THE AGENT ORANGE CONTROVERSY IN AUSTRALIA: A CONTRIBUTION TO THE DEBATE

COMMUNITY HEALTH STUDIES VOLUME I X , NUMBER 2, 1985

THE AGENT ORANGE CONTROVERSY IN AUSTRALIA: A CONTRIBUTION TO THE DEBATE*

Wayne Hall** and Donald MacPhee+

**Department of Psychiatry and Behavioural Science, University of Western Australia. Nedlands, W. A . 6009.

+Department of Microbiology. Latrobe University. Bundoora, Victoria, 3083

* This paper is based in part upon material presented at the 54th Annual Conference of the Australian and New Zealand Association for the Advancement of Science, Canberra, May, 1984.

Abstract This paper examines the claims made by the

Vietnam Veterans’ Association of Australia that the health of Vietnam veterans has been adversely affected by exposure to the herbicide Agent Orange and other pesticides while serving in Vietnam. Three claims are dealt with in detail: those concerning the effects of exposure to pesticides on the rates of birth defects among the children of Vietnam veterans and of psychiatric disorders and premature death among themselves. Epidemiological evidence on the rate a t which these adverse outcomes occur among Vietnam veterans is reviewed, as is evidence on the effects of occupational pesticide exposure on reproductive outcomes, mental health and premature death. The review indicates that there is little evidence to sustain any of the claims and much evidence against them. An analysis of the reasons for the persistence of the controversy in the face of negative evidence suggests that there has been an unfortunate confusion of two questions: are Vietnam veterans owed justice for the injustices they have suffered in the past? is their present suffering a consequence of their chemical exposure in Vietnam? The community owes it to Vietnam veterans and their families to distinguish the two questions to ensure that an affirmative answer to the first question does not depend upon an affirmative answer to the second.

Introduction In late 1978 the first claims were made in the

United States that psychiatric disorders, and cancers among Vietnam veterans, and birth abnormalities among their children, were the result

of the veterans’ exposure to herbicides while serving in Vietnam.’ One of the most widely used of the herbicides in Vietnam was “Agent Orange”, the US Army’s code name for the 50:SO combination of the two phenoxy herbicides 2,4-D and 2,4,5-T which was contaminated with the impurity 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD or “dioxin”). The code name of this herbicide has come to be used by the media as a shorthand for the controversy about the possible adverse effects of chemical exposure in Vietnam on the veterans and their families. The American veterans’ claims were taken up by Australian veterans who had experienced similar problems. The Vietnam Veterans’ Association of Australia (VVAA) was formed with the purpose ofachieving compensation and treatment for veterans said to be adversely affected by herbicides. This paper provides an analysis of the claims made by the VVAA whose leadership will be treated as the representatives of Vietnam veterans, a role they have been accorded by the Government and the press.

The Vietnam Veterans’ Association of Australia has claimed that exposure to the herbicide Agent Orange and other pesticides in Vietnam has produced an increase in the rates of birth defects among their children and of psychiatric disorders and cancers among themselves.2,-’ These claims presuppose: that Australian troops were exposed to pesticides in Vietnam; that the rates of birth defects among their children and of psychiatric disorders and cancers among themselves are higher than those in the general community; and that the increases in these rates are a consequence of pesticide exposure. A

HALL & MacPHEE I09 COMMUNITY HEALTH STUDIES

proper evaluation of the Agent Orange controversy requires separate evaluation of each of these assumptions.

Were Australian Troops Exposed to Pesticides? The question of the extent to which

Australian troops were exposed to pesticides (insecticides and herbicides) in Vietnam has been argued at great length. The controversy continues because of a conflict between the levels of exposure implied by surviving records (for example, the Herbs Tapes) and by the recollection of Vietnam veterans. The records imply minimal exposure; the recol lect ions imply extensive exposure . Documents and records preserved by Australian and United States’ Armies have been interpreted by the Department of Veterans’ Affairs as showing that the extent of exposure of Australian troops was minimal. The number of men affected is estimated to be no more than 5 per cent of those who served in Vietnam.2 Individual exposure to herbicides is estimated to have been confined to isolated occurrences of direct exposure from planes involved in spraying or from troop transits of sprayed areas. The recollections of some Australian servicemen provided by the VVAA suggest that exposure to herbicides and other chemicals was more extensive: that anyone who served in Vietnam WPS exposed by virtue of being there.*,’

Adjudication of this disagreement is complicated by the number of possible routes of exposure, and the range of chemical agents to which men may have been exposed. Australian troops may have been directly exposed to both herbicides and insecticides that were aerially sprayed by US forces. They may also have been exposed to ground-based spraying of herbicides and insecticides by Australian forces around base camps, and, in a small number of cases, to aerial spraying by the RAAF during crop destruction operations conducted by Australian forces.4 It is also possible that there was indirect exposure of troops through spray drift, the contamination of water supplies, and the accumulation of chemicals in the food chain.2

A further complication is the existence of major differences between the various chemicals in their potential for long-term adverse effects. The pesticide that is most widely credited with responsibility for adverse effects on the health of veterans and their families is the herbicide Agent Orange. However, the chemicals to which Australian troops were most extensively exposed

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were insecticides such as DDT and malathion which were used to control the mosquito vector of malaria.2 The evidence that the latter have adverse health effects is much less compelling. Because a variety of chemicals was involved it is also difficult to evaluate individual claims of exposure. We may know that a n individual has been exposed to some chemicals but we d o not know whether his exposure was to chemicals which may have adverse effects or to one whose adverse effects are minimal.

It is difficult to be optimistic about the prospects of resolving the disagreement about the extent of exposure to herbicides in Vietnam. There are obvious problems with any records and especially so in the present case. First, the records are incomplete4 and their incompleteness leaves open the objection that the missing records are those that matter. Second, written records are an uncertain guide to what actually happened: they may comprise orders that have been ignored, misunderstood or varied because of wartime exigencies, as we know was the case with the observance of safety precaut ions during Australian ground-based spraying operations.* Third, the deception and lying which it has been claimed were a feature of the American conduct of the Vietnam wars,6,7 make for scepticismabout the trustworthiness of official documents about the war.

Whatever the case about the aggregate exposure of Australian troops to pesticides in Vietnam, it is clear that a n index of exposure for individuals is unlikely to be developed. Many epidemiologists would argue that without a measure of individual exposure one cannot evaluate the claims made by Vietnam veterans. However, the veterans and their supporters are demanding a n immediate answer to their claims. For the purposes of providing one, we will assume that some veterans were exposed t o pesticides (herbicides and insecticides) and evaluate the available evidence with two questions in mind: have there been any increases in the rate of birth abnormalities, psychiatric disorders, and premature mortality among Vietnam veterans? and how likely are any such increases to be caused by pesticide exposure in Vietnam?

Has there been any increase in the rates of adverse health outcomes among Vietnam veterans and their families?

The evidence presented to the Senate Standing Committee on Science and the

COMMUNITY HEALTH STUDIES

Environment (SSCSE) by the VVAA consists of reports of birth defects, psychiatric disorders, and cancer deaths among its members.2 This evidence suffers from a number of deficiencies. First, it establishes only that these adverse outcomes occur among Vietnam veterans. This would be persuasive if each of the outcomes was exceedingly rare in the general community but they are not. Available evidence suggests that birth defects occur in between 2 and 4 per cent of live birth^,^.^ that severe psychiatric disorders such as those reported among veterans occur in as many as 3 per cent of the comrnunity,l0,l1 and that cancer would have been the cause of death in at least 0.2 per cent of men in the age group of Vietnam veterans in the period since the end of the Vietnam war.2

Second, the sample of Vietnam veterans who are members of the VVAA is unlikely to be representative of Vietnam veterans. This assumption is required if inferences are to be made about the rate of occurrence of birth defects, psychiatric disorder and cancer among Vietnam veterans. Any tendency for the occurrence of birth defects, psychiatric disorders, and cancer deaths to influence a veteran’s decision to join the VVAA would artifically inflate the rates of these conditions observed among VVAA members. The degree of selective recruitment into the VVAA need not be substantial to produce the observed rates of adverse outcome reported among VVAA members. For example, if only 10 per cent of the membership of the VVAAjoined because of a birth defect among their children. the rate of birth defects reported among VVAA family members ( 1 1.8 per cent)* would arise even if the rate among Vietnam veterans was the same as that in the general community (approximately 2 per cent).

Third, the manner in which the occurrences of birth defects, psychiatric disorders, and cancer deaths have been counted will affect any estimates of the rates with which they occur among VVAA members. In the case of birth defects there is good reason to believe that the definition has been over- inclusive: in the data presented by the VVAA to the Senate Standing Committee on Science and the Environment many childhood illnesses and disorders were counted as if they were birth defects (for example, asthma, enuresis, behaviour problems).2

These deficiencies in the VVAAs evidence do not refute the VVAA’s claims but they d o indicate that alternative explanations are available for the apparent increases in the reported rates of adverse outcomes among VVAA members. Ideally, these explanations would be excluded by comparing the

HALL & MacPHEE 1 1 1

rates of adverse health outcomes among veterans who have been exposed with the rates among veterans who have not been exposed. In the absence of an agreed upon index of individual exposure, such a study is impossible. Under these circumstances, the competing explanations of the VVAA claims can only be indirectly excluded by epidemiological research in which: (a) large representative samples of Vietnam veterans and appropriately selected controls are (b) compared with respect to the rates of occurrence of the adverse health outcomes by (c) standardised methods of diagnosis in which (d) the decision about the presence or absence of each of these outcomes is made independently of any knowledge of whether or not the person under study is a Vietnam veteran.

Epidemiological Evidence Direct and indirect epidemiological evidence

suggests that birth defects, psychiatric disorders, and cancer deaths do nof occur at an increased rate among Vietnam veterans. The direct evidence consists of two studies commissioned by the Commonwealth Governrnentl2,13,14 and the Ranchhand studies of the United States Air Force.” Indirect evidence is provided by the results of studies of reproductive outcomes in men who were occupationally exposed to herbicides and of studies of the reproductive effects of exposure of populations to known mutagenic agents.

Birth Defects The Commonwealth Institute of Health

(CIH) Case-Control Study of Birth Abnormalities failed to find any evidence that Vietnam veterans were at any greater risk of fathering a child with a birth abnormality than were their age peers who did not serve in Vietnam.12 This finding is especially important because there was sufficient power (90 per cent) to detect an increase of 50 per cent or greater in the rate of birth defects had one occurred. Some 8,517 case-control pairs were studied. These covered birth abnormalities recorded’ in 34 hospitals and 4 cytogenetics laboratories in Australian cities in the period 1966 to 1979. Careful matching was undertaken to eliminate sources of bias and sophisticated statistical analyses were used to adjust for the effects of known risk factors on which cases and controls differed. The odds ratio for the risk of a Vietnam veteran and a non-veteran fathering a child with a birth defect was 1.02 which was not statistically distinguishable from 1.00. The


confidence interval about this estimate was narrow (0.78 to 1.32) and various statistical adjustments had no effect upon it.j2,13

The CIH case-control study has not escaped criticism. Several critics have pointed out that it only provides a powerful test of the hypothesis that there has been an increase in the rate of birth defects among Vietnam veterans if all veterans were exposed to pesticides.~h,~7 If only a minority of veterans had been exposed (for example, 30 per cent), a two-fold increase in the rate of birth defects among exposed Vietnam veterans would have gone undetected in the CIH study17 since the rate among the exposed group would be "diluted" by the rate in the unexposed group which would be the same as in the general community.

There are three points to be made about the implications of this criticism for the VVAA's claim about the effects of pesticide exposure on the rate of birth defects among their children. First, the CIH study still provides reasonable grounds for rejecting the VVAA's original claim: if all Vietnam veterans were exposed then the study provides reasonable evidence that there has not been any increase in the rate of birth abnormalities among their children. Second, the suggestion that a smaller group of veterans were exposed is a weaker claim that is correspondingly harder to test. Indeed, if the proportion of veterans who were exposed was only 5 per cent, it would be impossible to test the claim that'there has been an increase in the rate of birth abnormalities, even if all the children born to Australian Vietnam veterans were studied.18 Third, the criticism of the CIH study is only a damaging one if there are good reasons for expecting a relationship between herbicide exposure and an increase in birth defects. Critics of the CIH study have not provided any.

In the nature of the case it is difficult, some would argue impossible, to prove the null hypothesis as was attempted in the CIH study. Nonetheless, good reasons may be provided for acting as if the null hypothesis were true.I9 These are provided by an analysis of epidemiological evidence on the effects of herbicide exposure on reproductive outcomes, and of evidence on the biological plausibility of the VVAA's claim.

Epidemiological evidence on the reproductive effects of herbicides affords support to the null results of the case-control study. Although there is evidence that 2,4,5-T has a teratogenic effect in mice?l there is no generally accepted evidence that this herbicide is teratogenic in humans. The widely quoted Alsea-ll Study22 has been claimed to show that exposure of pregnant women to phenoxy

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herbicides increased the rate of miscarriage. Its findings, however, have been severely criticised on methodological grounds, the most serious being that miscarriages were underascertained in all study areas, including the sprayed areas, and that there were geographical and demographic differences between the study and control areas, any one of which could have explained the apparent differences in miscarriage rate.23 Even if there were evidence that exposure of women to the phenoxy herbicides produced teratogenic abnormalities, this would be of minimal relevance to the present case where the issue of interest is the effect of male exposure on subsequent reproductive performance.

Five studies directly address the issue of the effects of male exposure to herbicides on subsequent reproductive outcomes. These are the studies of Lanthrop, Wolfle et all5, Smith, Fisher, Pearce et aP4, Townsend, Bodner, Van Peenen et UP, Suskind and Hertzberg26 and Tung (vide Dwyer).Qv

The studies of Smith et al, Suskind and Hertzberg, and Townsend et al investigated the occurrence of birth anomalies and miscarriages among the wives of men who had been occupationally exposed to phenoxy herbicides. Smith et a1 studied 548 agricultural spray operators and 441 agricultural workers as nonexposed controls while Suskind and Hertzberg studied 344 Dow Chemical employees (189 exposed and 155 not exposed) and Townsend et al studied 370 Dow Chemical employees and 345 controls. In none of these studies was there any evidence of an increase in the rate of birth anomalies, miscarriages or still-births. Although none of these studies is convincing in itself, as a group they provide good reason for believing that no increase has occurred. The number of cases studied was not substantial but in the Smith et a1 and Townsend et a1 studies the number of cases provided a reasonable degree of confidence that a two-fold increase would have been detected had one occurred. All studies relied upon the report of the subjects on the Occurrence of the adverse reproductive outcomes but this is more likely to have produced a bias in favour of finding a n increase in rate. And in all three studies the rate of birth anomaly and miscarriage in exposed and unexposed groups were those observed in the general population.

The study by Lanthrop, Wolfle et a1 was performed as part of the Ranchhand Morbidity Study in which the health of 1174 men who flew the Ranchhand spraying missions was compared with

COMMUNITY HEA L TH STUDIES

the health of 1531 controls who flew cargo planes into and within Vietnam. Self-reported reproductive outcomes were one of the many endpoints on which the two groups were compared. There were no statistically significant differences between Ranchhanders and controls in fertility or on any measures of sperm numbers or percentage of abnormalities. There was an apparent difference in the rate of miscarriages, with the Ranchhanders having the higher rate( 15.0 per cent versus 12.5 per cent), but both values were within the normal range (10-20 per cent) and the r a t e of r e p o r t e d m i s c a r r i a g e s a m o n g Ranchhanders was also higher among pregnancies that occurred before service in Vietnam ( 13.7 per cent versus 11.9 per cent).

Reports of birth defects showed a more complicated picture. The rates of reported birth defects in both groups were above those usually reportedq9 and the rate was higher among the Ranchhanders (8.7 per cent versus 6.5 per cent). Although on first impression these results seem to offer support for the veterans' claims, closer examination reveals reasons for doubt. The definition of birth defects seemed to be more inclusive among Ranchhanders in that fewer could be coded in terms of ICD-9 categories. Ranchhanders were also more inclined to report birth defects on the skin; the type of defect that one would expect an understandably anxious and vigilant parent to report more often. Individual levels of exposure to herbicides were estimated from the Herbs tapes and other sources. The relationship between exposure level and rate of abnormalities was suggestive of a dose response relationship but the relationship was not consistent between occupational s t ra ta within the Ranchhanders (for example, the most highly exposed officer group had the lowest rate of abnormalities).l5

The most widely quoted evidence of a higher rate of birth anomalies among the children of men presumed to have been exposed to phenoxy herbicides comes from the study by Tung.27 He compared the reproductive performance of North Vietnamese soldiers who served in South Vietnam (and had presumably been exposed to herbicides) with that of men who had only served in North Vietnam. The rates of birth anomaly in these groups of men were 3.6 per cent and 0.0 per cent respectively. These findings are unconvincing. The rate of anomalies among the exposed groups is within the range observed in the general population (2 to 4 per cent)*,9 and the absen'ce of any anomalies in the control group is suspicious.

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The most likely explanation of these results is that case-finding was more thorough among the men who were presumed to have been exposed.

Psychiatric Disorders There are no controlled epidemiological

studies of psychiatric disorder among Australian Vietnam veterans. The most relevant study is the US Air Force Ranchhand study of morbidity among the men who flew the herbicide spraying missions.15 The dimensions of health of greatest relevance to the present discussion were measured by: self-ratings of psychiatric symptoms (such as depression, anxiety, aggression, et cetera), standardised tests of cognitive impairment, and tests of neurological status.

The comparison of the Ranchhanders and controls showed a consistent difference in psychiatric symptoms similar to that reported among Australian Vietnam veterans, namely, higher ratings of depression, fatigue, isolation, and anger. Several features of the results, however, argue against their being interpreted as evidence in favour of the symptoms being a consequence of herbicide exposure. First, the difference in symptom ratings was confined to the men with high school education. Second, severity of symptoms was unrelated to the exposure index. Third, there was evidence from validity scales on the standardised psychological tests that the Ranchhanders were differentially reporting symptoms. Fourth, there was no evidence of cognitive impairment as would be expected if the men were suffering from "toxic neurasthenia" as has been claimed by van Tiggelin.28 Nor was there any evidence of a greater prevalence of neurological signs among the Ranchhanders. The results suggest that the small excess of symptoms among Ranchhanders was due t o a combination of over-reporting (probably because of the publicity given to the adverse effects of exposure to the herbicides they sprayed) and to the difference in combat exposure between men who flew cargo aircraft well outside enemy range and the Ranchhanders who flew their aircraft a t stalling speed at treetop level over enemy held positions.29

Modest support for the Ranchhand study findings comes from the study by Suskind and Hertzberg26 of the health of 367 men, of whom 204 had been occupationally exposed to dioxin in the course of the manufacture of the herbicide 2,4,5-T. Exposure to dioxin contaminated herbicide was indicated by the occurrence of chloracne (a reliable sign of dioxin exposure) in 86 per cent of cases. A comparison of exposed and non-exposed men on a


variety of health outcomes revealed that some symptoms and signs other than chloracne were suggestively associated with exposure (for example, upper gastrointestinal tract ulcers). There was little evidence of an increased prevalence of depressive symptoms on a crude measure of psychiatric symptoms of nervousness, anxiety or depression. Nor was there any evidence of changes in the peripheral nervous system as measured by conduction velocity of the ulnar, peroneal and sural nerves.26

Mortality The Commonwealth Institute of Health

Retrospective Mortality Study14 has provided ,good evidence against there having been, to date, any large increase in the rates of causes of death commonly linked with herbicide exposure, namely, cancer and suicide. This study tested whether death rates among 19,205 National Servicemen who had served in Vietnam was higher than those among 25,677 National Servicemen who had not served in Vietnam. The successful tracing to follow up and determination of vital status was exceptionally thorough, covering 94 per cent of both groups. The overall mortality rate in both groups was below that for men in the same age group in the general population, a finding previously reported among the veterans of earlier wars. There was a small but statistically significant exass of deaths overall (OR = 1.29, CI: 1.1-1.5). There was no evidence of an increase in the rate of cancer deaths (OR = .99, CI: 0.6-1.6). The rates of deaths due to suicide (OR = 1.5, CI: 0.9-2.3) and motor vehicle accidents (OR = 1.2, CI: 0.9-1.5) were not statistically significant but the width of the confidence intervals in each case suggests that the possibility of an increase should not be ruled out. There were variations between the various corps in which men had served in overall mortality rate. For example, there was an excess of deaths among the corps of the Royal Australian Engineers (odds ratio 2.4, confidence interval 1.4- 4.0); the causes of death that were responsible for the excess were motor vehicle accidents, other accidents, suicide and self-inflicted injury.14

Like every epidemiological study that has ever been done, the CIH mortality study is not without its interpretive problems. There are the possibilities of selection bias and confounding of possible chemical exposure with other aspects of Vietnam service that may affect mortality in the post-war period. As with the CIH birth defects study, there is also the issue of the proportion of Vietnam veterans who were exposed to pesticides

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in Vietnam. There is also a constraint imposed on the conclusions by the length of the follow up period. The period of follow up ( I 1 years on average) is too short to exclude the possibility of a subsequent increase in cancer deaths as more veterans enter the latency period.14

Doubtless, these features of the mortality study will provide the occasion for considerable argument as to the meaning of , its findings. Nonetheless, the study’s findings do permit some conclusions to be drawn about mortality rates among Vietnam veterans. The study’s results afford no support to the more extravagant claims in the press that there has been an “epidemic” of suicide among Vietnam veterans. The Australian (April 19, 1982, p9), for example, reported a 180- fold excess of suicides among Vietnam veterans. Nor do the study findings support the claim that the rate of deaths from cancer has been excessive to date. They suggest that any increase in mortality, to date, has been a modest one which has been largely due to causes that are not linked directly to herbicide exposure.

’

Summary of Epidemiological Evidence The epidemiological evidence of most

relevance to the VVAA’s claims has largely beFn negative. Although it has been broadly consistent, negative epidemiological evidence is less convincing than positive evidence: absence of evidence of adverse effects of pesticide exposure is not sufficient evidence that pesticides do not cause adverse effects on hea1th.m Additional evidence is required that the investigations had the statistical power to detect the effects expected. The ability of the studies of Australian Vietnam veterans to satisfy this depends upon the proportion of Vietnam veterans who were exposed to pesticides. In so far as the original VVAA claim is concerned, this condition has been satisfied in the CIH case- control study of birth defects. Corroboration of its null findings is provided by the studies of reproductive outcomes in men who have been occupationally exposed to herbicides.

The persuasiveness of the negative epidemiological findings can be further strengthened if there are good reasons for believing that the pesticides do not cause the type of adverse health effect claimed by the VVAA. We believe that such reasons emerge from an examination of the evidence and argument bearing on the question of whether increases in birth defects, psychiatric disorders and cancers are likely to be a consequence of exposure to pesticides.


Should We Expect a n Increase in Adverse Health Outcomes among Vietnam Veterans?

Birrh Defects Biological knowledge of the mechanisms of

birth defects supplies additional arguments for doubting that male exposure to chemicals can produce an increase in birth defects among children born several years after exposure. Much of the apparent plausibilty of the VVAA’s claim about birth defects derives from confusion about the mechanisms which can produce birth defects. I t is implicitly assumed, for example, that if pesticide exposure during pregnancy can produce birth defects- (by means of teratogenesis), then male exposure can produce birth defects in the same way. This is extremely unlikely. Teratogenic birth defects occur because of foetal exposure to chemicals during the process of development in urero. Birth defects of teratogenic origin could occur as a consequence of male exposure only if an extremely implausible sequence of events occurred, namely, long term storage of the chemical in the male’s body, transport from storage sites to the semen, and then, via the ejaculate, to the foetus in urero, and a specific action whereby the chemical induced a n abnormality rather than a miscarriage. Such events would occur so rarely that this cannot be seriously entertained as a cause of birth defects among the 42,000 men who served in Vietnam.2,)’

The possibility that birth defects of mutational origin have occurred among the children of Vietnam veterans cannot be excluded a priori. Exposure of males to potent mutagens could conceivably produce mutations in the male germ cells and these in turn could be transmitted to the offspring.2 While this is possible there is a good reason for believing that it would be an improbable occurrence. First, there is little evidence that any of the most likely candidate mutagens (for example 2,4-D, 2,4,5-T and dioxin) a re in fact mutagens: only dioxin has shown any evidence of being a mutagen and then only in bacterial systems.2’

Second, n o increase has ever been demonstrated in the rate of birth defects of mutagenic origin in human populations which have been exposed to a known mutagen. For example, the populations of Hiroshima and Nagasaki were exposed to a documented mutagen but inherited mutat ions have not been demonstrated in this population despite assiduous efforts to discover their occurrence in ‘two generations of the offspring of the persons who

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were exposed to atomic radiation. These attempts to discover an increase in the rate of inherited mutations included epidemiological studies of spontaneous abortions and stillbirths due to lethal mutations, infantile deaths, congenital malformations, and changes in the sex ratios of surviving offspring. Researchers have also conducted studies of the rate of chromosomal anomalies and an electrophoretic study of protein abnormalities among 10,000 exposed and 10,000 nonexposed persons which failed to find any evidence of an increase in the rate of inherited mutations.32 These results d o not exclude the possibility that mutations have been induced in the germ cells of exposed parents.33 They do, however, show that the rate of induction of mutations is such as to be undetected among 78,000 children of exposed parents in the bombed cities. Aforriori, a similar increase in mutations is unlikely to be detected in the smaller cohort of children born to the 42,000 men who served in Vietnam, and especially not if only a minority of Australian troops were exposed to pesticides.

Psychiatric Disorders The scientific study of psychiatric disorders

caused by chemical exposure is at a rudimentary stage of development. Evidence that the pesticides used in Vietnam can produce symptoms of depression, anxiety, and aggression is confined to poorly controlled studies of psychiatric disorder occurring among selected samples of men who have been accidentally exposed in industrial accidents or occupationally exposed over long periods during the manufacture of the herbicides.20,34,35

In the absence of direct epidemiological evidence, the claim made by van Tiggelinzs that the veterans’ psychiatric disorders are a consequence of their exposure to herbicide rests upon an implicit argument from analogy: occupational exposure to other chemicals can produce symptoms that are similar to those reported by veterans; therefore, the possibility cannot be excluded that the veterans’ psychiatric disorders are also due to chemical exposure.

The analogy is superficially attractive but closer examination reveals that it is a poor one as we have argued in detail elsewhere.29 Briefly, the reasons are as follows. First, the veterans’ symptoms are nonspecific: they occur after such a variety of different events, including industrial accidents in which no chemicals are involved,36.37 that no inference can be made as to their cause. Second, such evidence as exists suggests that these


symptoms are not a common consequence of exp0sure,2~ as is required to establish that there is a high probability that the veterans’ disorders are due to chemical exposure. Third, the analogy also involves a confusion between the immediate and delayed effects of exposure and it ignores diss imilar i t ies between t h e p a t t e r n s of occupational exposure that produce psychiatric disorders and the type of exposure claimed for Vietnam veterans.29

The strongest doubts about the plausibility of van Tiggelin’s analogy derive from the striking similarity between the symptoms of which the Vietnam veterans complain and those reported among the substantial numbers of psychiatric casualties who have occurred among the veterans of all modern wars. Psychiatrists who have dealt with the psychiatric consequences of war service in the veterans of the first and second world wars38-41 have reported the same pattern of symptoms (depression, anxiety, explosive rages, fatigue) and the phenomenon of delay in 0nset.2~ The VVAA’s reluctance to consider the possibility of a “war neurosis” probably derives from the false assumption that only psychiatric disorders that are caused by chemicals are “real” (for example, McCulloch)42; a not unnatural assumption in view of the expression of a similar view by a former senior administrtor in the Department of Veterans’ Affairs.43

Premature Deaths Recent epidemiological studies of men who

have been occupationally exposed to the phenoxy herbicides have suggested that these men have a n increased risk of developing soft tissue sarcomas.44 The relevance of these findings to Vietnam veterans is uncertain: these cancers are rare, the relative risk associated with exposure is small, and they are not the sort of cancers so far reported among Vietnam veterans. Because of the long latency period between exposure and the occurrence of cancer, the future occurrence of such cancers cannot be ruled out. In considering cancer deaths, attention should not be confined to cancers caused by exposures to pesticides; information suggests that there may be more to fear in the way of an increase in deaths due to alcohol and tobacco-related diseases since both substances were heavily used in Vietnam in part because of government subsidizing of prices.14 Nor should concern about premature mortality among Vietnam veterans be confined to chemically- related causes. There may be more cause for concern in increased rates of deaths due to

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behaviourally linked causes, such as suicide and accidents, which may be consequences of an increased rate of psychiatric disorders among war veterans.

Conclusions on the Claims at Issue We believe that the VVAA’s claims about the

effects of herbicides on the health of Vietnam veterans and their families can be rejected with varying degrees of confidence. The claim about an increase in birth defects can be most confidently rejected (1) because of the failure of a variety of epidemiological studies to discover any evidence of an increase in birth defects among the children of exposed men and (2) because there are good biological reasons for doubting that such an effect could occur as a result of male exposure. Our confidence in the reasons for rejecting the claim about psychiatric disorders is not as strong because it is possible for chemical exposure to produce psychiatric symptoms like those reported among Vietnam veterans. We nonetheless regard it as improbable because of the dissimilarities between toxic neurasthenia and the veterans’ disorders and because of the existence of a far more plausible explanation, namely, “war neurosis”.The claim about a n increased mortality rate is more open because of the relatively short length of the period of observation. But it is still possible to say that there is no available evidence which would support the assertion that there has been an “epidemic” of cancers and suicides among Vietnam veterans to date.

Why has the Controversy Resisted Resolution? Tbe controversy about the adberse effects of

alleged herbicide exposure on Vietnam veterans has proved peculiarly resistant to resolution. Seven years after the claims were first made they continue to be advanced and defended despite a number of scientific studies which have failed to substantiate them.l-’,14,15 We believe that an explanation for its persistence can be found in several features of the controversy.

First, the onus of proof has fallen not upon those who have made the claim about the adverse effects of chemical exposure in Vietnam but upon those who reject it. The reasons for this are not entirely clear but we suspect that the onus of proof which properly operates under Repatriation legislation has been carried over into the broader public and scientific arena. Under Repatriation legislation returned servicemen have historically been given the advantage when making claims for disease and disability connected with war service,


so that the responsibility for disproving the claim rests with the Department of Veterans' Affairs. This provision exists because returned soldiers have no recourse to usual legal remedies for harm caused by their war service since the Government enjoys immunity from litigation for damages suffered by soldiers in war-time.* We have no quarrel with such a provision but we think it is inappropriate to confuse the onus of proof provisions operating under special purpose legislation with the usual standard that operates in the community, namely, that he or she who makes a claim has to substantiate it.

The press coverage of the controversy has reinforced the reversal of the onus of proof. The reason for this is obvious: sensational claims sell newspapers; detailed rebuttals do not. Thus, unsubstantiated assertions about an "epidemic" of birth defects, psychiatric disorders and cancers among Vietnam veterans, which have been repeated often enough and which seem to have gone unanswered, have become accepted as "facts". In the face of the public perception of the controversy created 'by such press coverage, attempted rebuttals of the VVAA's claims have been unsuccessful. Part of the reason for this has been the absence of manifestly independent comment from scientists. Most of the running has been made by government employees whose rebuttals of the claims have been construed as part of a "cover-up" of "white-wash".

Second, the choice of epidemiological research as a strategy for resolving the controversy has entailed certain. disadvantages. The case- control study and the historical cohort study have

a number of features that reduces their c o n t r i b u t i o n t o a r e s o l u t i o n of t h e controversy: they take considerable time to design, enact, and produce findings; their findings are difficult to communicate in simple English; their interpretation is open to argument; and the researchers who conduct these studies are in the unhappy position of attempting to "prove a negative" which is a great deal more difficult to do than it is to establish a positive claim.'"

Third, the Agent Orange controversy shares a feature that is found at the centre of many controversies: a confusion of ethical and technical issues.45 In the Agent Orange controversy. the confusion is between the Vietnam veterans' right to fair treatment and the issue of what caused their suffering. Belatedly the public has acknowledged that Vietnam veterans have suffered an injustice because they were asked to fight an-unpopular war and their service was rewarded with contempt and ostracism. An appreciation of this injustice has become equated with accepting that there is a chemical cause for the veterans' suffering. While understandable, this confuses two separate issues and the failure to separate them may have unfortunate consequences for the Vietnam veterans and their families. The Vietnam veterans' case for fair treatment should not have to depend upon their demonstrating that they were poisoned by chemicals in Vietnam. The danger is that if it is made to depend upon such a demonstration, the eventual failure to sustain the veterans' claims about pesticides may lead to the unjustifiable rejection of their claim to be fairly treated.

References

Dux J, Young PJ. Agent Orange: The 5 . Bitter Harvest. Lane Cove: Hodder and Stoughton, 1980. 6. Senate Standing Committee on Science and the Environment. Pesticides and the Health 7. of Australian Vietnam Veterans. Canberra: Australian Government Publishing Service, 8. 1982. Senate Standing Committee on Science and the Environment. Reference: Pesticides and Vietnam. Veterans. Canberra: Austra- 9. lian Government Publishing Service. 1983. Report on the use of herbicides. insecticides

Hersh S. Kissinger: The Price of Power. Boston: Faber and Faber, 1983. Maclear M. Vietnam: The Ten Thousand Da.v War. London: Metheun, 1981. Shawcross W. Sideshow. L o n d o n : Fontana, 1980. Drew J H , Parkinson P, Walstrab J E et al. Incidences and types of malformations in newborn infants. Med J Ausr 1977; 1: 945- 949. Seward J F , Stanley F. Congenital mal format ions regis ter in Western Australia. Med J Aust 1981: I : 218-224.

and other chemicals by the Australian Army in South Vietnam. Presented to Parliament

pp5 1-52.

10. Andrews G, Tennant C, Brodarty H. The need for psychiatric care. Med f Aust 1981; I : 593-594.

I I . Goldberg D, Huxley P. Mental Illness and by Mr 1. Sinclair, December 1982, Book 111,

HALL & MacPHEE 1 I7 COMMUNITY HEALTH STUDIES

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

the Community: The Pathways to Psychiatric Care. London: Tavistock, 1980. Donovan JW, Adena MA, Rose G, et 01. Case-Control S tudy of Congeni tal Anomalies and Vietnam Service (Birth Defects Study). Canberra: Australian Government Publishing Service, 1983. Donovan JW, McLennan R, Adena M. Vietnam service and the risk of congenital anomalies: A case control study. Med J Aust 1984; 394-397. Fett MJ, Dunn M, Adena MA er al. The Mortality Srudr, Pair I: A Rerrospecrive Cohort Stud). of Mortalir). Among Australian Narional Servicenieti of the Vietnam Conflicr Era. Canberra: Australian Government Publishing Service. 1984. Lanthrop GD. Wolfle W H, Albanese RA er al. An epidemiological investigation of health effects in Air Force Personnel following exposure to herbicides. Air Force Morbidit). Stud? Results. USAF School of Aerospace Medicine, Aerospace Medicine Division (AFSC), 24 February, 1984. Somers RL. Vietnam service and congenital anomalies. Med J Aust 1984; 140, 688. Reznik R, Gold J and Mandrick J . Vietnam service and congenital anomalies. Med J

Simple calculations show that if only 5 per cent of Vietnam veterans were exposed to pesticides, a cohort study with in excess of 500,000 men in each of the “exposed” and “unexposed” groups would be required to detect a two-fold increase in the rate of birth defects among the chemically exposed Vietnam veterans. Cook T D and Campbell DT. Quasi- Experimentation: Design and Analysis Issues for Field Settings. Chicago: Rand McNally, 1979. J R B Associates. Review of Literature on Herbicides, Including Phenoxy Herbicides and Associated Dioxins, Two Volumes. A report prepared for the U.S. Veterans’ Administration, Washington, DC: 1981. Young AL, Calcagni JA, Thalken CE et al. m e Toxicology, Environmental Fate and Human Risk of Herbicide Orange and its Associated Dioxin. United States Air Force, O f f i c e o f E n v i r o n m e n t a l H e a l t h Laboratory, Technical Report 78-92, 1978. Environmental Protection Agency. Alsea I1 Study: Report of assessment of a field

Aust 1984; 140 194-195.

investigation of .six-year spontaneous abortion rates in three Oregon areas in relation to 2.4.5- T spra.ving practices. February 28, 1979.

23. Wagner SL, Witt JM, Norris LA et al. A Scientijic Critique of the EPA Alsea I1 Study and Report. Environmental Health Science Center, Oregon State University, Corbalis, October 25, 1979.

24. Smith AH, Fisher DO, Pearce N et 01. Congenital defects and miscarriages among New Zealand 2,4,5-T sprayers. Arch Environ Health 1982; 37: 197-200.

25. Townsend JC, Bodner KM, van Peenen P F D et al. Survey of reproductive events of wives of employees exposed to chlorinated dioxins. Am J Epidemioll982; I 15: 695-713.

26. Suskind RR, Hertzberg VS. Human health effects of 2,4,5-T and its toxic contaminant.

27. Tung, TT vide Dwyer JH. Summary of Proceedings of a Conference on Herbicide Exposure and Reproductive Epidemiology in Vietnam. Held April 10 1982 at Department of Medical Genetics, Mt Sinai School of Medicine.

28. Van Tiggelin C. Submission to Senate Standing Committee on Science and the Environment. Reference Pesticides Inquiry Volume 2, 874-924. Canberra: The Senate, 1983.

29. Hall W, MacPhee D. Do Vietnam veterans suffer from “toxic neurasthenia”? Ausr NZ J Psychiatry 1985, 19: 19-29.

30. Hall P, Sellinger B. Submission to Senate Standing Committee on Science and The Environment, 198 1. Reference: Pesticides Inquiry, Volume I . Canberra: The Senate, 1983.

31. Pearn JH. Teratogens and the male: An analysis with special reference to herbicide exposure. Med J Aust 1983; 2: 16-20.

32. Committee for the Compilation of Materials on Damage Caused by the Atomic Bombs in Hiroshima and Nagasaki. Hiroshima and Nagasaki: The Physical, Medical and Social Ef fects of the A t o m i c Bombings. (Translated by El lshoikawa and DL Swain) New York: Basic Books, 1981.

33. Upton AC. The biological effects of low- level ionizing radiation. Sci.Am 1982; 246:

34. Bashirov AA (1969) English language abstract in J R B Associates, Review 01 Literature on Herbicides. Including

J A M A 1984; 25 1: 2372-2380.

29-37.

HALL & MacPHEE 1 I8 COMMUNITY HEALTH STUDIES

Phenoxy Herbicides and Associated Dioxins. Volume 2, pp 92-95. A report p r e p a r e d f o r t h e US V e t e r a n s Administration, Washington, DC, 1981.

35. Bauer H et a1 (1961) English language abstract in J R B Associates, Review qf Literature o n Herbicides, Including Phenoxy Herbicides and Associated Dioxins, Volume 2, 19 - 20, A report p r e p a r e d f o r t h e U S V e t e r a n s Administration, Washington, DC, 1981.

36. Merskey H. The Analysis of Hysteria. London: Balliere-Tindall, 1978.

37. Miller H. Accident neurosis. Br MedJ 1961;

38. Archibald HC, Long DM, Miller C er a/. Gross stress reaction in combat - a 15 year follow up. A m J Psychiatry 1962; 119: 317- 322.

39. Archibald HC, Tuddenham RD. Persistent stress reaction after combat: A 20-year follow up. Arch Gen Psychiarry 1965; 12, 475-48 I .

I : 919-925.

HALL & MacPHEE 1 I9

40. Butler AG. The Australian Army Medical Services in the War of 19/4-1918. Volume 111. Canberra: Australian War Memorial, 1943.

41. Kardiner A. Traumatic neuroses of war. In: Arieti S. (Ed.) American Handbook of Psychiatry 1st Edition. New York: Basic Books, 1959.

42. McCulloch J. The unlucky veterans. Australian Socierv 1 February, 1984; 16-1 7.

43. Rose S. Submission to Senate Standing C o m m i t t e e o n S c i e n c e a n d t h e Environment, 1982. Reference: Pesticides Inquiry Canberra: The Senate, 1983.

44. Hardell L, Ericksson M. Lenner P, er al. Malignant lymphoma and exposure to chemicals, especially organic solvents, chlorphenols and phenoxy acids: A case- control study. BrJCancer 1981;43: 169-176.

45. Nelkin D. Controversy: Politics of Technical Decisions. Beverley Hills: Sage Publications. 1979.


THE AGENT ORANGE CONTROVERSY IN AUSTRALIA: A CONTRIBUTION TO THE DEBATE

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