Agent Orange Information
Department of Veterans Affairs
REPORT TO TO SECRETARY OF THE DEPARTMENT OF VETERANS AFFAIRS
ON THE ASSOCIATION BETWEEN ADVERSE HEALTH EFFECTS
AND EXPOSURE TO AGENT ORANGE
CONFIDENTIAL STATUS (1)
As Reported by Special Assistant
Admiral E.R. Zumwalt, Jr.
May 5, 1990
NOT FOR PUBLICATION AND
RELEASE TO THE GENERAL PUBLIC
On October 6, 1989 I was appointed as special assistant to
Secretary Derwinski of the Department of Veterans Affairs to assist the
Secretary in determining
whether it is at least as likely as not that there is a statistical association between exposure to Agent Orange and a specific adverse health effect.
As special assistant, I was entrusted with evaluating the
numerous data relevant to the statistical association between exposure to Agent
Orange and the specific
adverse health effects manifested by veterans who saw active duty in Vietnam. Such evaluations were made in accordance with the standards set forth in Public Law
98-542, the Veterans’ Dioxin and Radiation Exposure Compensation Standards Act and 38 C.F.R. 1.17, regulations of the Department of Veterans Affairs
concerning the evaluation of studies relating to health effects of dioxin and radiation exposure.
Consistent with my responsibilities as special assistant,
I reviewed and evaluated the work of the Scientific Council of the Veterans’
Advisory Committee on
Environmental Hazards and commissioned independent scientific experts to assist me in evaluating the validity of numerous human and animal studies on the effects of
exposure to Agent Orange and/or exposure to herbicides containing 2,3,7,8 tetrachlorodibenzo-para-dioxin (TCDD or dioxin). In addition, I reviewed and evaluated
the protocol and standards employed by government sponsored studies
to assess such studies’ credibility, fairness and consistency with generally accepted scientific practices.
After reviewing the scientific literature related to the
health effects of Vietnam Veterans exposed to Agent Orange as well as other
studies concerning the health
hazards of civilian exposure to dioxin contaminants, I conclude that there is adequate evidence for the Secretary to reasonably conclude that it is at least as likely as
not that there is a relationship between exposure to Agent Orange and the following health problems: non—Hodgkin’s lymphoma, chloracne and other skin
disorders, lip cancer, bone cancer, soft tissue sarcoma, birth defects, skin cancer, porphyria cutanea tarda and other liver disorders, Hodgkin’s disease,
hematopoietic diseases, multiple myeloma, neurological defects, auto—immune diseases and disorders, leukemia, lung cancer, kidney cancer, malignant melanoma,
pancreatic cancer, stomach cancer, colon cancer, nasal/pharyngeal/esophageal cancers, prostate cancer, testicular cancer, liver cancer, brain cancer, psychosocial
effects and gastrointestinal diseases.
I further conclude that the Veterans’ Advisory Committee
on Environmental Hazards has not acted with impartiality in its review and
assessment of the scientific
evidence related to the association of adverse health effects and exposure to Agent Orange.
In addition to providing evidence in support of the conclusions stated above, this report provides the Secretary with
a review of the scientific, political and legal efforts that have occurred
over the last decade to establish that Vietnam Veterans who have been exposed to
Orange are in fact entitled to compensation for various illnesses as service-related injuries.
II. AGENT ORANGE USAGE IN VIETNAM
Agent Orange was a 50:50 mixture of 2,4-D and 2,4,5-T. The
latter component, 2,4,5-T, was found to contain the contaminant TCDD or 2,3,7,
8-tetrachlorodibenzo-para-dioxin (i.e. dioxin), which is regarded as one of the most toxic chemicals known to man.1
From 1962 to 1971 the United States military sprayed theherbicide Agent Orange to accomplish the following objectives: 1)
1 See CDC Protocol for Epidemiologic Studies on the Health
of Vietnam Veterans (November, 1983), p. 4 ( The CDC Protocol also contains a
as of 1983 of the health effects on animals and humans exposed to herbicides and dioxin, pp. 63-78. The literature review documents health problems such as
chloracne, immunological suppression, neurological and psychological effects, reproductive problems such as birth defects, carcinogenic effects such as soft tissue
sarcomas, lymphomas and thyroid tumors, and various gastrointestinal disorders) ; See also General Accounting Office, "Report by the Comptroller General: Health
Effects of Exposure to Herbicide Orange in South Vietnam Should Be Resolved," GAO-CED-79-22 at 2 (April 6, 1979) (hereinafter GAO Report, 1979).
Dioxin is a family of chemicals (75 in all) that does not
occur naturally, nor is it intentionally manufactured by any industry. The most
toxic dioxin is called 2,3,7,8
— TCDD. Dioxins are produced as byproducts of the manufacture of some herbicides ( for example, 2,4, 5—T), wood preservatives made from trichlorophenals,
and some germicides. Dioxins are also produced by the manufacture of pulp and paper, by the combustion of wood in the presence of chlorine, by fires involving
chlorinated benzenes and biphenyls (e.g. PCBs), by the exhaust of automobiles burning leaded fuel, and by municipal solid waste incinerators
defoliate jungle terrain to improve observation and prevent enemy ambush; 2)
destroy food crops; and 3) clear Vegetation around military installations,
fire base camps, and trails 2
Unlike civilian applications of the components contained
in Agent Orange which are diluted in oil and water, Agent Orange was sprayed
undiluted in Vietnam.
Military applications were sprayed at the rate of approximately 3 gallons per acre and contained approximately 12 pounds of 2,4-D and 13.8 pounds of 2,4,5-T.3
Although the military dispensed Agent Orange in
concentrations 6 to 25 times the manufacturer’s suggested rate, "at that
time the Department of Defense (DOD)
did not consider herbicide orange toxic or dangerous to humans and took few precautions to prevent exposure to it."’ Yet, evidence readily suggests that at the time
of its use experts knew that Agent Orange was harmful to military personnel.5
2 See Bruce Myers, "Soldier of Orange: The
Administrative, Diplomatic, Legislative and Litigatory Impact of Herbicide Agent
Orange in South Vietnam," 8 B. C.
Env’t. Aff. L. Rev. 159, 162 (1979).
3 See GAO Report, 1979 at 2, 3 n.1; See also Myers, 8 B.C.
Env’t Aff. L. Rev, at 162. In contrast, civilian applications of 2,4,5—T
varied from 1 to 4 pounds
4 General Accounting Office, ‘Ground Troops in South Vietnam Were in Areas Sprayed with Herbicide Orange," FPCD 80-23, p.1 (November 16, 1979).
5 Letter from Dr. James R. Clary to Senator Tom Daschle
(September 9, 1988). Dr. Clary is a former government scientist with the
Chemical Weapons. Branch,.
BW/CW Division, Air Force Armament Development Laboratory, Eglin APE, Florida. Dr. Clary was instrumental in designing the specifications for the A/A 45y-l
spray tank (ADO 42) and was also the scientist who prepared the
The bulk of Agent Orange herbicides used in Vietnam were
reportedly sprayed from "Operation Ranch Hand" fixed wing aircraft.
Smaller quantities were applied
from helicopters, trucks, riverboats, and by hand. Although voluminous records of Ranch Hand missions are contained in computer records, otherwise known as the
HERBS and Service HERBs tapes, a significant, if not major source of exposure for ground forces was from non— recorded, non Ranch Hand operations.6
Widespread use of Agent Orange coincided with the massive buildup of U.S. military personnel in Vietnam, reaching a peak in
final report on Ranch Hand: Herbicide Operations in SEA, July 1979. According to Dr. Clary:
When we (military
scientists) initiated the herbicide program in the 1960’s, we were aware of
the potential for damage due to dioxin contamination in
the herbicide. We were even aware that the ‘military6 formulation had a higher dioxin concentration than the ‘civilian’ version due to the lower cost and
speed of manufacture. However, because the material was to be used on the ‘enemy’, none of us were overly concerned. We never considered a
scenario in which. our own personnel would become contaminated with the herbicide. And, if we had, we would have expected our own government to
give assistance to veterans so contaminated.
See also notes 13, 73-75 and accompanying text infra for additional information of the manufacturer’s awareness of the toxicity of Agent Orange.
6 Combat units, such as the ‘Brown Water Navy,’ frequently conducted
"unofficial" sprayings of Agent Orange obtained from out of channel,
and thus unrecorded
sources. Additionally, as Commander, U.S. Naval Forces, Vietnam, I was aware that Agent Orange issued to Allied forces was frequently used on unrecorded
1969 and eventually stopping in 1971. 7 Thus, according to an official of the
then Veterans Administration, it was "theoretically possible that about 4.2
American soldiers could have made transient or significant contact with the herbicides because of [the Ranch Hand Operation]." 8
A. REASONS FOR PHASE OUT
Beginning as early as 1968, scientists, health officials,
politicians and the military itself began to express concerns about the
potential toxicity of Agent Orange and
its contaminant dioxin to humans. For instance, in February 1969 The Bionetics Research Council Committee ("BRC’) in a report commissioned by the United States
Department of Agriculture found that 2,4,5-T showed a "significant potential to increase birth defects." 9 Within four months after the BRC report, Vietnamese
newspapers began reporting significant increases in human birth defects ostensibly due to exposure to Agent Orange.10
7 GAO Report 1979, supra note 1, at 29. See also note 82
and accompanying text infra for a discussion of the correlation between the
spraying of Agent Orange
and the hospitalization of Vietnam soldiers for disease and non-battle related injuries.
8 House Comm. on Veteran’s Affairs, 95th Cong., 2d Sess.,
Herbicide "Agent Orange". Hearings before the Subcommittee on Medical
Facilities and Benefits,
(Oct. 11, 1978) (Statement of Maj. Sen. Garth Dettinger USAF, Deputy Surgeon General USAF at 12).
9 Myers at 166.
10 Id While birth defects did significantly
increase in Saigon, critics contend that Saigon was not an area where the
preponderance of defoliation missions were
flown and argue that such increases were due primarily to the influx of U.S. medical personnel who kept better records of birth defects. Subsequent
By October, 1969, the National Institute of Health
confirmed that 2,4,5—T could cause malformations and stillbirths in mice,
thereby prompting the Department
of Defense to announce a partial curtailment of its Agent Orange spraying.11
By April 15, 1970, the public outcry and mounting
scientific evidence caused the Surgeon General of the United States to issue a
warning that the use of 2,4,5-T
might be hazardous to "our health". 12
On the same day, the Secretaries of Agriculture, Health
Education and Welfare, and the Interior, stirred by the publication of studies
that indicated 2,4,5-T was a
teratogen (i.e. caused birth defects), jointly announced the suspension of its use around lakes, ponds, ditch banks, recreation areas and
studies in Vietnam confirm the incidence of increased birth defects among
civilian populations exposed to Agent Orange. See e.g. Phuong, et. al. "An
Reproductive Abnormalities in Women Inhabiting Herbicide Sprayed and Non-herbicide Sprayed Areas in the South of Vietnam, 152-1981 18 Chemospere
843-846 (1989) (significant statistical difference between hydatidiform mole and congenital malformations between populations potentially exposed and not exposed
to TCDD); Phuong, et. al., "An Estimate of Differences Among Women Giving Birth to Deformed Babies and Among Those with Hydatidiform Mole Seen at the
OB-GYN Hospital of Ho Chi Minh City in the South of Vietnam," 18 Chemosphere 801-803 (1989) (statistically significant connection between frequency of the
occurrence of congenital abnormalities and of hydatidiform moles and a history of phenoxyherbicide exposure); Huong, et. al., "An Estimate of the Incidence of birth
Defects, Hydatidiform Mole and Fetal Death in Utero Between 1952 and 1985 at the OB-GYN Hospital of Ho Chi Minh City, Republic of Vietnam," 18
Chemosphere 805-810 (l989) (sharp increase in the rate of fetal death in utero, hydatidiform mole (with or without choriocarcinoma) and congenital malformations
from the pre 1965-1975 period, suggesting possible association to phenoxyherbicide exposure).
11 Myers at 167
homes and crops intended for human consumption.13 The Department of Defense simultaneously announced its suspension of all uses of Agent Orange.14
B. HEALTH STUDIES
As Agent Orange concerns grew, numerous independent
studies were conducted between 1974 and 1983 to determine if a link exists
between certain cancerous
diseases, such as non-Hodgkin’s lymphoma and soft-tissue sarcomas, and exposure to the chemical components found in Agent Orange. These studies suggested
just such a link.
In 1974, for example, Dr. Lennart Hardell began a study
which eventually demonstrated a statistically significant correlation between
exposure to pesticides
containing dioxin and the development of soft tissue sarcomas.15
13 Id. Although Dow Chemical Company, the primary
manufacturer of 2,45-T and 2,4-D, denied this teratogenicity, Dow’s own tests
confirmed that when dioxin
was present in quantities exceeding production specifications, birth defects did occur. See J. McCullough, Herbicides: Environmental Health Effects: Vietnam and the
Geneva Protocol: Developments During 1979, 13 (1970) (Congressional Research Report No. UG 447, 70—303SP). Pressure from industry subsequently led to
some relaxation of the limits placed on the 2,4,5—T and 2,4—D. The only current uses for these chemicals in the United States are on rice, pastures, rangelands and
rights of way.
14 Id. at 167. See also Dow Chemical v. Ruckelshaus, 477 F.2d 1317, 1319 (8th Cir. 1973) (secretaries announcement quoted in the opinion).
15 Hardell, L. and Sandstrom, A. "Case—control
Study: Soft Tissue Sarcomas and Exposure to Phenoxyacetic Acids or Chlorophenols,"
39 Brit. J. Cancer,
711—717 (1979). See also note 89 infra for the confirming results of follow-up studies by Hardell and others.
In 1974, Axelson and Sundell reported a two—fold
increase of cancer in a cohort study of Swedish railway workers exposed to a
variety of herbicides containing
By 1976, the Occupational Safety and Health Administration, established rigorous exposure criteria for workers working with 2,4, 5-T.1 17
In 1977 the International Agency for Research on Cancer (IARC),
while cautioning that the overall data was inconclusive, reported numerous
increased mortality rates in animals and humans exposed to 2,4-D or 2,4,5-T.18
16 Axelson and Sundell, "Herbicide Exposure,
Mortality and Tumor Incidence: An Epidemiological Investigation on Swedish
Railroad Workers," 11 Work Env’t.
Health 21-28 (1974).
17 U.S. Occupational Safety and Health Administration (1976), Air Contaminants; U.S. Code, Federal Register 29, Part 1910.93 at p. 27
18 With regard to 2,4-D, the IARC found the following
anomalies: elevated levels of cancer in rats; acute and short—term oral
toxicity in mice, rabbits, guinea pigs
and rats-—death, stiffness in the extremities, incoordination, stupor, myotonia, and other physical abnormalities; inmonkeys, injections caused nausea, vomiting,
lethargy, muscular incoordination and head droop, fatty degeneration of the liver, spleen, kidneys and heart; foetal anomaly increases in some species; post—birth
death rates increased in some. species; higher mortality rates and morphological alterations in pheasant embryos and their chicks when spraying took place under
simulated field conditions; higher mortality rates in rat pups in a 3 generation exposure; gene mutation after exposure to high concentrations; chromosomal aberrations
when cultured human lymphocytes were exposed; increased frequency of aberrant metaphases (2 to 4 times) in mice exposed to toxic concentrations.
In humans the IARC found that: a 23 year old farming
student, a suicide, had 6 grams of 2,4-D in his body, acute congestion of all
organs, severe degeneration of
ganglion cells in the central nervous system; 3 cases of peripheral neuropathy in humans sprayed with 2,4-D with initial symptoms of nausea, vomiting, diarrhea,
swelling and aching of feet and legs with latency, in individual cases, paresthesia in the extremities, pain in the legs, numbness and aching of fingers and toes, swelling
in hand joints, flaccid
In 1978, the Environmental Protection Agency issued an
emergency suspension of the spraying of 2,4,5-T in national forests after
finding "a statistically significant
increase in the frequency of miscarriages" among women living near forests sprayed with 2,4,5-T.19
In 1980, another provocative mortality study of workers
parapheresis; similar case reports in agriculture workers
sprayed by 2,4-D; workers associated with 2,4—D developed symptoms of
gastralgia, increased salivation, a sweet taste in the mouth, a sensation of drunkenness, heaviness of the legs and hyperacusea, rapid fatigue, headache, loss of
appetite, pains in the region of liver and stomach, weakness, vertigo, hypotension, bradycardia, dyspeptic symptoms, gastritis, liver disfunction, changes in metabolic
With regard to 2,4,5—Vs effect on animals the IARC
found: it can increase the frequency of cleft palates in some strains of mice;
fetal growth retardation may also
be observed; cystic kidneys were observed in two strains of mice; in purest available form, it induced some fetal effects and skeletal anomalies in rats as well as
behavioral abnormalities, changes in thyroid activity and brain serotonin levels in the progeny; increases in intrauterine deaths and in malformations in rats; fetal death
and teratogenic effects in Syrian golden hamsters; chromosomal abnormalities.
The IARC reported in 1977 with respect to 2,4,5-T’s
effects on humans that: workers exposed at a factory in the USSR had skin
lesions, acne, liver impairment,
and neurasthenic syndrome; similar findings were reported by Jerasneh, et al (1973, 1974) in a factory in Czechoslovakia which in 1965—68 produced 76 cases of
chloracne, 2 deaths from bronchogenic cancers. Some workers had porphyria cutanea tarda, urophryimuria, abnormal liver tests, severe neurasthenia, depression
syndrome, peripheral neuropathy; in a 1975 accident in West Virginia, 228 people were affected. Symptoms included chloracne, melanosis, muscular aches and
pains, fatigue, nervousness, intolerance to cold; 4 workers of 50 affected in a similar accident in the Netherlands in 1963 died within 2 years and at least 10 still had
skin complaints 13 years later.
19 June 1979 Congressional Hearings before House Commerce Committee.
Subcommittee on Oversight and Investigations, quoted in "Human Disease
Dioxin: Congress Calls for 2,4,5—T Ban After Dramatic Herbicide Hearings", 28 Bioscience 454 (August 1979). This study, otherwise known as the Alsea Study,
has been cited as showing the first correlation between 2,4,5—T (and presumably its TCDD contaminant) and teratogenic effects in humans.
involved in an accident at an industrial plant which manufactured dioxin
compounds suggested that exposure to these compounds resulted in excessive
neoplasms of the lymphatic and hematopoietic tissues. 20
On September 22, 1980, the U.S. Interagency Work Group to
Study the Long-term Health Effects of Phenoxy Herbicides and Contaminants
despite the studies’ limitations, they do show a correlation between exposure to phenoxy acid herbicides and an increased risk of developing soft-tissue tumors or
To be sure, there remain skeptics who insist that the
studies failed in one respect or another to establish a scientifically
acceptable correlation.22 Yet, it can fairly
be said that the general attitude both within and outside the scientific community was, and continues to be increasing concern over the mounting evidence of a
connection between certain cancer
20 Zack and Suskind, "The Mortality Experience of Workers Exposed to TCDD in a Trichlorophenol Process Accident," 22 Journal of Medicine 11—14 (1980).
21 See U.S. Interagency Workgroup to Study the Long-Term Health Effects of Phenoxy Herbicides and Contaminants (September 22, 1980) (executive summary).
22 See...e.g. "The Weight of the Evidence on the Human Carcinogenicity
of 2,4—D" (January 1990) (This report, sponsored by the National
Association of Wheat
Growers Foundation and a grant from the Industry Task Force II on 2,4—D Research Data, an association of manufacturers and commercial formulators of
2,4—D, concluded that the toxicological data on 2,4-D does not provide a strong basis for predicting that 2,4-D is carcinogenic to humans. Nevertheless, the panel
reviewing the evidence did conclude that "evidence indicates that it is possible that exposure to 2,4-D can cause cancer in humans.").
illnesses and exposure to dioxins.
III. VETERANS’ DIOXIN AND RADIATION EXPOSURE COMPENSATION
STANDARDS ACT OF 1984
With the increasing volume of scientific literature giving
credence to the belief of many Vietnam Veterans that exposure to Agent Orange
during their military
service was related to their contraction of several debilitating diseases -- particularly non-Hodgkin’s lymphoma, soft tissue sarcoma ("STS") (malignant tumors that
form in muscle fat, or fibrous connective tissue) and porphyria cutanea tarda ("PCT") (deficiencies in liver enzymes) --Vietnam Veterans rightfully sought disability
compensation from the Veterans Administration ("VA").
The VA determined, however, that the vast majority of
claimants were not entitled to compensation since they did not have service
connected illnesses. 23 As a
consequence, Congress attempted to alter dramatically the process governing Agent Orange disability claims through passage of the Veterans’ Dioxin and Radiation
Exposure Compensation Standards Act of 1984
23 By October 1, 1983, 9170 veterans filed claims for disabilities that they
alleged were caused by exposure to Agent Orange. The VA denied compensation to
7709 claimants on the grounds that the claimed diseases were not service connected. Only one disease was deemed associated with service related exposure to
Agent Orange, a skin condition known as chloracne. See House Report No. 98-592, reprinted in U.S.Code Cong. & Adm. News, 98th Cong. 2d Sess.,1984, at
4452. See also Nehmer v. U.S. Veterans Administration, 712 F.Supp. 1404, 1407 (1989).
(hereinafter the "Dioxin Standards Act") 24 To ensure that the VA
provided disability compensation to veterans exposed to herbicides containing
dioxin while serving
in Vietnam,25 Congress authorized the VA to conduct rulemaking to determine those diseases that were entitled to compensation as a result of a service--related
exposure to Agent Orange.26
In promulgating such rules, the Dioxin Standards Act
required the VA to appoint a Veterans’ Advisory Committee on Environmental
Hazards (the "Advisory
Committee") -- composed of experts in dioxin, experts in epidemiology, and interested members of the public -- to review the scientific literature on dioxin and
submit periodic recommendations and evaluations to the Administrator of the 27 Such experts were directed to evaluate the scientific evidence pursuant to regulations
promulgated by the VA, and thereafter to submit recommendations
24 Veterans’ Dioxin and Radiation Exposure Compensation Standards Act, Pub.
L. 98—542, Oct. 24, 1984, 98 Stat. 2727 (hereinafter the Dioxin Standards
In passing the Act Congress found that Vietnam Veterans were "deeply concerned about possible long term health effects of exposure to herbicides containing
dioxin,"(Section 2 (1)), particularly since "(t)here is scientific and medical uncertainty regarding such long—term adverse health effects." (Section 2 (2)). In
responding to this uncertainty, Congress mandated that "thorough epidemiological studies of the health effects experienced by veterans in connection with exposure .
to herbicides containing dioxin" be conducted, (Section 2(4)), especially in light of the fact that "[t)here is some evidence that chloracne, porphyria cutanea tarda, and
soft tissue sarcoma are associated with exposure to certain levels of dioxin as found in some herbicides." (Section 2 (5)).
25 Id. at Section 3.
26 Id. at Section 5.
27 Id. at Section 6.
and evaluations to the Administrator of the VA on whether "sound
scientific or medical evidence" indicated a connection to exposure to Agent
Orange and the
manifestation of various diseases.28
In recognition of the uncertain state of scientific
evidence and the inability to make an absolute causal connection between
exposure to herbicides containing dioxin
and affliction with various rare cancer diseases,29 Congress mandated that the VA Administrator resolve any doubt in favor of the veteran seeking compensation. As
stated in the Dioxin Standards Act:
It has always been the
policy of the Veterans Administration and is the policy of the United States,
with respect to individual claims for service
connection of diseases and disabilities, that when, after consideration of all the evidence and material of record, there is an approximate balance of
positive and negative evidence regarding the merits of an issue material to the determination of a claim, the benefit of the doubt in resolving each such
issue shall be given to the claimant. 30
A. NEHMER V. U.S. VETERANS ADMINISTRATION
Despite Congressional intent to give the veteran the benefit of the doubt, and in direct opposition to the stated purpose of
28 Id. at Section 5.
29 See Nehmer v. U.S. Veterans Admin., 712 F. Supp. 1404,
1408. (N.D. Cal. (1989). wherein the court found after reviewing the legislative
history of the Act
"that Congress intended service connection to be granted on the basis of "increased risk of incidence" or a "significant correlation" between dioxin and various
diseases," rather than on the basis of a casual relationship.
30 See Dioxin Standards Act at Section 2 (23).
the Dioxin Standards Act to provide disability compensation to Vietnam
Veterans suffering with cancer who were exposed to Agent Orange, the VA
deny compensation improperly to over 31,000 veterans with just such claims. In fact, in promulgating the rules specified by Dioxin Standards Act, the VA not only
confounded the intent of the Congress, but directly contradicted its- own established practice of granting compensable service-connection status for diseases on the
lesser showing of a statistical association, promulgating instead the more stringent requirement that compensation depends on establishing a cause and effect
Mounting a challenge to the regulations, Veterans groups prosecuted a
successful legal action which found that the VA had "both imposed an
demanding test for grantingservice connection for various diseases and refused to give the
31 See e.g. 38 C.F.R. 3.310(b) (compensation granted for
cardiovascular diseases incurred by veterans who suffered amputations of legs or
feet); Nehmer at
The significance of the distinction between a statistical
association and a cause and effect relationship is in the burden of proof that
the veteran must satisfy in order
to be granted benefits. A statistical association "means that the observed coincidence in variations between exposure to the toxic substance and the adverse health
effects is unlikely to be a chance occurrence or happenstance," whereas the cause and effect relationship "describes a much stronger relationship between exposure
to a particular toxic substance and the development of a particular disease than ‘statistically significant association’ does." Nehmer, 712 F.Supp. at 1416.
Thus, the regulation promulgated by the VA established an
overly burdensome standard by incorporating the causal relationship test within
the text of the regulation
itself. 38 C.F.R. 1 3.311(d) ("(s] ound scientific and medical evidence does not establish a cause and effect relationship between dioxin exposure" and any diseases
except some cases of chloracne) (emphasis added).
veterans the benefit of the doubt in meeting the demanding standard."
Nehmer v. U.S. Veterans Administration, 712 F. Supp. 1404, 1423 (1989) (emphasis
original). As a result, the court invalidated the VA’s Dioxin regulation which denied service connection for all diseases other than chloracne; ordered the VA to
amend its rules; and further ordered that the Advisory Committee reassess its recommendations in light of the court’s order.32
Thus, on October 2, 1989, the VA amended 38 C.F.R. Part 1,
which among other things set forth various factors for the Secretary and the
to consider in determining whether it is "at least as likely as not" that a scientific study shows a "significant statistical association" between a particular exposure to
herbicides containing dioxin and a specific adverse health effect.33 Equally important, the
32 Nehmer, 712 F. Supp at 1423.
33 38 C.F.R. 1.17 (b) & (d). 38 C.F.R. 1.17 states:
(a) From time to time, the Secretary shall publish evaluations of scientific or medical studies relating to the adverse health effects of exposure to a herbicide containing
2,3,7,8 tetrachlorodibenzo-p-dioxin (dioxin) and/or exposure to ionizing radiation in the "Notices" section of the Federal Register.
(b) Factors to be considered in evaluating scientific studies include:
(1) Whether the study’s findings are statistically significant and replicable.
(2) Whether the study and its findings have withstood peer review.
(3) Whether the study methodology has been sufficiently described to permit replication of the study.
(4) Whether the study’s findings are applicable to the veteran population of interest.
(5) The views of the appropriate panel of the Scientific Council of the Veteran’ Advisory Committee on Environmental Hazards.
(c) When the Secretary determines, based on the evaluation of
regulation permits the Secretary to disregard the findings of the Advisory Committee, as well as the standards set forth at 38
scientific or medical studies and after receiving the advice of the
Veteran’s Advisory Committee on Environmental Hazards and applying the
doctrine as set forth in paragraph (d) (1) of this section, that a significant statistical association exists between any disease and exposure to a herbicide containing
dioxin or exposure to ionizing radiation, 3.311a or 3.311b of this title, as appropriate, shall be amended to provide guidelines for the establishment of service
(d) (1) For purposes of paragraph (c) of this section a "significant statistical association" shall be deemed to exist when the relative weights of valid positive and
negative studies permit the conclusion that it is at least as likely as not that the purported relationship between a particular type of exposure and a specific adverse
health effect exists.
(2) For purposes of this paragraph a valid study is one which:
(i) Had adequately described the study design and methods of data collection, verification and analysis;
(ii) Is reasonably free of biases, such as selection, observation and participation biases; however, if biases exist, the investigator has acknowledged them and so
stated the study’s conclusions that the biases do not intrude upon those conclusions; and
(iii) Has satisfactorily accounted for known confounding factors.
(3) For purposes of this paragraph a valid positive study is one which satisfies the criteria in paragraph (d) (2) of this section and whose findings are statistically
significant at a probability level of .05 or less with proper accounting for multiple comparisons and subgroups analyses.
(4) For purposes of this paragraph a valid negative study is one which satisfies the criteria in paragraph (d) (2) of this section and has sufficient statistical power to
detect an association between a particular type of exposure and a specific adverse health effect if such an association were to exist.
(e) For purposes of assessing the relative weights of valid positive and negative studies, other studies affecting epidemiological assessments including case series,
correlational studies and studies with insufficient statistical power as well as key mechanistic and animal studies which are found to have particular relevance to an
effect on human organ systems may also be considered.
(f) Notwithstanding the provisions of paragraph (d) of this section, a "significant statistical association" may be deemed to exist between a particular exposure and
a specific disease if, in the Secretary’s judgment, scientific and medical evidence on the whole supports such a decision.
C.F.R. § 1.17 (d) and determine in his own judgment that the scientific and
medical evidence supports the existence of a "significant statistical
association" between a
particular exposure and a specific disease. 38 C.F.R. § 1.17 (f).
The Secretary recently exercised his discretionary
authority under this rule when he found a significant statistical association
between exposure to Agent Orange
and non—Hodgkin’s lymphoma, notwithstanding the failure of his own Advisory Committee to recommend such action in the face of overwhelming scientific data.34
B. . THE WORK OF THE VETERANS’ ADVISORY COMMITTEE ON ENVIRONMENTAL HAZARDS
To assess the validity and competency of the work of the Advisory Committee, I asked several impartial scientists to
34 After reviewing numerous scientific studies, at least four of which were
deemed to be valid positive in demonstrating the link . between exposure to
containing dioxin and non--Hodgkin’s lymphoma, the Advisory Committee still concluded that:
The Committee does not
find the evidence sufficient at the present time to conclude that there is a
significant statistical association between exposure to
phenoxy acid herbicides and non—Hodgkin’s lymphoma. However, the Committee cannot rule out such an association.
The Secretary should be interested to note that a new mortality study
positively confirms that farmers exposed to herbicides containing 2,4-D have an
of developing non-Hodgkin’s lymphoma. See Blair, "Herbicides and Non-Hodgkin’s Lymphoma: New Evidence From a Study of Saskatchewan Farmers," 82
Journal of the National Cancer Institute 575--582 (1990).
review the Advisory Committee transcripts. Without exception, the experts who
reviewed the work of the Advisory Committee disagreed with its findings and
questioned the validity of the Advisory Committee’s review of studies on non—Hodgkin’s lymphomas .
For instance, a distinguished group at the Fred Hutchinson
Cancer Research Institute in Seattle, Washington, upon reviewing the Advisory
concluded "that it is at east., as likely as not that there is a significant association (as defined by the Secretary of Veterans Affairs) between (exposure to phenoxy
acid herbicides and non-Hodgkin’s lymphoma.)" 35 This same group further asserts that the Committee’s work was "not sensible" and "rather unsatisfactory" in its
review and classification of the various studies it reviewed. Additionally, these scientists regarded Dr. Lathrop’s views as "less than objective" and felt that the
possibility exists that "his extreme views (e.g., in respect to the role of dose--response testing) may have unduly affected the Committee’s work." Finally, the
Hutchinson scientists argue that the issue of chemical-specific effects, in which animal studies have been sufficient to demonstrate the carcinogenicity of dioxin, is an
important factor "not well cons idered by the Committee." (emphasis in original)
A second reviewer of the Committee’. work, Dr. Robert
35 Letter to Admiral Zumwalt from Dr. Robert W. Day, Director of the Fred Hutchinson Cancer Research Center of Seattle, Washington (Feb. 20, 1990).
Hartzman (considered one of the U.S. Navy’s top medical researchers),
effectively confirms the views of the Hutchinson group. Dr. Hartzman states that
preponderance of evidence from the papers reviewed [by the Advisory Committee) weighs heavily in favor of an effect of Agent Orange on increased risk for
non—Hodgkin’s lymphoma."36 Dr. Hartzman also attests that:
an inadequate process is being used to evaluate scientific publications for
use in public policy. The process uses scientific words like
‘significant at the 5% level’ and
a committee of scientists to produce a decision about a series of publications. But in reality, the Committee was so tied by the process, that a decision which should
have been based on scientific data was reduced to vague impressions... Actually, if the reading of the rules of valid negative found in the transcript is correct (‘a valid
negative must be significant at the p=.05 level’ that is statistically significant on the negative side) none of the papers reviewed are valid negatives. 37
A third reviewing team, Dr. Jeanne Hager Stellman, PhD
(Physical Chemistry) and Steven D. Stellman, PhD (Physical Chemistry), also echo
expressed by the Hutchinson Group and Dr. Hartzman on the validity of the Committee’s proceedings and conclusions. In fact, the Stellmans’ detailed annotated
bibliography and assessment of numerous cancer studies relevant to herbicide exposure presents a stunning indictment of the Advisory Committee’s scientific
interpretation and policy judgments regarding the link between Agent Orange and Vietnam
36 Letter to Admiral Zumwalt from Dr. R.J. Hartzman Capt. MC USN (March 7, 1990).
37 Id. at p.3
Veterans . 38
A fourth reviewer, a distinguished scientist intimately
associated with government sponsored studies on the effects of exposure to Agent
Orange, states the same
conclusions reached by the other reviewers:
The work of the
Veterans’ Advisory Committee on Environmental Hazards, as documented in their
November 2, 1989 transcript, has little or no
scientific merit, and should not serve as a basis for compensation or regulatory decisions of any sort...
My analysis of the NHL
articles reviewed by the committee reveals striking patterns which indicate to
me that it is much more likely than not that a
statistical association exists between NHL and herbicide exposure.
As these various reviewers suggest, the Advisory
Committee’s conclusions on the relationship between exposure to Agent Orange
lymphoma were woefully understated in light of the clear evidence demonstrating a significant statistical association between NHL and exposure to phenoxy acid
herbicides such as Agent Orange.
Perhaps more significant than the Committee’s failure to
sake such obvious findings is the distressing conclusion of the independent
reviewers that the Committee’s
process is so flawed
38 See Stellman & Stellman, "A Selection of
Papers with Commentaries Relevant to the Science Interpretation and Policy:
Agent Orange and Vietnam Veterans,’
(March 1, 1990) . See also note 51 and accompanying text infra for additional discussion of the Stellmans’ work.
39 A copy of the anonymous reviewer’s analysis can be madeavailable for the
Secretary’s personal .inspection and review. In another paper, this same
"I estimate that the Vietnam Veterans are experiencing a 40% to 50% increase in sarcomas and non--Hodgkin’s lymphoma rates."
as to be useless to the Secretary in making any determination on the effects
of Agent Orange. From a mere reading of Committee transcripts, these reviewers
detected overt bias in the Committee’s evaluation of certain studies. In fact, some members of the Advisory Committee and other VA officials have, even before
reviewing the evidence, publicly denied the existence of a correlation between exposure to dioxins and adverse health effects.40 This blatant lack of impartiality lends
credence to the suspicion that certain individuals may have been unduly influenced in their evaluation of various studies. Furthermore, such bias among Advisory
committee members suggests that the Secretary should, in accordance with the Dioxin Standards Act, appoint new personnel to the Advisory Committee.
III. THE CDC STUDIES
Were the faulty conclusions, flawed methodology and
noticeable bias of the Advisory Committee an isolated problem, correcting the
misdirection would be more
manageable. But, experience with other governmental agencies responsible for specifically analyzing and studying the effects of exposure to
40 For instance, Dr. Lawrence B. Hobson (Director, Office of Environmental
Medicine, Veterans Health Services and Research Administration), claims that
‘presents no threat from the exposures experienced by the veterans and the public at large," and virtually accuses scientists who find that such health effects do exist
to be nothing more than witch doctors. See Hobson, ‘Dioxin and Witchcraft" presented at the 5th InternatiOnal Symposium on Chlorinated Dioxins and Related
Compounds (September 1985) .
Agent Orange strongly hints at a discernible pattern, if not outright
governmental collaboration, to deny compensation to Vietnam Veterans for
with exposure to dioxin .
A case in point is the Centers for Disease control ("CDC")
. As concerns grew following the first studies of human exposure to Agent
commissioned a large scale epidemiological study to determine the potential health effects for Vietnam Veterans exposed to Agent Orange. Initially, this study was to
be conducted by the VA itself. When evidence surfaced, however, of the VA’s footdragging in commencing the study (and initial disavowal of any potential harm
from exposure to Agent Orange), Congress transferred the responsibility for the study to the CDC in 1983. 41
Unfortunately, as hearings before the Human Resources and
Intergovernmental Relations Subcommittee on July 11, 1989 revealed, the design,
conclusions of the CDC study were so ill conceived as to suggest that political pressures once again interfered with the kind of professional, unbiased review
Congress had sought to obtain.42
The Agent Orange validation study, for example, a study of
41 See 135 Congressional Record, Statement of Senator Tom Daschle (November 21, 1989); See also Agent Orange Hearings at p.37.
42 Oversight Review of CDC’s Agent Orange Study: Hearing Before the Human
Resources and Intergovernmental Relations Subcommittee of the Committee on
Government Overations House of Representatives, 101st Cong., 1st Sess. at p. 71 and 330 (1989) [hereinafter cited as Agent Orange Hearing].
the long—term health effects of exposures to herbicides in Vietnam, was
supposedly conducted to determine if exposure could, in fact, be estimated.43
years and approximately $63 million in federal funds, the CDC concluded that an Agent Orange exposure study could not be done based on military records. 44 This
conclusion was based on the results of blood tests of 646 Vietnam Veterans which ostensibly demonstrated that no association existed between serum dioxin levels
and military— based estimates of the likelihood of exposure to Agent Orange.45 Inexplicably, the CDC then used these "negative" findings to conclude that not only
could an exposure study not even be done, but that the "study" which was never even conducted proves that Vietnam Veterans were never exposed to harmful doses
of Agent Orange.
Even more disturbing, when the protocol for this
"study" and the blood test procedures were examined further, there
appeared to be a purposeful effort to
sabotage any chance of a meaningful Agent Orange exposure analysis. For , the original protocol for the Agent Orange exposure study understandably called for
subject veterans to be tracked by company level
43 Id. at 37; See also, Protocol for Epidemiologic Studies of the Health of
Vietnam Veterans, Centers for Disease Control, Public Health Service, U.S.
of Health and Human Services (November, 1983).
44 Agent Orange Hearings at 13 (Statement of Dr. Vernon Houk).
45 Id. at 12—13.
location.46 By tracking company level units of 200 men, rather than
battalions of 1,000 men, the location of men in relation to herbicide
applications would be known
with greater precision, thereby decreasing the probability that study-subjects would be misclassified as having been or not been exposed to Agent Orange.
However, in 1985 the CDC abruptly changed the protocol to
have battalions, rather than companies, serve as the basis for cohort selection
and unit location. 47
By the CDC’s own admission, changing the protocol to track veterans on the broader batta1ion basis effectively diluted the study for the simple reason that many of
the 1,000 men in a battalion were probably not exposed to Agent Orange. Why then did the CDC change the protocol in 1985?
According to Dr. Vernon Houk, Director of the Center for
Environmental Health and Injury control, the department within the CDC
responsible for conducting the
Agent Orange study, the protocol was changed because the CDC concluded that company— specific records were unreliable and contained too many gaps of
information. As a result, military records could simply not be used to assess exposure.48
46 Id. at 4l.
47 Id. at 38.
48 Agent Orange Hearing: Testimony of Dr. Vernon Houk at
38-40 and 69. Dr. Houk sports an unbounded skepticism for the health hazards of
recently endorsed the lessening of the dioxin dumping standard in the State of Georgia at a rate 500 times more lenient than EPA recommended guidelines. See
Letter from Dr. Vernon N. Houk to Leonard Ledbetteber, Commissioner Georgia Department of Natural Resources (November 27, 1989).
Richard Christian, the former director of the
Environmental Study Group of the Department of Defense ("ESG")
testified that not only was this conclusion false, but
that he had personally informed the CDC that adequate military records existed to identify company—specific movements as well as spray locations.49 Furthermore,
in a February 1985 report to the Congressional Office of Technology Assessment, the CDC reported that in analyzing 21 of 50 detailed computer HERBs tapes
developed by the ESG on company movements that it was possible to correlate the exposure data to areas sprayed with Agent Orange with consistent results.50
Indeed, a peer reviewed study sponsored by the American Legion conclusively demonstrated that such computerized data could be used to establish a reliable
exposure classification system essential to any valid epidemiologic study of Vietnam Veterans.51
In addition to altering the protocol from company units to
battalions, the CDC further diluted the study by changing the protocol on the
length of time study
subjects were to have served in Vietnam. Whereas the original protocol required subjects to have served a minimum of 9 months in combat companies, the CDC
reduced the minimum to 6 months. Furthermore, the CDC eliminated
49 Agent Orange Hearing, Testimony of Richard Cheristian at 41.
50 Interim Report, Agent Orange Study: Exposure
Assessment: Procedures and Statistical Issues. See Also American Legion Magazine
Special Issue, "Agent
Orange" (1990) at p. 12.
51 Agent Orange Hearing 155-220 (Testimony of Steven and
Jeanne Stellman); American Legion and Columbia University Vietnam Experience
Environmental Research (December, 1988).
from consideration all veterans who served more than one tour in Vietnam.
Finally, while the original protocol called only for subjects who served in
1967 to 1968, the years that Agent Orange spraying was at its height, the CDC added an additional 6 months to this time period. The net effect of these various
changes was seriously to dilute the possibility that study subjects would have been exposed to Agent Orange, which in turn would impair any epidemiological study’s
ability to detect increases in disease rate.52
Although the above referenced problems cast serious suspicion on the work of the CDC, perhaps its most controversial
52 Agent Orange Hearing at 46-49. This "dilution
effect" is considered the classic flaw in epidemiological study design.
most epidemiologists would try to optimize
the chances of observing an effect by including, rather than excluding, the subjects who are most likely to have been exposed to the suspected disease causing agent.
This statistical ability to observe an effect if one is present is generally referred to as the "statistical power" of a given study.
When the CDC chose to generalize exposure to Agent Orange
to groups of veterans who were less likely, rather than more likely, to be
exposed, the power of
the study was diluted. For example, if we assume that 1 out of every 5 men who served in Vietnam was exposed to Agent Orange, any possible effects of the
exposure will be diluted when the 4 non—exposed men are averaged in. If we assume further that exposure to Agent Orange caused a doubling of the incidence of
cancers among the 20% of men exposed, the effect would largely be obscured since 80% of the group being studied would not have been sprayed with Agent
Orange and would thus have a normal background rate of cancer. Consequently, only exceptionally large increases in the cancer rate would be discovered and or
reach statistical significance in a study group so diluted from the outset. See Agent Orange Hearing at 149 (Testimony of John F. Sommer, Jr., Director National
Veterans Affairs and Rehabilitation commission the American Legion).
See also Agent Orange Legislation and Oversight: Hearing
Before the Committee on Veterans’ Affairs, United States Senate, 100th
Cong.,(May 12, 1988)
(Testimony of Dr. Joel Nichalek) at pp. 65, 66 and 668.
action was to determine unilaterally that blood tests taken more than 20
years after a veteran’s service in Vietnam were the only valid means of
veteran’s exposure to Agent Orange. In addition, Dr. Houk further "assumed" that the half—life for dioxin in the blood was seven years. 53 When the underlying data
for Houk’s assumptions were recently reviewed, however, 11 percent of the blood tests were invalid (i.e. study subjects had higher values of dioxin in their blood in
1987 than in 1982 even though the subjects had no known subsequent exposure to dioxin) and the half lives of dioxin in the remaining study subjects ranged from a
low of 2 to a high of 740 years! 54 Yet despite this tremendous variance in the data and the high incidence of false results, Houk and the CDC concluded, rather
remarkably, that a large scale exposure study was simply not possible since "negative" blood tests appeared to "confirm" that study subjects were not even exposed
to Agent Orange.
Such conclusions are especially suspect given the fact
that scientists have consistently cautioned against the use of blood tests as
the sole basis for exposure
classification. Although blood and adipose tissue tests can be used to confirm that
53 Agent Orange Hearing at 59. Dr. Houk’s assumption was based on a study
of only 36 former Ranch Handers (members of "Operation Ranch Hand,"
Force herbicide defoliation program) who had volunteered blood samples in 1982 and 1987.
54 American Legion Magazine Reprint "Agent Orange" at 12 See also
Agent Orange Hearing at p. 67 (testimony of Dr. Houk revealed that the
the Agent Orange project believed that the dioxin blood analysis was so flawed there is a substantial likelihood that there is no correlation between the exposure
scores and the blood levels).
Vietnam veterans were heavily exposed to Agent Orange and the contaminant
dioxin55, even the CDC’s own researchers have unequivocally stated that
has to be learned about the kinetics of dioxin metabolism and half-life before current levels can be used to fully explain historic levels of exposure."56
While the CDC’s changes in protocol have been "justified",
however unreasonably, on the basis of "scientific" explanations57,
what cannot be justified is the evidence
of political interference in the design, implementation and drafting of results of the CDC study by Administration officials rather than CDC scientists. As early as
1986, the Subcommittee on Oversight and Investigations of the Committee on Energy and Commerce documented how untutored officials of the Office of
Management and Budget (0MB) interfered with and second-guessed the professional judgments of agency scientists and multidisciplinary panels of outside peer
55 See Kahn, "Dioxins and Dibenzofurans in Blood and
Adipose Tissue of Agent Orange Exposed Vietnam Veterans and Matched
Controls," 259 Journal of the
American Medical Association 1661 (1988). This report found that "Vietnam veterans who were heavily exposed to Agent Orange. exceeded matched control
subjects in both blood, and adipose tissue levels of 2,3,7, 8—tetrachlorodibenzo-p— dioxin (TCDD) but not in the levels of the 12 other 2,3,7,8-substituted dioxins
and dibenzofurans that were detected. Since only TCDD among these compounds was present in Agent Orange but all are present in the population of the
industrialized world, it is likely that the elevated TCDD levels arose from wartime exposure."
56 Patterson, "Levels of Polychlorinated Dibenzo-p-dioxins
and Dibenzofurans in Workers Exposed to 2,3,7,8 --tetrachlorodibenzo-p—dioxin,.
Journal of Industrial Medicine 135, 144 (1989).
57 See generallv, Agent Orange Hearing (Testimony of Dr. Vernon Houk) at 44--50.
effectively to alter or forestall CDC research on the effects of Agent
Orange, primarily on the grounds that "enough" dioxin research had
already been done.58 These
Agent Orange Hearings revealed additional examples of political interference in the CDC~s Agent Orange projects by members of the White House Agent Orange
Dr. Philip 3. Landrigan, the former Director of the
Environmental Hazards branch at the CDC, upon discovering the various
irregularities in CDC procedures
concluded that the errors were so egregious as to warrant an independent investigation not only of the methodology employed by the CDC in its validation study, but
also a specific inquiry into what actually transpired at the Center for Environmental Health of the CDC.60
With these suspicions in mind, it should come as no
surprise that those familiar with the CDC~s work found little credence in the
conclusions reached by the CDC
in its recently released Selected Cancers Study. Even though the CDC has previously stated that it believes exposure to Agent Orange is impossible to assess, it
found no difficultly in reporting to the press upon the release of the Selected Cancers Study that exposure to Agent
58 OMB Review of CDC Research: Impact of the Paperwork
Reduction Act; A Report Prepared for the Subcommittee on Oversight and
Investigations of the
Coumittee on Energy and Commerce, 99th Cong. 2nd Sess. (October 1986).
59 See Agent Orange Nearing at 49-54 (Testimony of Dr. Vernon Houk).
60 Agent Orange Hearing at 229 and 330
Orange does not cause cancer. This conclusion was reached despite the fact
that the CDC made no effort to determine, through military records or
tissue tests, if study subjects were, indeed, exposed to dioxins; nor did the CDC attempt to verify exposure to Agent Orange of those study subjects who actually
contracted cancerous diseases. In fact, according to scientists who have made preliminary reviews of the CDC’s findings, the statistical power of any one cancer
grouping, with the exception of non—Hodgkin’s lymphoma, was so low as to make any conclusion virtually impossible.
IV. RANCH HAND STUDY
Unfortunately, political interference in government
sponsored studies associated with Agent orange has been the norm, not the
exception. In fact, there appears to
have been a systematic effort to suppress critical data or alter results to meet preconceived notions of what alleged scientific studies were meant to find.61 As recently
as March 9, 1990 Senator Daschle disclosed compelling evidence of additional political interference in the Air Force Ranch Hand study, a separate government
sponsored study meant to examine the correlation between exposure to Agent Orange and harmful health effects among Air Force veterans who participated in
Agent Orange spraying
61 See generallv Agent Orange Nearing; Congressional Record, S
2550 (March 9, 1990); Congressional Record, (November 21, 1989) (Statements of
missions under Operation Ranch Hand. As Senator Daschle explained:
In January 1984, the
scientists in charge of the Ranch Hand Study issued a draft baseline morbidity
report that described some very serious health
problems in the Ranch Hand veterans and stated that the Ranch Handers, by a ratio of five to one, were generally less well than the veterans in the
control group. The opening sentence of the draft report’s conclusion was clearly stated: "It is incorrect to interpret this baseline study as ‘negative.’
After the Ranch Hand
Advisory Committee, which operates under the White House Agent Orange Working
Group of the Domestic Policy Council, got
its hands on the document, the final report was changed in some very important ways. Most notably, the table and exposition explaining that the Ranch
Handers were generally less well than the controls was omitted, and the final conclusion was altered substantially. The statement that the baseline study
was not negative was completely omitted and the study was described as "reassuring." 62
By altering the study’s conclusion, opponents of Agent
Orange compensation were able to point to "irrefutable proof" that
Agent Orange is not a health problem: if
those veterans most heavily exposed to Agent Orange did not manifest any serious health problems, they argued, then it could safely be deduced that no veteran
allegedly exposed to Agent Orange in smaller doses could have health problems. Yet, when Senator Daschle questioned Air Force scientists on why discrepancies
existed between an Air Force draft of the Ranch Hand Study and the final report actually released to the press, the answers suggested not merely disagreements in
data evaluation, but the perpetration of fraudulent conclusions. In a word, the major premise was badly
62 See Congressional Record S 2550 (March 9, 1990)
For example, in 1987 Ranch Hand scientists confirmed to
Senator Daschle that an unpublished birth defects report shows that birth
defects among Ranch Hand
children are double those of children in the control group and not "minor" as originally reported in l984.63
This increase in birth defects takes on added significance
when one considers that the original CDC birth defects study, which found no
increase in birth defects,
merely examined birth defects as reported on birth certificates, rather than as reported by the child’s parent or physician. The CDC never recorded hidden birth
defects, such as internal organ malformations and other disabilities that only became apparent as the child developed. Consequently, it is very likely that the CDC’s
negative findings on birth defects were also vastly understated.64
In addition to elevated birth defects, Ranch Handers also
showed a significant increase in skin cancers unrelated to overexposure to the
sun as originally suggested
in the 1984 report. Air Force scientists also admitted that Air Force and White House Kanagement representatives were involved in
63 Congressional Record, (November 21, 1989) (Statement of Senator Thomas Daschle).
64 The CDC birth defects study was confined to Vietnam
Veterans located in the Atlanta, Georgia region. The study was not an Agent
Orange birth defects study
since no effort was made to determine whether the veterans had even been exposed to Agent orange. See notes 10 and 18 supra for additional information on birth
scientific decisions in spite of the study’s protocol which prohibited such involvement.65
On February 23, 1990, the Air Force released a follow-up
morbidity report on the Ranch Handers. That report, "1987 Followup
Examination Results," described
statistically significant increases in health problems among Ranch Handers including: all cancers —— skin and systemic combined, both verified and suspected; skin
cancers alone; hereditary and degenerative neurological diseases and other problems. The Air Force-concluded, however, that these and other problems cannot
necessarily be related to Agent Orange/dioxin exposure, as they do not always show a "dose-response" relationship — particularly since the exposure index used in
the data analysis "is not a good measure of actual dioxin exposure." 66
With this conclusion, the Air Force for the first time
officially acknowledged that the conclusions reached in its original 1984 Ranch
Hand study are not simply
moot, but that the Ranch Hand study is not, at this date, an Agent Orange study at all since dioxin exposure could not be determined reliably in the first place. In
other words, the Air Force could just as easily have concluded that the health problems associated with the Ranch Handers were not necessarily related to eating
65 Congressional Record, S 2551 (March 9, 1990) (Statement of Senator Daschle).
66 Wolfe, St. al., Air Farce Health Study and
Epidemiologic Investigation of Health Effects in Air Force Personnel Following
Exposure to Herbicides (Feb. 1990)
at p. vi.
For the Air Force to have made the statement in 1990 of no
evidence of a link between exposure to Agent Orange and the cancer problems
Ranch Handers is, as Senator Daschle notes, "patently false."67. Although not yet conclusive, what the Ranch Hand and CDC studies demonstrate is that there is
evidence of a link between health problems and dioxin exposures which may become definitive when a new and reliable exposure index is used to evaluate the data.
As stated by Dr. James Clary, one of the scientists who prepared the final Ranch Hand report:
The current literature on dioxin and non--Hodgkin’s lymphoma and soft tissue sarcoma can be characterized by the following:
1. It underestimates (reduced risk estimates) the effect of dioxins on human
tissue systems. As additional studies are completed we can
expect to see even stronger correlations of dioxin exposure and NHL/STS.
2. Previous studies were not sensitive enough to detect small, but statistically
significant increases in NHL/STS. As time progresses, and
additional evidence is forthcoming, it will be increasingly difficult for anyone to deny the relationship between dioxin exposure and
V. INDEPENDENT STUDIES
Shamefully, the deception, fraud and political interference that has characterized government sponsored studies on the health
67 Congressional Record 5. 2551 (March 9, 1990). See also
Letter from Maj. Gen. James G. Sanders, U.S.A.F. Deputy Surgeon General to
Daschle (February 23, 1990).
68 Letter from Dr. James Clary to Senator Tom Daschle (September 9, 1988).
effects of exposure to Agent Orange and/or dioxin has not escaped studies
ostensibly conducted by independent reviewers, a factor that has only further
compounded the erroneous conclusions reached by the government.
For instance, recent litigation against the Monsanto
corporation revealed conclusive evidence that studies conducted by Monsanto
employees to examine the
health effects of exposure to dioxin were fraudulent. These same fraudulent studies have been repeatedly cited by government officials to deny the existence of a
relationship between health problems and exposure to Agent Orange. According to court papers:
Zack and Gaffey, two Monsanto employees, published a
mortality study purporting to compare the cancer death rate amongst the Nitro
workers who were
exposed to Dioxin in the 1949 explosion with the cancer death rate of unexposed workers. The published study concluded that the death rate of the exposed worker
was exactly the same as the death rate as the unexposed worker. However, Zack and Gaffey deliberately and knowingly omitted 5 deaths from the exposed group
and took 4 workers who had been exposed and put these workers in the unexposed group, serving, of course, to decrease the death rate in the exposed group and
increase the death rate in the unexposed group. The exposed group, in fact, had 18 cancer deaths instead of the reported 9 deaths (P1. Ex. 1464), with the result
that the death rate in the exposed group was 65% higher than expected (emphasis in original)69.
69 Brief of Plaintiffs-appellees in Kemner. et. al. v.
Monsanto Company, No. 5--88--0420 (5th Dist., Illinois Appellate Court) (Oct. 3,
1989) (as the facts were
proven at trial, the appeal only considered appealable matters of law). Plaintiff’s brief refers to Zack and Gaf fey, "A Mortality Study of Workers Employed at the
Monsanto Company Plant in Nitro, WV,. man Environmental Risks of Chlorinated Dioxins and Related Compounds (1983) pp. 575--591. It should be noted that
the Advisory Committee classified this report as "negative" in evaluating compensation for NHL
The brief also states that another study of the workers exposed in the 1949 accident was also fraudulent (e.g. R.R. Suskind
Similarly, recent evidence also suggests that another study heavily relied
upon by those opposed to Agent Orange compensation to deny the existence of a
between dioxin and health effects was falsified. Three epidemiologic studies and several case report studies about an 1953 industrial accident in which workers at a
BASF plant were exposed to dioxins concluded that exposure to TCDD did not cause human malignancies.70 A reanalysis of the data that comprised the studies, all
of which was supplied by the BASF company itself, revealed that some workers suffering from chloracne (an acknowledged evidence of exposure to dioxin) had
actually been placed in the low--exposed or non--exposed cohort groups. Additionally, 20 plant supervisory personnel, not believed to have been exposed, were
placed in the exposed group.
When the 20 supervisory personnel were removed from the
exposed group, thereby negating any dilution effect, the reanalysis revealed
increases in cancers of the respiratory organs (lungs, trachea, etc.) and
and V.S. Hertzberg, "Human Health Effects of 2,4,5-T and Its Toxic
Contaminants," Journal of the American Medical Association, Vol. 251, No.
18 (1984) pgs.
2372-2380.) The study reported only 14 cancers in the exposed group and 6 cancers in the unexposed group. Trial records conclusively demonstrated, however,
that there were 28 cancers in the group that had been exposed to dioxins, as opposed to only 2 cancers in the unexposed group.
70 See e.g. Thiess, Frentzel-Beyme, Link,
"Mortality Study of Persons Exposed to Dioxin in a Trichlorophenol Process
Accident that occurred in the BASF AG
on November 17 , 1953", 3 American Journal of Industrial Medicine 179—189 (1982)
cancers of the digestive tract.71 According to the scientist who conducted
this study, "t)his analysis adds further evidence to an association between
and human malignancy."72
Recent evidence also reveals that Dow Chemical, a manufacturer of Agent
Orange was aware as early as 1964 that TCDD was a byproduct of the manufacturing
process. According to Dow’ s then medical director, Dr. Benjamin Holder, extreme exposure to dioxins could result in "general organ toxicity" as well as
"psychopathological" and "other systemic" problems. 73 In fact, a
71 Friedemann Rohleder, "Dioxins and Cancer Mortality
Reanalysis of the BASF Cohort," presented at the 9th International
Symposium on Chlorinated Dioxins
and Related Compounds, Toronto, Ontario (Sept. 17-22, 1989). BASF recently published a study in an attempt to refute the allegations that the original studies
related to the accident were fraudulent. See Zobier, Messerer & Huber, "Thirty Four Year Mortality Follow Up of BASF Employees, 62 Occupational
Environmental Health 139-157, (Oct. 19, 1989). While the company states that "there was no significant increase in deaths from malignant neoplasms," the study
does conclude that:
There was, however, a
significant excess for all cancers combined among the chloracne victims 20 or
more years after initial exposure when an excess
would be most likely to occur. In addition, there is the notable finding on one case of liver cancer without cirrhosis in a worker with an exceptionally high
level of TCDD in the blood.
Id. at 155. See also id. at 139 ("In general, our
results do not appear to support a strong association between cancer mortality
and TCDD, but they do suggest
that some hazard may have been produced.) (emphasis added) and 149 ("Although TCDD blood levels were available for only 5 of the 10 subjects, the three highest
levels were found in subjects with liver cancer, leucosis and Merkell—cell carcinoma of the skin.").
72 Wanchinski, "New Analysis Links Dioxin to Cancer," New Scientist, (Oct. 28, 1989) p. 24.
73 See L. Casten, Patterns of Secrecy: Dioxin and Agent
Qrange (1990) (unpublished manuscript detailing the efforts of government and
industry to obscure the
serious health consequences of exposure to dioxin).
recent expert witness who reviewed Dow Chemical corporate documents on behalf
of a plaintiff injured by exposure to dioxin who successfully sued Dow74 states
unequivocally that "the manufacturers of the chlorphenoxy herbicides have known for many years about the adverse effects of these materials on humans who were
exposed to them."75
VI. CURRENT SCIENCE ON HEALTH EFFECTS OF HERBICIDES AND DIOXIN
Despite its poor record in carrying out its responsibility to ascertain the
health effects of exposure to Agent Orange, the CDC has been candid in some of
As early as 1983, for instance, the CDC stated in the protocol of its proposed Agent Orange Studies "(t)hat the herbicide contaminant TCDD is considered to be
one of the most toxic components known. Thus any interpretation of abnormal findings related to 2,4,5—T must take into consideration the presence of varying or
74 Peteet v. Dow Chemical Co., 868 F.2d 1428 (5th Cir. 1989) cert...denied 110 S.Ct. 328 (1989).
75 Letter from Daniel Teitelbaum, M.D., P.C. to Admiral E.R. Zumwalt, Jr. (April 18, 1990). Dr Teitelbaum additionally states:
What I do think...may bear on the Agent Orange issue, is the fact that in
review of Dow’s 2,4-D documentation I found that there are significant
potentially carcinogenic materials present in 2,4-D which have never been made known to the EPA, FDA, or to any other agency. Thus, in addition to the problem of
the TCDD which, more likely than not, was present in the 2,4,5--T component of Agent Orange, the finding of other dioxins and closely related furans and xanthones
in the 2,4--D formulation was of compelling interest to me.
amounts of TCCD." 76
In 1987, after first being leaked by the New York Times, a
VA mortality study was released indicating a 110 percent higher rate of
non-Hodgkin’s lymphoma in
Marines who served in heavily sprayed areas as compared with those who served in areas that were not sprayed. 77 The study also found a 58 percent higher rate of
lung cancer among the same comparative groups . 78
Also in 1987, a second VA study found a suggestive eight-fold increase in soft tissue sarcoma among veterans most likely to
76 CDC Protocol, see note 1 supra The CDC went on to state
that a wide variety of health effects have been observed following the
administration of TCDD to
experimental animals including soft tissue sarcomas and lymphoma1 nasal and nasopharyngeal cancers, birth defects, changes in thymus and lymphoid tissues, and
other numerous cancers. Additionally, the CDC acknowledged the toxic effects of occupational exposure to dioxin, including evidence that exposure "may be
associated with an increased risk of soft tissue sarcoma and lymphoma" and perhaps nasal and nasopharyngeal cancers.
77 Breslin, et. al. "Proportionate Mortality Study of U.S. Army and U.S. Marine Corps Veterans of the Vietnam War," Veterans Administration (1987).
78 Id. Some scientists, including the Advisory Committee
have attempted to denigrate these significant findings on the basis that Army
personnel did not show
similar results. The explanation for this lack of comparative Army findings is directly attributable to the dilution effect caused by including logistics personnel as part of
the Army study. Marines were studied as a separate group. The Marine’s logistical support personnel (i.e. the Navy), were not included. Thus, the increased cancers
among Marines were clearly associated with field exposure to Agent Orange.
The Army study, on the other hand, combined field
personnel with personnel on logistics assignments who were unlikely to have been
exposed to Agent Orange.
As a result, the Army findings were drastically diluted. Additionally, Army personnel generally engaged the enemy and returned to base, whereas Marines consistently
remained in areas presumably sprayed by Agent Orange to provide medical, health and engineering assistance to the local population. Such "pacification" efforts gave
Marines additional opportunities to be exposed to dioxins.
have been exposed to Agent Orange.79
A proportionate mortality study of deaths in pulp and
paper mill workers in New Hampshire from 1975 to 1985 showed that one or more of
experienced by such workers (dioxin is a byproduct of pulp and paper production) posed a "significant risk" for cancers of the digestive tract and lymphopoietic
tissues . 80
Another case control study of farmers in Hancock County,
Ohio, showed a "statistically significant" rise in Hodgkin’s disease
and non-Hodgkin’s lymphoma.
Although the study speculates that exposure to phenoxy herbicides may be the cause of such elevated cancers, the study recognizes that, given the size of its cohort,
the only credible conclusion that can be drawn is that it "adds to the growing body of reports linking farming and malignant lymphoma, particularly NHL." 81
A study of disease and non—battle injuries among U.S.
Marines in Vietnam from 1965 to 1972 showed a significantly higher rate of first
Marines stationed in Vietnam as opposed to Marines stationed elsewhere, particularly
79 Kang, et. al., "Soft-Tissue Sarcoma and Military Service in Vietnam:
A Case Control Study," 79 Journal of the National Cancer Institute 693
The increases were not statistically significant as reported. Nonetheless, the results are remarkable.
80 E · Schwartz, "A Proportional Mortality Ratio of Pulp and Paper Mill Workers in New Hampshire," 45 British Journal of Industrial Medicine, 234—238 (1988).
81 Dubrow, Paulson & Indian, "Farming and Malignant Lymphoma in Hancock county, Ohio," 45 British Journal of Industrial Medicine 25—28 (1988).
for neoplasms, diseases of the blood and blood forming organs and diseases of
the circulatory and respiratory systems.82 Of particular significance is the
fact that the
rate of first hospitalization for disease and non—battle injuries among Vietnam personnel rose steadily, reaching a peak in 1969, while the rate of non—Vietnam
personnel remained relatively constant.83 This rise in hospitalization for non—combat injuries coincides exactly with the increased use of Agent Orange, reaching a
peak in 1969, and declining thereafter until its elimination in 1971.
In a recently published article entitled "2,4--D,
2,4,5 --T, and 2,3,7,8 --TCDD: An Overview", the authors acknowledge that
at least three weaknesses in
research related to dioxins are sufficient to cast doubt on the validity of any study. 84 The
82 Palinkas & Coben, "Disease and Non—Battle Injuries Among U.S. Marines in Vietnam, 153 Military Medicine 150 (March, 1988).
83 Id. at 151. It should be noted that the year of
greatest combat activity, as measured by the number of personnel wounded in
action, 1968, had the smallest
disease and non-battle injury vs. wounded in action ratio. Id. at 152.
84 Lilienfeld and Gallo "2,4-D, 2,4,5—T and
2,3,7,8-TCDD An Overview," Epidemiologic Review, Vol. II (1989). Three
major criteria must be considered in
evaluating the numerous epidemiologic studies of phenoxy herbicides and 2,3,7,8-TCDD: 1) the accuracy of exposure assessment; 2) the studies’ statistical power;
and 3) the adequacy of follow-up. Problems in any one of the three areas leaves the study open to criticism and subject to manipulation.
For instance, in retrospective studies, various proxies of
exposure to herbicides and 2,3,7,8,—TCDD have been used such as military
service in Vietnam or
residence in an area in which the herbicides were sprayed. The weakness in such an approach is that unless the proxy corresponds to exposure, the "exposed group"
is diluted with the individuals who have NOT been exposed, thereby reducing the magnitude of the strength of the association. In fact, such reduction may be of such
a degree as to preclude detection of any
authors report that while the data on soft tissue sarcoma and phenoxy acids
are too inconsistent to allow for any comment at this time, there is evidence of
association between STS and the suspect chemicals in 2 of the 8 studies analyzed in their article. Furthermore, the birth defect studies analyzed "suggest that adverse
reproductive effects can be caused by (dioxin) . 85
Recent studies in Vietnam continue to show statistically
significant reproductive anomalies and birth defects among women, and children
of women presumably
exposed to Agent Orange spraying.86
of a serum marker for 2,3,7,8-TCDD by Kahn may provide the means of identifying persons who have been exposed.
Furthermore, studies concerning Agent Orange have nearly
all been conducted in the past decade. This 10 year latency period is generally
thought to be insufficient
for many cancers to be clinically detected .
86 See note 10 supra. It should be noted that as early as
1977 information about Agent Orange’s potential for genetic damage was known
to the VA. For
example, a "NOT FOR RELEASE" VA document expressly noted Agent Orange’s "high toxicity" and "its effect on newborn, deformed children —— similar to the
thalidomide situation." See L. Casten, Patterns of Secrecy note 73 supra at Department of Veteran Affairs p.4. Similarly, in March of 1980, Senator Tom Daschle
and Rep. David Bonior received an anonymous memorandum written on VA stationery which stated:
2,4,5-T and 2,4-D commonly known as Agent Orange and Agent Blue, are mutagenic
and teratogenic. This means they intercept the
genetic DNA message processed to an unborn fetus, thereby resulting in deformed children being born. Therefore, the veteran would appear to have no
ill effects from the exposure but he would produce deformed children due to this breakage in his genetic chain.... . .Agent Orange is 150,000 times more
toxic than organic arsenic.
Id. See also Wolfe & Lathrop, "A Medical Surveillance Program for
Scientists Exposed to Dioxins and Furans," Human and Environmental Risks of
Dioxins and Related Compounds, 707—716 (1983)
In the December 1, 1989, issue of Cancer, a study of the
cancer risks among Missouri farmers found elevated levels of lip and bone cancer
as well as nasal cavity
and sinuses, prostrate, non-Hodgkin’s lymphoma and multiple myeloma. Smaller elevations, but elevations nonetheless, were found for cancers of the rectum, liver,
malignant melanoma, kidney and leukemia. According to the authors, evidence of the cause for the elevated risks for these illnesses "may be strongest for a role of
agricultural chemicals, including herbicides, insecticides and fertilizers." 87
Both the U.S. Environmental Protection Agency (EPA) and
the International Agency for Research on Cancer (IARC) have concluded that
dioxin is a "probable
human carcinogen." 88
In a work entitled "Carcinogenic Effects of
Pesticides" to be issued by the National Cancer Institute Division of
Cancer Etiology, researchers conclude that while
confirmatory data is lacking there is ample evidence to suggest that NHL, STS, colon, nasal and nasopharyngeal cancer can result from exposure to phenoxy
A just released case control study of the health risks of exposure to dioxins confirmed previous findings that exposure to
(Proceedings of International Symposium on Chlorinated Dioxins and Related
Compounds, Arlington, VA, October 25—29, (1981)). The article explains the
possible mechanism for paternally transmitted birth defects.
87 Brownson, et. al. "Cancer Risks Among Missouri Farmers," 64 Cancer 2381, 2383 (December 1, 1989) .
88 Agency for Toxic Substances and Disease Registry, pp. 7,, 61—68, 94 reprinted in Rachel’s Hazardous Waste News # 173 (March 21, 1990)
phenoxyacetic acids or chlorophenols entails a statistically significant increased risk (i.e. 1.80) for soft tissue sarcoma.89
As recently as February 28, 1990 an additional study found
that farmers exposed to various herbicides containing 2,4—D may experience
elevated risks for
certain cancers, particularly cancers of the stomach, connective tissue, skin, brain, prostate, and lymphatic and hematopoietic systems."90
This week a scientific task force, after reviewing the
scientific literature related to the potential human health effects associated
with exposure to phenoxyacetic acid
herbicides and/or their associated contaminants (chlorinated dioxins) concluded that it is at least as likely as not that exposure to Agent Orange is linked to the
following diseases: non—Hodgkin’s lymphoma, soft tissue sarcoma, skin disorders/chloracne, subclinical hepatotoxic effects (including secondary coproporphyrinuria
and chronic hepatic porphyria), porphyria cutanea tarda, reproductive and developmental effects, neurologic
89 Eriksson, Hardell & Adami, "Exposure to
Dioxins as a Risk Factor for Soft Tissue Sarcoma: A Population--Based
Case--Control study," 82 Journal of the
National Cancer Institute 486—490 (March 21 1990) . It should be noted that in this study the median latency for phenoxyacetic acid and chlorophenols exposure
was 29 and 31 years respectively, thereby suggesting that many of the veterans who are at risk have not yet manifested symptoms of STS.
90 Blair, "Herbicides and Non-Hodgkin’s Lymphoma: New Evidence From a Study of Saskatchewan Farmers," 82 Journal of the National cancer
effects and Hodgkin’s disease.91
On the same day that this scientific task force reported a
statistically significant linkage between exposure to the dioxins in Agent
Orange and various cancers and
other illnesses, the Environmental Protection Agency reported that the cancer risk posed by the release of such a "potent carcinogen" as dioxin in the production of
white paper products is "high enough to require tighter controls on paper mills."92
As many of the studies associated with Agent Orange and dioxins attest,
science is only at the threshold of understanding the full dimension of harmful
from environmental agents on various components of the human immune system. 93 In
91 Report of the Agent Orange Scientific Task Force of the
American Legion, Vietnam Veterans of America, and the National Veterans Legal
reported by McAllister, "Viet Defoliant Linked to More Diseases, Washington Post, May 1, 1990 at AS, col. 4. The report also found that there are other disorders
for which there is evidence suggesting an association with exposure to Agent Orange, but for which statistically significant evidence is not currently available. Those
diseases include: leukemias, cancers of the kidney, testis, pancreas, stomach, prostate, colon hepatobiliary tract, and brain, psychosocial effects, immunological
abnormalities, and gastrointestinal disorders.
92 Weisskopf, "EPA Seeking to Reduce Dioxin in White Paper: Cancer Risk Said to Justify Mill Restrictions," Washington Post, May 1, 1990 at AS, col. 1.
93 A recent report in the Washington Post suggests that
there is an inherent uncertainty in trying to measure the dangers posed by the
chemicals humans eat, drink
and breathe. Since human experimentation is impossible to assess the effect of varied doses of a chemical on human health, scientists are ultimately required
fact, a whole new discipline — immunotoxicology — has developed to
explore further the effects of environmental chemicals on human health and to
test results to humans.94
Immunotoxicology has established, however, at a minimum
that at least three classes of undesirable effects are likely occur when the
immune system is disturbed
by environmental exposure to chemicals such as dioxin, including: 1) immunodeficiency or suppression; 2) alteration of the host defense mechanism against mutagens
and carcinogens (one theory is that the immune system detects cells altered by mutagens or other carcinogenic trigger and destroys these cells. Thus, an impaired
immune system may not detect and destroy a newly forming cancer); and 3) hypersensitivity or allergy to the chemical antagonist. Because of dioxin’s ability to be
both an immunosuppressant and a carcinogen, as early as 1978 immunologists were suggesting that "(a) gents such as TCDD.. .may be far more dangerous than
those possessing only one of these properties."95
While scientists are not in agreement, some
immunotoxicologists argue that one molecule of a carcinogenic agent, like dioxin
in the right place and at the right time
to speculate or guess as to the health effects of a given chemical to the
human body. See Measuring Chemicals’ Dangers: Too Much Guesswork?"
March 23, 1990.
94 Silbergeld & Gaisewicz, "Dioxins and the Ah Receptor," 16 American Journal of Industrial Medicine 455, 468—69 (1989).
95 Inadvertent Modification of the Immune Response — The
Effect of Foods, Drugs, and Environmental Contaminants; Proceedings at the
symposium; U.S. Naval Academy (August 28-30, 1978), p. 78.
cause the human immune system to turn on itself, manifesting such breakdowns
in the form of cancer. Indeed, even some courts have accepted this theory of
causation in matters specifically related to exposure to dioxin.96
With additional evidence from Vietnam suggesting that
Agent Orange contaminants have the ability to migrate away from actual spray
locations via river channels
and the food chain, the opportunity for a Vietnam Veteran to have been exposed to dioxin contaminant molecules increases significantly.97
It cannot be seriously disputed that any large population
exposed to chemical agents, such as Vietnam Veterans exposed to Agent Orange, is
likely to find among
its members a number who will develop malignancies and other mutagenic effects as a result of being exposed to harmful agents.
To be sure, decisions today with regard to the seriousness of Agent Orange health effects must be made while the science of
96 See Peteet V. Dow Chemical Co. , 868 F.2d 1428, 1433 (5th Cir. 1989) cert denied 110 S.Ct. 328 (1989).
97 See e.g. Schecter, et. al., "Levels of 2,3,7,8—TCDD
in Silt Samples Collected Between 1985—86 From Rivers in the North and South
of Vietnam," 19
Chemosphere 547—550 (1989) (suggestive findings that the predominant dioxin isomer in Agent Orange has moved into downstream rivers in the South of
Vietnam); Olie, et. al., "Chlorinated Dioxin and Dibenzofuran Levels in Food and Wildlife Samples in the North and South of Vietnam," 19 Chemosphere 493-496
(1989) (food and wildlife specimens in South Vietnam had a higher relative abundance of 2,3,7,8-TCDD suggesting contamination from Agent Orange); Schecter, et
· al. "Chlorinated Dioxin and Dibenzofuran Levels in Food Samples Collected Between 1985—87 in the North and South of Vietnam," 18 Chemosphere 627—634
(1989) (Agent Orange contaminants, specifically 2,3,7,8-TCDD found at relatively elevated levels in food and wildlife samples 15-2 5. years after environmental
contamination with compound in South of Vietnam
immunotoxicology is in its infancy. After having evaluated and considered all
of the known evidence on Agent Orange and dioxin contaminants, it is evident to
enough is known about the current trends in the study of dioxins, and their linkage with certain cancers upon exposure, to give the exposed Vietnam Veteran the
benefit of the doubt.
This benefit of the doubt takes on added credence given
two separate means for determining exposure to Agent Orange — 1) HERBs and
Service HERBs tapes
establishing troop location for comparison with recorded Ranch Hand spraying missions; and 2) blood testing from living Veterans,to ascertain elevated dioxin levels.
The inexplicable unwillingness of the CDC to utilize this data has had the effect of masking the real increase in the rate of cancers among the truly exposed. There is,
in my opinion, no doubt that had either of these methods been used, statistically significant increased rates of cancer would have been detected among the Veterans
for whom exposure can still be verified.
Since science is now able to conclude with as great a
likelihood as not that dioxins are carcinogenic directly and indirectly through
immunosuppression, and since a
large proportion of those exposed to dioxin can be so ascertained, I am of the view that the compensation issue for service—related illnesses associated with
exposure to Agent Orange should be resolved in favor of Vietnam Veterans in one of the two following ways:
COMPENSATION FOR SERVICE RELATED ILLNESSES
Any Vietnam Veteran, or Vietnam Veteran’s child who has
a birth defect, should be presumed to have a service—connected health effect
if that person suffers
from the type of health effects consistent with dioxin exposure and the Veteran’ s health or service record establishes 1) abnormally high TCDD in blood tests; or 2)
the veteran’s presence within 20 kilometers and 30 days of a known sprayed area (as shown by HERBs tapes and corresponding company records); or 3) the
Veteran’ s presence at fire b se perimeters or brown water operations where there is reason believe Agent Orange have- occurred.
Under this alternative compensation would not be provided
for those veterans whose exposure came from TCDD by way of the food chain; silt
sprayed areas into unsprayed waterways; some unrecorded U.S. or allied Agent Orange sprayings; inaccurately recorded sprayings; or sprayings whose wind drift
was greater than 20 kilometers. Predictably, problems generated by the foregoing oversights, the mass of data to be analyzed as claims were filed, and the known
loss of many service records would invalidate many veterans’ legitimate claims
Any Vietnam Veteran or child of a Vietnam Veteran who
experiences a TCDD—like health effect shall be presumed to have a
service—connected disability. This
alternative is admittedly
broader than the first, and would provide benefits for some veterans who were
not exposed to Agent Orange and whose disabilities are not presumably truly
service—connected. Nevertheless, it is the only alternative that will not unfairly preclude receipt of benefits by a TCDD exposed Vietnam Veteran.
Furthermore, this alternative is consistent with the
Secretary’s decision regarding the Service—connection of non— Hodgkin’s
lymphoma, as well as legal
precedent with respect to other diseases presumed by the Department of Veterans Affairs to be connected to one or more factors related to military service (i.e.
veterans exposed to atomic radiation and POW’s with spastic colon).
PRESUMPTIONS OF AGENT ORANGE RELATED HEALTH EFFECTS
I have also given considerable thought to which health
effects are to be presumed likelier than not to be related to TCDD exposure and
service—connected. Any such determination must be made in light of: 1) the review of the scientific literature, including animal studies where human data does not
exist or has been manipulated; 2) the inappropriate processes of the Veterans Advisory Committee on Environmental Hazards; 3) the past political manipulations of
Ranch Hand and CDC studies; and 4) the recent discoveries of manipulation by scientists hired by chemical manufacturers of dioxin contaminants to evaluate the
potentially best epidemiological data concerning TCDD’s effects on humans.
My evaluation of the evidence has been made with just such
considerations in mind. Additionally, I have conferred with several experts
in the field. After evaluating all the evidence and material of record, I am
there is better than "an approximate balance of positive and negative evidence" on a series of Agent Orange related health effects.
It can, in my judgment, be concluded, vith a very high
degree of confidence, that it is at least as likely as not that the following
are caused in humans by exposure to
TCDD: non—Hodgkin’ s lymphoma, chloracne and other skin disorders, lip cancer, bone cancer, soft tissue sarcoma, birth defects, skin cancer, lung cancer,
porphyria cutanea tarda and other liver disorders, Hodgkin’s disease, hematopoietic diseases, multiple myeloma, neurological defects and auto—immune diseases
In addition, I am most comfortable in concluding that it
is at least as likely as not that liver cancer, nasal/pharyngeal/esophageal
cancers, leukemia, malignant
melanoma, kidney cancer, testicular cancer, pancreatic cancer, stomach cancer, prostate cancer, colon cancer, brain cancer, psychosocial effects, and
gastrointestinal disease are service-- connected.
I have separated the two foregoing subsets subjectively
only because there is somewhat more data to support the former than the latter.
immunological and toxicological theory supports both subsets and fully justifies, in my view, the inclusion of both subsets of the foregoing health effects in determining
a service--connected injury.
Such a resolution of the embarrassingly prolonged Agent
Orange controversy would be on the order of decisions to compensate U.S.
soldiers who contracted
cancer after exposure to radiation from atomic tests and U.S. soldiers involved, without their knowledge, in LSD experiments. With the scientific basis now available
for it to be stated with confidence that it is at least as likely as not that various health effects are related to wartime exposure to Agent Orange, there is the opportunity
finally to right a significant national wrong committed against our Vietnam Veterans.
1. That the Secretary undertake a prompt reevaluation of
the compensation decision impacting on Vietnam Veterans exposed to Agent Orange
in light of
accumulating scientific evidence that discredits earlier "findings" of an insufficient linkage between dioxin contaminants in Agent Orange and rare disease, such as
2. To the extent that the Secretary deems it necessary to
use the Veterans’ Advisory Committee on Environmental Hazards to assist in his
reevaluation, the current
members should be dismissed -— having demonstrated a disturbing bias in their review to date of the scientific literature related to Agent Orange and dioxin -- and
new members should be appointed in accordance with Section G of the Veterans’ Dioxin and Radiation Exposure Compensation Standards Act, including persons
with recognized scientific and medical expertise in fields pertinent
to understanding the health effects of exposure to dioxin. The Committee meeting currently scheduled for May 16th and May 17th should be cancelled.
3. That the Secretary in making his decision regarding
Agent Orange compensation for Vietnam Veterans do so on the basis of his
independent evaluation of the
existing scientific and medical evidence on the health effects of exposure to dioxins, as cataloged and discussed in this Report, and in full recognition that the standard
to be applied -- as mandated by both Congress and the courts -- requires the resolution of doubts as to a number of cancers linked to dioxins in favor of the Vietnam
TABLE 1-1 Updated (1998) Summary of Findings in Occupational,
Environmental, and Veterans Studies Regarding the Association Between
Specific Health Outcomes and Exposure to Herbicides
Sufficient Evidence of an Association
Evidence is sufficient to conclude that there is a positive association. That is, a
positive association has been observed between herbicides and the outcome in
studies in which chance, bias, and confounding could be ruled out with
reasonable confidence. For example, if several small studies that are free from
bias and confounding show an association that is consistent in magnitude and
direction, there may be sufficient evidence for an association. There is sufficient
evidence of an association between exposure to herbicides and the following
Limited/Suggestive Evidence of an Association
Evidence is suggestive of an association between herbicides and the outcome
but is limited because chance, bias, and confounding could not be ruled out with
confidence. For example, at least one high-quality study shows a positive
association, but the results of other studies are inconsistent. There is
limited/suggestive evidence of an association between exposure to herbicides
and the following health outcomes:
Respiratory cancers (lung/bronchus, larynx, trachea)
Acute and subacute transient peripheral neuropathy
Spina bifida in the children of veterans
Porphyria cutanea tarda
Inadequate/Insufficient Evidence to Determine Whether an Association
The available studies are of insufficient quality, consistency, or statistical power to
permit a conclusion regarding the presence or absence of an association. For
example, studies fail to control for confounding, have inadequate exposure
assessment, or fail to address latency. There is inadequate or insufficient
evidence to determine whether an association exists between exposure to
herbicides and the following health outcomes:
Female reproductive cancers (cervical, uterine, ovarian)
Urinary bladder cancer (category change in 1998)
Birth defects (other than spina bifida)
Neonatal/infant death and stillbirths
Inadequate/Insufficient Evidence to Determine Whether an Association
Childhood cancer in offspring
Abnormal sperm parameters and infertility
Chronic peripheral nervous system disorders
Metabolic and digestive disorders (diabetes, changes in liver enzymes,
lipid abnormalities, ulcers)
Immune system disorders (immune suppression and autoimmunity)
Limited/Suggestive Evidence of No Association
Several adequate studies, covering the full range of levels of exposure that human
beings are known to encounter, are mutually consistent in not showing a positive
association between exposure to herbicides and the outcome at any level of
exposure. A conclusion of "no association" is inevitably limited to the conditions,
level of exposure, and length of observation covered by the available studies. In
addition, the possibility of a very small elevation in risk at the levels of exposure
studied can never be excluded. There is limited/suggestive evidence of no
association between exposure to herbicides and the following health outcomes:
Gastrointestinal tumors (stomach cancer, pancreatic cancer, colon cancer,
NOTE: "Herbicides" refers to the major herbicides used in Vietnam:
(2,4-dichlorophenoxyacetic acid); 2,4,5-T (2,4,5-trichlorophenoxyacetic acid) and its contaminant
TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin); cacodylic acid; and picloram. The evidence regarding
association is drawn from occupational and other studies in which subjects were exposed to a
variety of herbicides and herbicide components
Health Outcomes with Sufficient Evidence of an Association
In Update 1996, the committee found sufficient evidence of an association
between exposure to herbicides and/or TCDD
and four diseases: soft-tissue sarcoma, non-Hodgkin's lymphoma, Hodgkin's disease, and chloracne. The recent scientific
literature continues to support the classification of these diseases in the category of sufficient evidence. Based on the recent
literature, there are no additional diseases that satisfy this category's criteria--that a positive association between herbicides and
the outcome must be observed in studies in which chance, bias, and confounding can be ruled out with reasonable confidence.
The committee regards evidence from several small studies that are free from bias and confounding, and that show an
association that is consistent in magnitude and direction, as sufficient evidence for an association. The evidence that supports
the committee's conclusions for the three cancers is detailed in Chapter 7 and for chloracne in Chapter 11.
Health Outcomes with Limited/Suggestive Evidence of Association
In Update 1996, the committee found limited/suggestive evidence of an
association for six classes of diseases, three
cancers--respiratory (larynx, lung/bronchus, and trachea) cancer, prostate cancer, and multiple myeloma--and three other
health outcomes--spina bifida in the children of veterans, acute and subacute (transient) peripheral neuropathy, and porphyria
cutanea tarda. The recent scientific literature continues to support the classification of these diseases in the limited/suggestive
category of sufficient evidence. Based on the recent literature, there are no additional diseases that satisfy this category's
For outcomes in this category, the evidence must be suggestive of an association
with herbicides, but the association may
be limited because chance, bias, or confounding could not be ruled out with confidence. Typically, at least one high-quality
study indicates a positive association, but the results of other studies may be inconsistent.
Since the last update, there have been several studies of respiratory cancer
among occupationally exposed groups and
Vietnam veterans. Newly published studies of phenoxy herbicide production workers (Kogevinas et al., 1997) and workers
exposed as a result of an industrial accident (Ott and Zober, 1996) show small but statistically significant excesses of lung
cancer mortality. Results in both studies indicate higher estimated risk for individuals with higher estimated exposure. One other
occupational study (Ramlow et al., 1996) reports a relative risk indistinguishable from 1. A study of rice farmers in Italy
(Gambini et al., 1997) found lower lung cancer incidence than observed in the general population, a result similar to that found
in studies of U.S. farmers, which may reflect lower incidence of smoking in this occupational group. New data from the Seveso
accident (Bertazzi et al., 1997) do not indicate any increase in lung cancer mortality in this environmentally exposed group, but
an insufficient number of years have passed since exposure to draw conclusions about any effect that the accidental exposure
may have had. Increases in respiratory cancers were seen in new studies of U.S. and Australian Vietnam veterans, although
there is evidence that cigarette smoking was more prevalent among Vietnam veterans than among non-Vietnam veterans or the
general public. In summary, the most recently published studies continue to support placing respiratory cancers in the category
of limited/suggestive evidence. Although smoking undoubtedly plays a role in these cancers, the consistency of the finding
across several studies argues against the notion that it is the sole explanatory factor.
New studies of production workers continue to show weak but consistent evidence
of effects on prostate cancer mortality,
whereas new research on agricultural workers shows no indication of increased risk. A detailed and well-conducted analysis of
Australian male Vietnam veterans' mortality (Crane et al., 1997) found a statistically significant relationship between Vietnam
service and prostate cancer. The committee's summary evaluation, based on all of the epidemiologic evidence, was that the
data continue to support the classification of prostate cancer in the limited/suggestive category.
The evidence that supports the committee's conclusions for multiple myeloma is
detailed in Chapter 7 and is not
substantially changed from Update 1996.
In Update 1996 the committee identified three studies of the offspring of
Vietnam veterans that were suggestive of an
association between exposure to the herbicides considered in this report and spina bifida, although a number of methodologic
issues limited the interpretation of these results. Since the publication of that report, occupational studies of the offspring of
fathers employed in British Columbia sawmills (Dimich-Ward et al., 1996) and the offspring of Norwegian farmers (Kristensen
et al., 1997), and a multicenter case-control study of paternal occupation and risk of spina bifida conducted in the Netherlands
(Blatter et al., 1997), have provided some additional support for the association with this specific birth defect, although
concerns remain including control of confounding, exposure determination, and isolation of exposure to specific herbicides and
No additional evidence has been published since Update 1996 regarding acute and
subacute transient peripheral
neuropathy or porphyria cutanea tarda.
Health Outcomes with Inadequate/Insufficient Evidence to Determine Whether an
The scientific data for many of the cancers and other diseases reviewed by the
committee were inadequate or insufficient to
determine whether an association exists. For diseases in this category, the available studies are of insufficient quality,
consistency, or statistical power to permit a conclusion regarding the presence or absence of an association. For example,
studies fail to control for confounding or have inadequate exposure assessment. This group includes hepatobiliary cancers
(cancers of the liver and intrahepatic bile duct), nasal and nasopharyngeal cancer, bone cancer, skin cancers (including basal
cell carcinoma, squamous cell carcinoma, and non-melanocytic skin cancers), breast cancer, cancers of the female
reproductive system (including cervix, endometrium, and ovaries), testicular cancer, urinary bladder cancer, renal cancer
(cancers of the kidney and renal pelvis), and leukemias. The scientific evidence regarding each of these cancers is detailed in
Based on an evaluation of all the epidemiologic evidence, including studies
published since the release of Update 1996, the
committee felt that urinary bladder cancer should be added to this category. Although there is no evidence that exposure to
herbicides or dioxin is related to this cancer, relative risks in some of the largest cohorts tended to be greater than 1,
weakening the committee's prior conclusion that there was positive evidence of no relationship. The co-exposure to TCDD
and a variety of known bladder carcinogens makes it very difficult to isolate any possible additional effect of herbicides,
although little total effect was seen.
A recent community based case-control study examining herbicide exposure and
skin cancers drew the attention of the
committee (Gallagher et al., 1996). This study, which controlled for a number of factors known to influence skin cancer rates,
found increasing risk of squamous cell carcinoma with increasing lifetime exposure to herbicides. Although there are concerns
regarding the study's control of confounding and the adequacy of the exposure assessment, the committee concluded that the
study was the best of its kind to date. The available evidence is insufficient to determine whether an association exists between
herbicide exposure and any of the forms of skin cancer. However, the committee encourages further study of basal and
squamous cell skin cancer incidence among working and Vietnam veteran populations. In any future studies, careful attention
should be paid to exposure assessment, as well as to controlling for confounding from UV exposures. Efforts to examine the
carcinogenicity of organic arsenicals are also encouraged.
Several reproductive effects are classified in this category, including
spontaneous abortion, birth defects other than spina
bifida, neonatal or infant death and stillbirths, low birthweight, childhood cancer in offspring, and abnormal sperm parameters
and infertility. The scientific evidence for reproductive effects is detailed in Chapter 9. Neurobehavioral effects that are
classified in this category include cognitive and neuropsychiatric disorders, motor or coordination dysfunction, and chronic
peripheral nervous system disorders. The scientific evidence for these effects is detailed in Chapter 10.
Other health effects that are classified in this category include metabolic and
digestive disorders, immune system disorders,
circulatory disorders, and respiratory disorders. The scientific evidence for these effects is detailed in Chapter 11.
Diabetes is a health outcome of special interest to the DVA. When viewed in the
context of the total literature the
committee concludes that, at this time, there is inadequate/insufficient evidence to determine whether an association exists
between herbicide or dioxin exposure and increased risk of diabetes. Further analyses and full publication of existing studies
may justify a reevaluation of this conclusion.
Many animal studies provide potential biological mechanisms for an association
between herbicide exposure and diabetes
risk. Although the majority of earlier reports on humans suggest little association, the potentially more definitive 1997 report
from the Ranch Hand study (Henriksen et al., 1997) raises the possibility that the highest-exposure group (highest TCDD
level) may have an increased risk. Such a conclusion may be supported by a currently unpublished NIOSH study of exposed
workers. It is important to note that both these studies used serum TCDD levels as the measure of exposure. At this time,
questions concerning case definition and full control for obesity, or other confounders (in the Ranch Hand study) preclude
determining whether or not an association exists between herbicide exposure and diabetes in these studies. The committee
strongly urges that the NIOSH study be documented more completely and published in the peer-reviewed literature, so that its
potentially important findings can be evaluated fully. It strongly recommends that the Ranch Hand study develop a fully
adjusted multivariate model (e.g., Cox Proportional Hazard with time to diabetes as the outcome), fully controlling for baseline
age and obesity (BMI) and, if possible, for family history of diabetes, central fat distribution, diabetogenic drug exposure, and
a measure of obesity at the time of Vietnam service. The committee recommends consideration be given to a combined
analysis of the Ranch Hand and NIOSH studies to further examine the possibility that herbicide exposure leads to an increased
risk of diabetes.
Health Outcomes with Limited/Suggestive Evidence of No Association
In VAO, the committee found a sufficient number and variety of well-designed
studies to conclude that there is
limited/suggestive evidence of no association between a small group of cancers and exposure to TCDD or herbicides. This
group includes gastrointestinal tumors (colon, rectal, stomach, and pancreatic) and brain tumors. Recent scientific evidence
continues to support the classification of such cancers in this category and is detailed in Chapter 7. Based on the recent
literature, there are no additional diseases that satisfy the criteria necessary for this category.
For outcomes in this category, several adequate studies covering the full range
of levels of herbicide exposure that human
beings are known to encounter are mutually consistent in not showing a positive association between exposure and health risk
at any level of exposure. These studies have relatively narrow confidence intervals. A conclusion of "no association" is
inevitably limited to the conditions, level of exposure, and length of observation covered by the available studies. In addition,
the possibility of a very small elevation in risk at the levels of exposure studied can never be excluded.
The Relationship Between the Length of Time Since Exposure and the Possible Risk
The importance of latency effects and other time-related factors in determining
cancer risk has long been recognized, and
statistical methodologies have been developed to study this issue. A variety of practical difficulties relating to exposure
assessment and other data requirements, however, have limited the use of these methods in epidemiologic studies of
environmental carcinogens. In response to the request from the DVA to explore latency issues related to herbicides used in
Vietnam, the committee attempts in Chapter 8 to establish a methodology to address the timing of herbicide exposure and the
risk of cancer. This chapter also reviews the literature on herbicide exposure and some cancers for results that describe how
the timing of exposure affects the relative risk due to exposure.
One of the committee's tasks was to assess the likelihood that exposure to
herbicides used in Vietnam resulted in or will
result in increased risk of disease in Vietnam veterans. Currently, any such inference would have to be based on extrapolation
from the findings about disease experience of other groups exposed to TCDD or herbicides generally. Given that we know
when the potential exposure to TCDD and other herbicides used in Vietnam began and ended, it would appear reasonable to
examine time-related factors for those who served in Vietnam, but to date, no adequate analysis of time-related factors for
cancer occurrence in Vietnam veterans has been published. Extrapolation from other types of studies is problematic for several
reasons. Brief exposures, such as occurred in Seveso, and chronic occupational exposures may not apply to Vietnam veterans
because of the different exposure situation. For example, there is evidence in the literature (e.g., for respiratory cancer) that
latency can vary not only among individuals, but also according to other aspects of the exposure scenario, such as the
magnitude of exposure. Thus, if high exposures in an occupational setting result in a certain pattern of relative risks for a given
time since first exposure, this pattern may not hold for lower level exposures such as occurred in Vietnam. Similarly, direct
evidence was not presented to evaluate the impact of age at exposure to herbicides. It is possible that the age at which
exposure was received could influence the pattern of latency that would be observed (e.g., exposures incurred at younger ages
could be more potent, but the impact might not be seen for a longer time period; conversely, exposures at older ages might be
more harmful, particularly in the short run). Unfortunately, the data are not available to evaluate the hypothesis that age at
exposure is important. A major limitation of the analyses discussed in this chapter is the failure of most studies to conduct
analyses of latency that also controlled for factors such as duration of exposure, age, and calendar time of exposure (or
analyses of age at exposure that controlled for time since exposure), particularly for occupational cohorts with protracted
Another consideration is the long retention time of TCDD and other highly
chlorinated herbicides. Since body burdens from
any exposure, no matter how brief, result in continuing exposures to internal organs, the concept of time since exposure ended
has a different meaning than for chemical agents that are eliminated quickly.
A third issue concerns the distinction between morbidity and mortality. As
discussed in Chapter 8, the latency between
exposure and death is composed of two parts: (1) latency until disease appears and (2) time between disease occurrence and
death. For diseases with low survival rates, such as respiratory cancer, the time between disease occurrence and death is
generally short; therefore, a study focusing on mortality will give a good approximation of the latency period. However, for
diseases that are not always fatal or that have a long survival time such as prostate cancer, it is preferable to examine incidence
rather than mortality. Thus, further data on prostate cancer incidence would be of great help, since relatively few men with
prostate cancer die from it.
Overall, the data on latency do not alter the committee's conclusions with
regard to the categories of evidence for individual
cancer sites, but they do provide some information on how long the effects of herbicide exposures last. The evidence suggests
that if respiratory cancer does result from exposure to herbicides used in Vietnam, the greatest relative risk for lung cancer may
be in the first decade after exposure, but until further follow-up has been carried out for some of the cohorts, it will not be
possible to put an upper limit on the length of time these herbicides could exert their effect. For prostate cancer, the published
data are largely uninformative, and conclusions must await more definitive studies, preferably using incidence rather than
mortality. For non-Hodgkin's lymphoma, effects are seen in the second decade after exposure begins and continue to be
observed more than 20 years after external exposure ends. Because of the long retention times of TCDD, internal exposures
can continue long after external exposures cease.
Increased Risk of Disease Among Vietnam Veterans
One of the three primary charges contained in the Agent Orange Act of 1991
(Public Law 102-4, subsequently codified as
38 USC Sec. 1116) states:
For each disease reviewed, the Academy shall determine (to the extent that
available scientific data permit meaningful
determinations) . . . the increased risk of the disease among those exposed to herbicides during service in the Republic of
Vietnam during the Vietnam era. . . .
Although there have been numerous health studies of Vietnam veterans, most have
been hampered by relatively poor
measures of exposure to herbicides or TCDD, in addition to other methodological problems. Most of the evidence on which
the findings regarding disease association are based comes from studies of people exposed to dioxin or herbicides in
occupational and environmental settings, rather than from studies of Vietnam veterans. The committee found this body of
evidence sufficient for reaching the conclusions about statistical associations between herbicides and the health outcomes.
However, the lack of adequate data on Vietnam veterans per se complicates the quantification of any increased risk of disease
among individuals exposed to herbicides during service in Vietnam. Given the large uncertainties that remain about the
magnitude of potential risk from exposure to herbicides in the epidemiologic studies that have been reviewed (Chapters 7, 9,
10, and 11), the inadequate control for other important risk factors, and the uncertainty about the nature and magnitude of
exposure to herbicides in Vietnam (Chapter 5), the necessary information to undertake a quantitative risk assessment is
Thus, the committee cannot quantify the degree of risk likely to be experienced
by those exposed to herbicides during
service in the Republic of Vietnam during the Vietnam era. For those outcomes in the "Sufficient" and "Limited/Suggestive"
categories, what can be said is that too little is known about the herbicide exposure of veterans to make a meaningful
determination of the increased risk, if any, of these outcomes among Vietnam veterans. As discussed above, the epidemiologic
analyses to date have many limitations which prevent a more quantitative exposure-response analysis. Where there is
inadequate/insufficient evidence to determine whether an association exists between herbicide exposure and a particular health
outcome, there is also inadequate/insufficient information to assess the increased risk, if any, of that outcome. Finally, a finding
of "limited/suggestive evidence of no association" between herbicide exposure and a health outcome means that the evidence
suggests there is no increased risk of that outcome among Vietnam veterans. These conclusions are inevitably limited to the
conditions, level of exposure, and length of observation covered by the studies reviewed by the committee. There are certain
diseases where the committee can draw more specific conclusions, and this information is related in the discussion of those
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affected: 38 CFR §3.309
Date of Regulation: July 9, 2001
Secretary Approved Regulation: April 19, 2001
Register Citation: 66 FR 23166
The purpose of the following information on this new VA regulation is to
inform all concerned why it is being promulgated.
This information is not regulatory.
Department of Veterans Affairs (VA) has amended its adjudication regulations
concerning presumptive service connection for certain diseases for which there
is no record during service. This amendment is necessary to implement a decision
of the Secretary of Veterans Affairs under the authority granted by 38 U.S.C.
1116 that there is a positive association between exposure to herbicides used in
the Republic of Vietnam during the Vietnam era and the subsequent development of
Type 2 diabetes. The intended effect of this amendment is to establish
presumptive service connection for that condition based on herbicide exposure.
April 19, 2001.
J. Principi, Secretary of Veterans Affairs.
For the reasons set forth in the preamble, 38 CFR part 3 is amended as
A--Pension, Compensation, and Dependency and Indemnity Compensation
1. The authority citation for part 3, subpart A continues to read as
Authority: 38 U.S.C. 501(a), unless otherwise noted.
2. In Sec. 3.309, paragraph (e), the listing of diseases is amended by
adding ``Type 2 diabetes (also known as Type II diabetes mellitus or adult-onset
diabetes)'' between ``Chloracne or other acneform disease consistent with
chloracne'' and ``Hodgkin's disease'' to read as follows:
3.309 Diseases subject to presumptive service connection.* * * * *
(e) * * *
Type 2 diabetes (also known as Type II diabetes mellitus or adult-onset
* * * * * (Authority: 38 U.S.C. 501(a) and 1116