be "miniscule" if any at all.

The Veteran, however, argues that the August 2103 IME report does not adequately answer the question of how much residual herbicide remained in the soil at Fort Drum in 1964, 1965 and 1967.  In support of his claim, the Veteran has submitted an article entitled "Yale scientist tells Congress Agent Orange research is flawed, exposure more widespread than reported."  This article reflects the congressional testimony of a Yale School of Nursing Research Scientist who referenced a Canadian scientist led soil sampling that found high levels of dioxin concentrations at former military bases presumably many years after use of Agent Orange.

The Board has had the opportunity to conduct legal research for other cases involving alleged herbicide exposure at Fort Drum.  The Board has found particularly pertinent information in the case of Malinowski v. Gibson, No. 13-0016, WL 2768851 (June 19, 20142014), which involved the case of another Veteran who was stationed at Fort Drum 1974.  In pertinent part, this non-precedential Memorandum Decision cited the following evidence which had been presented in support of the claim:

According to a July 1981 reported prepared by the Chemical Systems Laboratory at the Aberdeen Proving Ground, chemicals found in Agent Orange were discovered at Fort Drum in five-gallon metal cans stored in an "an unheated wooden frame building with a wooden floor."  R. at 198.  This rustic facility did "not meet present day requirements for storage of pesticides."  R. at 226.  Another building was undergoing renovations so that it could be used to "properly store" herbicides and other pesticides.  R. at 198.
 
The report also reveals that the following occurred at Fort Drum: (1) in 1961 Dow Chemical Company "tested an experimental defoliant"; (2) in the 1950s a "large quantity of herbicide ... was sprayed from a helicopter over a site in the main impact area"; (3) from 1969 to 1978, herbicides were "used to control vegetation along fences and ... used to control brush along [two roads] in the main impact area"; and (4) from the 1950s through the early 1970s herbicides were used "on range impact areas ... to improve the line of vision from observation points to target impact areas."  Id.
 
In February 1984, an official at the U.S. Army Toxic and Hazardous Materials Agency wrote that an "exploratory survey at [Fort Drum] has been designed to determine whether or not site specific contaminants are migrating or have the potential to migrate beyond the installation's boundaries."  R. at 70.  Raw data for the survey was to be generated by testing groundwater, surface water, sediment, and soil for "the presence of chemical contamination," the official wrote.  Id.  The data would then "be used to assess any environmental or health hazard caused by existing or potential contamination [and] additional work or corrective actions may be warranted."  Id.  The official stated that samples collected for the survey would be tested for the presence of chemicals associated with Agent Orange because "this particular herbicide was used on the range impact areas to improve the line of vision from observation points to target impact areas ... during the 1960s through the early 1970s."  Id.

Nonetheless, in that case, the United States Armed Services Center for Research of Unit Records only conceded that four square miles of Fort Drum were treated with Agent Orange in 1959 and found no additional records of "spraying, testing, transporting, storage, or usage of Agent Orange at Fort Drum, New York." 

The Board notes that it may take judicial notice of evidence not subject to reasonable dispute - particularly if favorable to the Veteran.  See Smith (Brady) v. Derwinski, 1 Vet. App. 235, 238 (1991).  The evidence cited in the Malinowski case raises significant doubt regarding whether herbicides were stored and used at Fort Drum after 1959.  The July 1981 report prepared by the Chemical Systems Laboratory at the Aberdeen Proving Ground actually found five-gallon Agent Orange barrels improperly stored in a wooden structure.  This report also discusses that, in 1961, the Dow Chemical Company "tested an experimental defoliant" and that "from the 1950s through the early 1970s herbicides were used "on range impact areas ... to improve the line of vision from observation points to target impact areas."  As noted by the Court in Malinowski, the 1984 report by the U.S. Army Toxic and Hazardous Materials Agency, investigating whether Agent Orange sprayed onto vegetation at Fort Drum in the 1960s and 1970s still may have been present in the surrounding environment, "strongly suggest[ed] that experts, at least in 1984, believed that Agent Orange may remain extant and hazardous a decade or more after it was applied."

Notably, the Malinowski Court also noted that a June 2004 Board decision had conceded that a Veteran was exposed to herbicides at Fort Drum in 1962 by relying on the 1984 report by the U.S. Army Toxic and Hazardous Materials Agency.  This Board decision, under Docket Number 03-26 757, further elaborates that the February 1984 letter from the Department of the Army, U.S. Army Toxic and Hazardous Materials Agency stated that herbicide 2,4,5-T was utilized during the 1960s through the early 1970s at Fort Drum, New York, to improve the line of vision from observation points to target impact areas as well as to control brush along roads in the main impact area.  Notably, 2,4,5-T and its contaminant TCDD is listed as a qualifying herbicide under 38 U.S.C.A. § 1116(a)(4) and 38 C.F.R. § 3.307(a)(6)(i).  

The Board observes that prior Board decisions have no precedential value in subsequent Board decisions.  Nonetheless, the validity of the July 1981 report prepared by the Chemical Systems Laboratory at the Aberdeen Proving Ground and the 1984 report by the U.S. Army Toxic and Hazardous Materials Agency cited above were accepted by the Board and the Court in prior proceedings.  The Board, at this time, has no reason to doubt the validity of these two government agency reports.

Given the above, the Board finds the August 2013 IME opinion regarding the extent of the Veteran's herbicide exposure in 1964, 1965 and 1967 has substantially reduced probative weight as that examiner did not have all procurable information before her regarding the extent of herbicide use at Fort Drum.  See Nieves-Rodriguez v. Peake, 22 Vet. App. 295 (2008) (citing to Fed.R.Evid. 702 as guiding factors to be used by VA adjudicators in evaluating the probative value of a medical opinion; whether (1) the testimony is based upon sufficient facts or data; (2) the testimony is the product of reliable principles and methods; and (3) the expert witness has applied the principles and methods reliably to the facts of the case).

Resolving reasonable doubt in favor of the Veteran, and in light of the February 1984 letter from the Department of the Army, U.S. Army Toxic and Hazardous Materials Agency stating that the herbicide 2,4,5-T was utilized during the 1960s through the early 1970s at Fort Drum, New York, the Board finds that the Veteran was exposed to herbicides during his active military service while stationed at Fort Drum.  38 U.S.C.A. § 5107(b).

Thus, the remaining dispositive issue on appeal concerns whether the Veteran's chronic peripheral neuropathy results from his exposure to herbicides in service.  As noted above, the Veteran concedes that his peripheral neuropathy manifested many years after service and, as such, service connection is not warranted for chronic peripheral neuropathy on a presumptive basis.  38 C.F.R. § 3.307(a)(6)(ii) (providing for presumptive service connection for "early-onset" peripheral neuropathy which manifested to a degree of 10 percent or more within a year after the last date on which the Veteran was exposed to a herbicide agent during active military, naval, or air service).

However, the Veteran may still establish his entitlement to service connection under the general laws governing service connection claims by proving direct causation.  Combee, 34 F.3d 1039, 1042 (Fed. Cir. 1994).

The record on appeal includes opinions for and against the claim.  The earlier opinions of Dr. S.N.M. and Dr. K.D.S. indicate that the Veteran's mixed polyneuropathy and neuropathic features on examination could be consistent with toxic neuropathy, but no conclusive opinion was reached.  Additionally, two recent opinions from orthopedic surgeons have opined that it is at least as likely as not that the Veteran's peripheral neuropathy is due to the Veteran's herbicide exposure in service.

On the other hand, a Board Certified Neurologist and a Board Certified Specialist in Occupational Medicine have opined that the Veteran's peripheral neuropathy is not due to the Veteran's herbicide exposure in service.  Both of these opinions are based, in part, on the assumption that the Veteran had minimal, if any, herbicide exposure at Fort Drum.

As discussed above, the IME examiner opinions were formed without knowledge of the 1984 letter from the Department of the Army, U.S. Army Toxic and Hazardous Materials Agency stating that the herbicide 2,4,5-T was utilized during the 1960s through the early 1970s at Fort Drum, New York.  Thus, these opinions have substantially reduced probative value.

As for the opinions in favor of the claim, the Board observes that the Veteran has reported a history of exposure to ether and urethane while working in a shoe factory.  However, this history was considered by Dr. S.N.M. who drew no conclusions that such exposure was the cause of the Veteran's peripheral neuropathy.  In fact, no examiner has offered an opinion that the Veteran's peripheral neuropathy is due to his workplace exposure to toxins.

On the other hand, the recent opinions from the orthopedic surgeons which attribute the Veteran's peripheral neuropathy to his herbicide exposure in service are based upon an accurate review of the factual history in this case.  The December 2013 opinion noted that TCDD concentrated in tissues and body cells which had high levels of fat, and that the peripheral nerve had a high fat content.  The orthopedic surgeon opinions are generally consistent with the opinions of Dr. S.N.M. and Dr. K.D.S. that the Veteran's mixed polyneuropathy and neuropathic features on examination could be consistent with toxic neuropathy.  Resolving reasonable doubt in favor of the Veteran, the Board finds that the Veteran's chronic peripheral neuropathy is due to his herbicide exposure in service.  Thus, the claim of entitlement to service connection for chronic peripheral neuropathy as due to herbicide exposure is granted.


ORDER

The claim of entitlement to service connection for chronic peripheral neuropathy, to include as due to exposure to Agent Orange, is granted.



____________________________________________
MARJORIE A. AUER
Veterans Law Judge, Board of Veterans' Appeals



Department of Veterans Affairs