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Use and effects of chemical agents on Australian personnel in Vietnam - Royal Commission (Hon. Mr Justice P. Evatt) - Final report, dated 31 July 1985 - Report - Volume 5 - Mental well-being


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The Parliament of the Commonwealth of Australia

ROYAL COMMISSION ON THE USE AND EFFECTS OF CHEMICAL AGENTS ON

AUSTRALIAN PERSONNEL IN VIETNAM

Commissioner: The Hon. Mr Justice P. Evatt, DSC, LLB

Final Report—July 1985

Volume 5: Mental Well-being

Presented 22 August 1985 Ordered to be printed 19 September 1985

Parliamentary Paper No. 292/1985

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m m m tea *

ROYAL COMMISSION ON THE USE AND EFFECTS OF CHEMICAL AGENTS ON AUSTRALIAN PERSONNEL IN VIETNAM

Commissioner: The Hon. Mr Justice Phillip Evatt DSC, LLB.

A Judge of the Federal Court of Australia

FINAL REPORT

July 1985

VOLUME 5

Australian Government Publishing Service Canberra 1985

© Commonwealth of Australia 1985

ISBN 0 644 04339 3 Set of Volumes ISBN 0 644 04344 X Report Volume Five

Printed by Canberra Publishing and Printing Co., Fyshwick, A.C.T.

ROYAL COMMISSION ON THE USE AND EFFECTS OF CHEMICAL AGENTS ON AUSTRALIAN PERSONNEL IN VIETNAM -1). A U S T R A L I A ,Α.

Commissioner: The Hon. Mr Justice Phillip Evatt DSC

Secretary: Mr B.D. Meade

31 July 1985

G.P.O. Box 4842 Sydney, N.S.W. 2001 Telephone: (02) 239 6222

Your Excellency,

In accordance with Letters Patent issued to me on 13 May 1983, 27 June 1984, 3 August 1984 and 23 April 1985, I have the honour to present to you the Final Report of my inquiry.

I believe that the Report complies with those Letters Patent and that my task is therefore completed.

Yours sincerely

JUSTICE PHILLIP EVATT Royal Commissioner

His Excellency the Right Honourable Sir Ninian Stephen, A.K., G.C.M.G., G.C.V.O., K.B.E. Governor-General and Commander-in-chief Government House CANBERRA A.C.T. 2600

File Ref.:

TABLE OF CONTENTS

VOLUME 5

CHAPTER IX

THE MENTAL HEALTH AND WELL-BEING OF AUSTRALIAN PERSONNEL AND OF THEIR SPOUSES

GLOSSARY 1. INTRODUCTION 1

2. WAR TIME STRESS 2

2.1 World War II 3

2.2 Korean War 4

3. PATTERN OF NEUROPSYCHIATRIC DISORDER WORLD WAR II, KOREA VIS-A-VIS VIETNAM 5

4. HOW "UNIQUE1 WAS THE VIETNAM WAR? 6

4.1 Homecoming 11

4.2 Arthur S. Blank, Jnr M.D. 12

4.2.1 Stresses Typical of all Wars 12

4.2.2 Unusual Stresses Found in the Vietnam War 13

4.2.3 Psychological Stresses Secondary to The General Political Character of the War 13

4.2.4 Atrocity 13

4.2.5 Additional Emotional Trauma 14

4.2.6 Stresses of the Immediate Homcoming Period 14

4.2.7 Long Term Effects Exacerbating the Effects of War Stress 14

4.2.8 Major Delayed and Chronic Stress Symptoms Seen in Vietnam Veterans 14 5. THE NATURE OF READJUSTMENT 17

5.1 American Studies 20

5.1.1 President's Commission on Mental Health; Mental Health Problems of Vietnam Era Veterans 20

5.1.1(a) Psychiatric Disorders: The Paradox of Vietnam 21

5.1.1(b) Clinical Symptoms of War Stress 22 5.1.1(c) Delayed Combat Reaction 22

5.2 Drug Abuse & Alcoholism (American Studies) 24 5.3 Stigmatisation 25

5.4 Failure of Social Integration 26

5.5 Family Breakdown 27

6. DEFINITIONS: THE CLASSIFICATION OF MENTAL ILLNESS 27 6.1 International Classification of Diseases 27 6.2 American Psychiatric Association Diagnostic and Statistical Manual 29

6.2.1 Diagnostic and Statistical Manual (DSM) 29

6.2.2 Promulgation of DSM I, II, and III 30

v

6 .3 Post Traumatic Stress Disorder (PTSD) 32

6.3.1 Diagnostic Criteria for PTSD 35

6.4 Conclusion 38

7. AUSTRALIAN ARMY TESTING OF PSYCHOLOGICAL FITNESS 38 7.1 On Recruitment 39

7.2 In Vietnam 40

7.3 On Discharge 40

7.4 Conclusion 42

8. THE PSYCHOLOGICAL EVIDENCE 8.1 Submissions Relevant to this Chapter 42

8.1.1 The Returned Services League of Australia 43

8.1.2 Royal Australian and New Zealand College of Psychiatrists 44

8.1.3 W AA 's Case - Alleged Neurotoxicity of Chemical Agents 45

8.1.3.1 As Revealed from Issues of "Debrief" The National Journal of W A A 45

8.1.3.2 From W A A ' s Submission to the Commission (i) Initial Submission 52

2.4- D 54

2.4.5- T 60

TCDD 60

Cacodylic Acid 60

Malathion 64

Paraquat 65

Chlordane 65

Dieldrin 66

Lindane 69

(ii)Toxicology Submission 69

2.4- D 70

2.4.5- T and TCDD 76

Cacodylic Acid 81

DDT 8 8

Dieldrin 91

Malathion 92

Chlordane 94

Dapsone 94

Picloram 95

Lindane 95

9. EVIDENCE IN SUPPORT OF W AA' S NEUROTOXICITY ALLEGATIONS 9.1 Dr van Tiggelen 96

9.1.1 "Organic Neurasthenic Depressive Syndrome 96

9.1.2 Rejection of Dr Van Tiggelen's Views - Reasons 100

9.2 Dr John Poliak 109

9.3 Dr Shearer 112

9.3.1 2,4-D 112

9.3.2 Cacodylic Acid 113

9.3.3 Malathion and Diazinon 115

9.3.4 Lindane 119

vi

9.3.5 Dieldrin 120

9.3.6 N-Hexane 121

9.4 Dr Silbergeld 122

9.4.1 TCDD-2.4.5-T 123

9.4.2 2,4-D 134

9.4.3 DDT, Dieldrin. Lindane and Chlordane 136

9.4.4 Malathion 140

10. THE CASE PRESENTED BY ROSS LONNIE 141

10.1 Dr Peter Orris 141

11. THE FINAL SUBMISSION OF W A A 144

12. WAA'S CASE ANSWERED 14 5

12.1 Dr Ellard 145

12.2 Dr Spragg 146

12.3 Displacement - Dr Blackburn and Dr Ellard 147

12.4 Drs Hall and MacPhee 147

12.5 Professor J.G. Andrews 149

12.6 Rejection of a Neurotoxic or Neurasthenia Cause 149

13. DOES THE VIETNAM VETERANS' SYNDROME EXIST 150 13.1 Conclusion 163

14. LITERATURE 14.1 Australian Literature 163

14.2 British/European Literature 165

14.3 American/Canadian Literature 166

15. DR MICHAEL MAXWELL BARR 168

16. MENTAL AND PHYSICAL HEALTH AND WELL-BEING OF THE SPOUSES OF VIETNAM VETERANS 175

17. PSYCHIATRIC AND PSYCHOLOGICAL TREATMENT OF VIETNAM VETERANS 180

17.1 Repatriation General Hospital (RGH/s) 180

17.2 Vietnam Veterans Counselling Service (WCS) 186

17.3 The Treatment of Vietnam Combat Veterans The Combat Veteran as Survivor 189 17.3.1 Philosphy 190

17.3.2 Family Therapy Implications 191 17.3.3 Treatment Issues 192

17.3.4 "Flooding" as a Therapeutic Technique 193

18. EVIDENCE OF TREATMENT OF PSTSD 195

18.1 Review of Treatment Literature by Professor Andrews 195

18.2 Other Sources of Such Evidence 196

18.3 RANZCP Submission 197

19. CONCLUSIONS 199

vii

19.1 Initial Testing 200

19.2 Psychiatry in Vietnam 200

19.3 Psychological Debriefing 202

19.4 Post Traumatic Stress Disorder and its Applicability to Vietnam Veterans 204

19.5 The Results of Combat 205

19.6 The Counselling Service 205

20. RECOMMENDATIONS 208

ENDNOTES 213

viii

TABLE OF CONTENTS - REPORT

VOLUME 1 - INTRODUCTION and EXPOSURE

Prologue

I Introduction II Standard of Proof III Ascertainment of Claims IV Exposure

VOLUME 2 - TOXICOLOGY and GENERAL HEALTH

V Toxicology and Safe Doses VI Health Effects General

VOLUME 3 - BIRTH ANOMALIES

VII Health Effects, Reproductive Outcomes and Birth Anomalies

VOLUME 4 - CANCER

VIII Health Effects, Cancer

VOLUME 5 - MENTAL WELL-BEING

IX Health Effects, Mental

VOLUME 6 - MORTALITY CLASS ACTION W A A and SECTION 47

X Mortality XI Class Action XII Status of W A A XIII Interim Report and S .47

VOLUME 7 - BENEFITS and TREATMENT

XIV Benefits and Treatment

VOLUME 8 - CONCLUSIONS. RECOMMENDATIONS and EPILOGUE

XV Conclusions and Recommendations Epilogue

VOLUME 9 - EXHIBIT LISTS AND BIBLIOGRAPHY

ix

APPENDIX III

Abreaction

Actualization

Acute

Acute Exposure

Acute Effects

Acute Situational Stress Reaction

Ad iustment

Aetiology

GLOSSARY

A process by which repressed

material, particularly a painful experience or a conflict, is

brought back to consciousness. In the process of abreacting, the person not only recalls but

relives the repressed material, which is accompanied by the

appropriate affective response.

Process of mobilizing one's

potentialities or making them concrete.

A term usually associated with the short term, often used to

indicate something which is

sudden and/or severe.

Usually means that exposure is brief although it may occur on more than one occasion over a

relatively short period of time.

Are those which occur a very

short time after exposure to a harmful agent and their severity usually shows an obvious

relationship to the dose.

or A severe emotional reaction resulting from extreme

environmental stress. such as death, disaster, or similar life threatening situations.

A person's relation to his

society and of his inner self.

The study of the causes of a

disease.

x

Affective Psychosis

Aggression

Alienation

Alpha-Blocker

Amphetamine

Antianxiety Drug

Antidepressant Drug

A psychosis in which disturbance of mood is a primary

characteristic; disturbances in thinking and behaviour are the secondary characteristics.

Forceful, goal-directed behaviour that may be verbal or physical. It is the motor counterpart of the affects of rage, anger, and

hostility.

A psychiatric term used variously to describe a person's feelings of detachment from his self or

society, to denote one's avoidance of emotional experiences, or to describe a person's efforts to

estrange himself from his own

feelings. ,

A drug used in pharmacotherapy, eg. clonidine. When used in PTSD treatment prevents muscle

constriction aroused by unpleasant combat memories.

A central mervous system

stimulant. Its chemical structure and action are closely related to ephedrine and other

sympathomimetic amines.

Drug used to reduce pathological anxiety and its related symptoms without influencing cognitive or perceptual disturbance. It is also known as a minor tranquilizer and an anxiolytic drug.

Meprobamate derivatives and

diazepoxides are typical

antianxiety drugs.

Drug used in the treatment of

pathological depression. It is also known as a thymoleptic drug and a psychic energizer. The two main classes of antidepressant drugs are the tricyclic drugs and

the monoamine oxidase inhibitors.

xi

Antimanic Drug

Antipsychotic Drug

Anxiety

Anxiety Neurosis

Apa thy

Aphasia

Drug, such as Lithium, used to

alleviate the symptoms of mania. Lithium is particularly effective in preventing relapses in

manic-depressive illness. Other drugs with antimanic effects are haloperidol and chlorpromazine.

Drug used to treat psychosis,

particularly schizophrenia. It is also known as a major tranquilizer and a neuroleptic drug.

Phenothiazine derivatives,

thioxanthene derivatives, and butyrophenone derivatives are typical antipsychotic drugs.

Unpleasurable affect consisting of psychophysiological changes in response to an intrapsychic

conflict. In contrast to fear, the danger or threat in anxiety is unreal. Physiological changes consist of an uncomfortable

feeling of impending danger,

accompanied by overwhelming

awareness of being powerless, inability to perceive the

unreality of the threat, prolonged feeling of tension, and exhaustive readiness for the expected danger.

A neurosis characterized by panic and anxious overconcern.

Want of feeling or affect; lack of interest and emotional involvement in one's surroundings. It is

observed in certain types of

schizophrenia and depression.

Disturbance in speech due to

organic brain disorder. It is

characterized by an inability to express thoughts verbally. There are several types of aphasia:

(l)motor aphasia: inability to speak, although understanding remains; (2)sensory aphasia: inability to comprehend the

xii

meaning of words or the use of

objects; (3)nominal aphasia: difficulty in finding the right name for an object; (4)syntactical aphasia: inability to arrange words in proper sequence.

Aphonia Loss or absence of voice

Autonomic Relating to the autonomic

(cerebrospinal) nervous sytem.

Autonomic Nervous System

Behavioural. Psychotherapy

Beta-blockers

The part of the nervous sytem that functions outside of

consciousness and that directs such functions as breathing, heart rate, and digestion.

A type of therapy that focuses on overt and objectively observable behaviour, rather than on thoughts and feelings. It aims at

symptomatic improvement and the elimination of suffering and

maladaptive habits. Various conditioning and

anxiety-eliminating techniques derived from learning theory are combined with didactic discussions and techniques adapted from other systems of treatment.

A drug in pharmacotherapy, eg. propranolol. When used in PTSD treatment prevents muscle

relaxation and slows heart beat induced as a peripheral effect of recall of combat.

Borderline State A state in which the symptoms are (Borderline Psychosis) so unclear or transient that it is difficult to classify the patient as psychotic or nonpsychotic.

Brief Psychotherapy A form of psychotherapy in which the sessions are limited to 10 to 15 in number and during which time attempts to modify behaviour

occur. This approach is used in both individual and group settings.

xiii

Catharsis Release of ideas, thoughts, and

repressed materials from the

unconscious, accompanied by an affective emotional response and release of tension. Commonly

observed in the course of

treatment, both individual and group, it can also occur outside therapy.

Central Nervous The spinal cord and brain. System (CNS)

Character Disorder A pattern of personality

characterized by maladaptive, inflexible behaviour.

Chlorpromazine

Choreiform Movements

Chronic

Chronic Exposure

Chronic Effects

A phenothiazine derivative used primarily as an antipsychotic agent and in the treatment of

nausea and vomiting. The drug was synthesized in 1950 and was used in psychiatry for the first time in 1952. At present,

chlorpromazine is one of the most widely used drugs in medical

practice.

Involuntary unco-ordinated

movements, usually transient.

A term usually associated with events which take place over a

relatively long period of time.

Usually means that exposure takes place over a considerable period of time and usually carries the implication that the concentration of any potentially harmful

chemical involved is quite low. This may not always be the case.

Are often defined as those effects which tend to persist over a long period without any obvious crisis occurring. Often, of course,

chronic exposure to a particular agent may be accompanied by

chronic effects, especially where exposure is to a relatively low level of a particular agent.

x i v

Cognition Mental process of knowing and

becoming aware. One of the ego

functions. it is closely

associated with judgment. Groups that study their own processes and dynamics use more cognition than do encounter groups, which

emphasize emotions. Also known as thinking. See cognitive

Cognitive Cognitive or personality changes

following organic brain damage are chronic, mild states of memory disturbance and intellectual deterioration. often accompanied by increased irritability,

querulousness„ lassitude and complaints of physical weakness.

Cognitive Psychology See psychology.

Combat Fatigue A strong physical and mental

reaction to the stresses of

military battle.

Compensation Conscious or, usually, unconscious defence mechanism by which a

person tries to make up for an

imagined or real deficiency, physical or psychological, or both.

Crisis Intervention A brief therapeutic approach used in emergency rooms of general or psychiatric hospitals that is ameliorative, rather than

curative, or acute psychiatric emergencies. Often, treatment factors focus on environmental modification, although

interpersonal and intrapsychic factors are also considered. Individual, group, family, or drug therapy is used within a

time-limited structure of several days to several weeks.

XV

Decompensation

Depression

De sensitization

Diagnostic and Statistical Manual of Mental Disorders

Dissociation

In medical science, the failure of normal functioning of an organ, as in cardiac decompensation; in psychiatry, the breakdown of the psychological defence mechanisms that maintain the person's optimal psychic functioning.

In psychiatry, a morbid state

characterized by mood alterations, such as sadness and loneliness; by low self-esteem associated with self-reproach; by psychomotor retardation and at times

agitation; by withdrawal from interpersonal contact and at times a desire to die; and by such

vegetative symptoms as insomnia and anorexia.

The act of removing an emotional complex. See also systematic

desensitization.

A handbook for the classification of mental illnesses. Formulated by the American Psychiatric

Association, it was first issued in 1952 (DSM-I). The second

edition (DSM-II), issued in 1968, correlates closely with the World Health Organization's

International Classification of Diseases. The third edition

(DSM-III) issued in 1980,

introduced the concept of Post Traumatic Stress Disorder (PTSD).

An unconscious defense mechanism by which an idea is separated from its accompanying affect, as seen in hysterical dissociative states; an unconscious process by which a group of mental processes is split off from the rest of a person's

thinking, resulting in an

independent functioning of this group of processes and thus a loss of the usual interrelationships.

xvi

DSM See Diagnostic and Statistical

Manual of Mental Disorders.

DSM III Diagnostic and Statistical Manual„

Edition III. American Psychiatric Association, 1980.

Dyad A pair of persons in an

interactional situation, such as husband and wife, mother and

father, co-therapists, or patient and therapist

Dysfunction Difficult or abnormal function.

ECT (Electroconvulsive Therapy)

A treatment, usually for depression, that uses electric currents to induce unconsciousness and convulsive seizures.

EEG (electroencephalogram) A recording of the electrical impulses emanating from the brain.

Ego-dystonic Repugnant to or at variance with

the ego. A symptom or personality train that is recognized by the individual as unacceptable and undesirable and is experienced as

alien.

Emotional Lability A propensity for emotions to be easily evoked and to quickly

subside; emotional changeability.

Epidemiology In psychiatry, the study of the

prevalence and distribution of mental disorders within a

particular population.

Endogenous Originating or produced within the

organism or one of its parts.

Endogenous Depression A severe psychiatric illness, with specific symptomatology of weight loss, early morning waking, loss of contact with reality,

difficulty with concentration.

Exogenous Originating or produced outside of

the organism.

xvii

Flooding A type of behaviour therapy in

which the patient, at the

beginning of therapy as the

therapeutic strategy, imagines the most anxiety-producing scene and fully immerses (floods) himself in it, as opposed to systemtic

desensitization, (q.v.).

Fugue A long period in which a person

has almost complete amnesia for his past. Habits and skills are usually unaffected. He leaves home and starts a new life with

different conduct. Afterward, earlier events are remembered, but those of the fugue period are

forgotten.

Grief Alteration in mood and affect

consisting of sadness appropriate to a real loss.

Group Psychotherapy A type of psychiatric treatment that involves two or more patients participating together in the presence of one or more

psychotherapists. who facilitate both emotional and rational

cognitive interactions to effect changes in the maladaptive

behaviour of the members.

Guilt Affect associated with

self-reproach and need for

punishment. In psychoanalysis, guilt refers to a neurotic feeling of culpability that stems from a conflict between the ego and the superego. It begins

developmentslly with parental disapproval and becomes

internalised as conscience in the course of super-ego formation. Guilt has normal psychological and social functions, but special

intensity or absence of guilt

characterizes many mental

disorders, such as depression and

x vi i i

Homeostasis

Hyperchondriasis (Hypochondriacal Neurosis)

Hysteria

antisocial personality,

respectively. Some psychiatrists dis tinquish shame as a less

internalised form of guilt.

The tendency to maintain a

constant balance among bodily processes to ensure optimal

functioning.

Exaggerated concern with one's physical health. The concern is not based on real organic

pathology. Unrealistic

interpretation of physical signs or sensations as abnormal, leading to preoccupation with the fear or belief of having a disease.

Mental disorders in which motives, of which the patient seems

unaware, produce either a

restriction of the field of

consciousness or disturbances of motor or sensory function which may seem to have psychological advantage or symbolic value. It may be characterized by conversion

phenomena or dissociative

phenomena. In the conversion form the chief or only symptoms consist of psychogenic disturbance of function in some part of the body, e .g .. paralysis, tremor,

blindness, deafness, seizures. In the dissociative variety, the most prominent feature is a narrowing of the field of consciousness

which seems to serve an

unconscious purpose and is

commonly accompanied or followed by a selective amnesia. There may be dramatic but essentially

superficial changes of personality sometimes taking the form of a

fugue (wandering state).

Behaviour may mimic psychosis or, rather, the patient's idea of

psychosis.

xix

I CD

Idealization

Ideational Shield

Idiopathic

Labile

Linquo-mental Reflex

Malingerinq

International Classification of Disease. The manual of

International Statistical

Classification of Diseases,

injuries and causes of death,

published by the World Health

Organization. The 9th edition was adopted in 1975 and has been used by the Department of Veterans' Affairs since 1980.

A defence mechanism in which a

person consciously or, usually, unconsciously overestimates an attribute or an aspect of another person.

An intellectual, rational defense against the anxiety that a person would feel if he became vulnerable to the criticisms and rejection of others. As a result of his fear

of being rejected. he may feel

threatened if he criticises

another person, an act that is

unacceptable to him. In both

group and individual therapy, conditions are set up that allow the participants to lower this ideational shield.

Without known cause.

Unstable; characterized by rapidly changing emotions.

A primative reflex in which the mentalis muscle (in the chin) is made to contract by the stroking of the tongue. The presence of

this reflex is claimed to indicate damage of the temporal lobe of the brain.

The deliberate feigning of illness or disability in order to evade an obligation or to obtain

compensation.

x x

Poorly adjusted or pathological behaviour pattern.

A state of emotional well-being in which a person is able to function comfortably within his society and in which his personal achievements

and characteristics are

satisfactory to him.

Questionnaire type of psychological test for ages 16 and over. with

550 true-false statements that are coded in 14 scales, ranging from a social to a schizophrenia scale. Group and individual forms are

available.

Neurasthenia An obsolete diagnostic term that

was used to describe a neurosis in which the principal symptoms are excessive fatigue and bodily

accompaniments or depression.

Neurosis Mental disorder characterised by

anxiety. The anxiety may be

experienced and expressed

directly. or, through an

unconscious psychic process, it may be converted, displaced, or somatized. Although neuroses do not manifest depersonalization or

overt distortion of reality, they can be severe enough to impair a person's functioning. The

neuroses, also known as

psychoneuroses, include the

following types: anxiety,

hysterical, phobic,

obsessive-compulsive, depressive, neurasthenic, depersonalization, and hypochondriacal.

Norepinephrine A catecholamine that functions as a neurohumoral mediator liberated by postganglionic adrenergic nerves. It is also present in the adrenal medulla and in many areas

in the brain, with the highest concentration in the

Maladaptive Wav

Mental Health

Minnesota Multiphasic Personality Inventory (MMPI) ........

hypothalamus. A disturbance in the metabolism of norepinephrine is considered to be an important

factor in the causation depression.

Nosology The science of

of diseases. the classification

Numbing Inhibition or suppression of

sensitivity and compassion; the anaesthetizing reactions. of empathic

Organic Relating to an organic; in

theories on mental disorders, often referring to organic lesions.

Organic Disease An illness that is caused by

actual structural or biochemical change in an organ or tissue.

Orthopsychiatry A combined mental hygiene approach using psychiatry, psychology, and other sciences to promote healthy emotional development and growth.

Personality Disorder Mental disorder characterized by maladaptive patterns of adjustment to life. There is no subjective anxiety, as seen in neurosis, and no disturbance in the capacity to recognize reality, as seen in

psychosis. The types of

personality disorders include passive-aggressive, antisocial, schizoid, hysterical, paranoid, cyclothymic. explosive,

obsessive-compulsive, asthenic, and inadequate.

Compound derived from phenothiazine. It is particularly known for its antipsychotic

property. As a class, the

phenothiazine derivatives are among the most widely used drugs in medical practice particularly in psychiatry. Chlorpromazine.

triflupromazine, fluphenazine, perphenazine, and thioridazine are some examples of phenothiazine derivatives.

Phenothiazine Derivative

x xi i

Phenoxy Herbicides A general term for a group of the chemicals which includes 2,4-D and 2,4,5-T. These chemicals are

structurally related to one

another, but work in different ways and on different plant

species.

Porphyria A metabolic disease that is

accompanied by abdominal pain and certain mental symptoms.

Post Traumatic Stress A diagnostic category or anxiety Distorder (PTSD) neurosis first propounded in DSM III(q.v.). Its essential feature is the development of

characteristic symptoms following a psychologically traumatic event generally outside the range of usual human experience. The

characteristic symptoms involve reexperiencing the traumatic event; numbing of responsiveness to, or reduced involvement with, the external world; and a variety of autonomic, dipphoric, or

cognitive symptoms. Subtypes are Acute, Chronic, or Delayed PTSD.

Psychiatry The medical speciality dealing

with mental disorders. The

diagnosis and treatment of mental diseases.

Psychoactive Drug Drug that alters thoughts,

feelings, or perceptions. Such a drug may help a person in either individual or group therapy

overcome depression. anxiety, or rigidity of thought and behaviour while he learns new methods of

perceiving and responding.

Psychology The profession, scholarly

discipline and science concerned with the behaviour of man and

animals, and related mental and physiological processes.

Cognitive psychology attempts to

xxi ii

integrate into one whole disparate knowledge from the subfields of perception, hearing, memory, intelligence, and thinking.

Psychopathology Branch of science that deals with morbidity of the mind.

Psychopharmacoloqy The study of how certain drugs affect mental and behavioural processes.

Psycholophvsiological Disorder Mental disorder characterized by physical symptoms of psychic

origin. It usually involves a single organ system innervated by the automonic nervous system. The physiological and organic changes stem from a sustained emotional disturbance. It was previously known as psychosomatic disorder.

Psychosis Mental disorder in which a

person's mental capacity,

affective response, and capacity to recognize reality, to

communicate, and to relate to

others are impaired enough to

interfere with his capacity to deal with the ordinary demands of life. The psychoses are

subdivided into two major

classifications according to their origin: psychoses associated with organic brain syndromes and

functional psychoses.

Psychotic A term indicating gross impairment

in reality testing. It may be

used to describe the behavior of an individual at a given time, or a mental disorder in which at some time during its course all

individuals with the disorder have grossly impaired reality testing. When there is gross impairment in reality testing, the individual

incorrectly evaluates the accuracy of his or her perceptions and

thoughts and makes incorrect

x x i v

Psychotherapy

Psychotropic Drug

RAP

inferences about external reality, even in the face of contrary

evidence. The term psychotic does not apply to minor distortions of reality that involve matters of relative judgment.

Form of treatment for mental

illness and behavioural

disturbances in which a trained person establishes a professional contract with the patient and

through definite therapeutic communication. both verbal and nonverbal, attempts to alleviate the emotional disturbance, reverse or change maladaptive patterns of

behaviour, and encourage

personality growth and

development. Psychotherapy is distinguished from such other forms of psychiatric treatment as the use of drugs, surgery,

electric shock treatment, and insulin coma treatment.

Drug that affects psychic function and behaviour. Also known as a

phrenotropic drug. it may be

classified as an antipsychotic drug, antidepressant drug,

antimanic drug, antianxiety drug, or hallucinogenic drug.

RAP groups: informal group

meetings of veterans for "honest speaking" under the active

leadership and involvement of a counsellor/therapist: psychological group therapy. First implemented at New York in

1970.

Schiziod Personality A personality disorder in which the person is shy, oversensitive, and sometimes eccentric. People with schizoid personalities are usually detached and seemingly unemotional in the face of

upsetting events and experiences.

X XV

Sensitize

Shell-shock

Syndrome

Systematic De sensitization

Toxic Encephalopathy

Toxic Neurasthenia

Toxic Psychosis

To render sensitive; to induce sensitivity.

A traumatic neurosis; term used especially during and after World War I to denote psychiatric

illness consequent to battle.

A grouping of symptoms that occur together and that constitute a recognizable condition. The term "syndrome" is less specific than

"disorder" or "disease". The term "disease" generally implies a specific aetiology or

pathophysiological process.

Reciprocal inhibition (2); a type of behaviour therapy for

eliminating phobias or anxieties; the patient and therapist

construct a list of imagined

scenes eliciting the phobia,

ranked from the least to the most anxiety-producing; the patient then is trained in deep muscle

relaxation, and is repeatedly asked to imagine himself in the presence of the least

anxiety-producing scene on the list until he feels himself fully relaxed; the procedure is repeated for each scene on the list until the patient develops the capacity to feel relaxed with any of the

anxiety-producing scenes; real life scenes are then substituted for the imagined scenes.

Pathological changes in the brain caused by a toxic agent.

Neurasthenia caused by a toxic agent.

A psychosis caused by toxic

substances produced by the body or introduced into it in the form of chemicals or drugs.

xxvi

Trauma In psychiatry, a significant,

upsetting experience or event that precipitates or aggravates a

mental disorder.

Visual Evoked Response A recording of electrical activity (VER) of the brain usually made from the

surface of the skull following the presentation of a visual

stimulus. The recordings are

typically made many times and

averaged. Various components of the resultant wave-form have been attributed to neural activity in particular parts of the brain. Thus a recording which shows part of the wave-form to be absent or delayed, may reflect impairment of

that part of the brain associated with that wave-form.

War Neurosis A neurotic disorder caused by

war-time experiences,

characterised by anxiety,

depression and various bodily complaints. Acute war neuroses are those that are seen under

war-time conditions. Chronic war neuroses are those that persist beyond war-time conditions into civilian life.

xxv ii

C H A P T E R IX

THE MENTAL HEALTH AND WELL-BEING OF AUSTRALIAN PERSONNEL AND OF THEIR SPOUSES

"If a man will begin with certainties, he shall end in doubts, but if he will be content to begin with doubts, he shall end in certainties."

Francis Bacon1

C H A P T E R IX

THE MENTAL HEALTH AND WELL-BEING OF

AUSTRALIAN PERSONNEL AND OF THEIR SPOUSES

1. INTRODUCTION

Paragraph (i) of the Commission's Letters Patent directs

it to inquire particularly into

...evidence relating to the effects of any

exposure to chemical agents on the mental and physical health and well-being of Australian personnel and any effects on mental and physical health and well-being of their spouses...

The inquiry, however, is not confined merely to chemical

causation in respect of the subject matter of that

reference. The Commission is further directed, in making

such inquiry to:

...have regard to any other matters which may appear to you to be relevant...

As well, logically any examination of causation involves

consideration of alternative possible causes ("confounding

variables"). In considering this aspect, the Commission

has had regard to expert evidence directed to

IX-1

chemical-causation. and to literature, concerning the

stresses of war, war-time conditions and other factors

unique to Vietnam.

2. WAR-TIME STRESS

The concept of stress related to combat is not at all

novel. It was first studied after the American Civil War

but prior to World War I psychological casualties

resulting from war were considered to be weak, lacking

military discipline or both.

World War I produced the diagnosis of "shell-shock" for a

syndrome involving one or more of paralysis,

pseudo-confusion, blindness, hypochondria, phobic or

anxiety symptoms, freezing, catatonic stupor,

irritability, overwhelming depression, startle reaction to

noises, somatic symptoms, gross tremors, restlessness,

insomnia, nightmares or repetitive battle dreams.

After World War I large numbers of men were treated for

combat-related stress, which became known as "war

neurosis" or "traumatic neurosis". However the prevailing

opinion was that, although precipitated by combat, the

disorder was a result of predisposing character or

personality defects.

IX-2

2.1 World War II

Neuro-psychiatric admission rates were quite high in the

various war theatres. Annual admission rates for combat

divisions serving in the European theatre were

approximately 25%, although for infantry battalions

characteristically exposed to the greatest amounts of

combat, rates were 20%. 2 The rates were higher in the

South-western Pacific theatre which is considered to have

been stressful, not only because of the battle conditions,

but also because of the location. The heat, lack of

recreation, excessive physical demands, tropical diseases,

isolation, monotony and other discomforts were additional

sources of stress. Such conditions were similar to those

in South-east Asia.

In all wars fought by Americans, predispositional factors

were assumed to account for most psychiatric casualties.

World War II was no exception. The incidence of these

disorders increased 300% over World War I, even though the

pre-induction psychiatric rejection rate was three to four 3 times higher.

Various terms were adopted to describe these psychiatric

casualties, for example, "psycho" or "troppo". Later the

IX-3

US Army Commander in Tunisia ordered that all psychiatric

disorders in the combat zone - regardless of the

manifestation - were to be called "exhaustion". This was

a tactic designed to discount the mentally debilitating

potential of battle. Hanson (1949), claimed that the term

"exhaustion" more accurately described the disorder

because physical fatigue played an important role in 4 psychiatric breakdown.

Glass (1957) points out that low neuro-psychiatric

casualty rates in combat should be regarded with

5

scepticism. The stigma of mental illness was

associated with ineffective commanders and low unit

morale. This lowered the rate of official diagnosis of

neuro-psychiatric fatigue.

2.2 Korean War

During this War a distinction of "combat fatigue" as

different from exhaustion due to physical fatigue

developed. The lower combat-related psychiatric casualty

rates in Korea were credited to the rotation policy of

nine-months maximum in a combat zone.

IX- 4

PATTERN OF NEUROPSYCHIATRIC DISORDER - WORLD WAR II. 3 .

KOREA VIS-A-VIS VIETNAM

The pattern of neuropsychiatric disorder of combatants of

World War II and Korea is quite different from that of

Vietnam.

For both World War II and the Korean War. the incidence of

neuropsychiatric disorder among combatants increased as

the intensity of the wars increased. As those wars wound

down. there was a corresponding decrease in these

disorders until the incidence closely resembled pre-war

periods. Prolonged or delayed symptoms during the

post-war periods were obscure and few in number. No great

significance was attached to them.

The Vietnam experience proved different. As the war

increased in intensity. there was no corresponding

increase in neuropsychiatric casualties. It was when the

war was winding down that neuropsychiatric disorders began

to increase. After the conflict the number of veterans

presenting with neuropsychiatric disorders began to

increase markedly.6

During the 1970s, people who had experienced traumatic

episodes other than combat, eg plane crashes. natural

IX-5

disasters, fire, acts of terrorism presented with

syndromes similar to that of troubled Vietnam veterans.

The new classification of Post Traumatic Stress Disorder

(PTSD) in The Diagnostic and Statistical Manual of Mental

Disorder, Third Edition (1980) (DSM III) was the result of

research by veterans1 task forces and the recommendations

of those involved in psychiatric treatment of civilian

victims of trauma.

4. HOW "UNIQUE" WAS THE VIETNAM WAR?

The Commission found a paucity of Australian literature on

stress and this conflict. (See under Literature infra).

It must be borne in mind when reading this Chapter,

particularly references to American publications, that

there were significant differences between the Australian

and the American involvement in the Vietnam conflict.

Dr. Peter G. Bourne, in his foreword to "Stress Disorders

Among Vietnam Veterans: Theory, Research and Treatment",

edited by Dr. C.R. Figley, cites the following factors as

unigue to the Vietnam war:

IX- 6

(i) America remained fundamentally detached from the

war, maintaining business as usual, despite

opposition at home and the nightly combat scenes

on television.

(ii) The Vietnam veteran returned to the United States

to apathetic indifference or hostile repudiation.

(iii) The conduct of the war differed. For Americans

brief periods of intense combat were mixed with

relaxed existence in the major cities of Asia and

Australia.

(iv) It was a guerilla war with no fixed battle lines.

(v) There were. no protracted artillery duels or

aerial bombardments on American troops which

characterised the two World Wars and Korea.

(vi) There was a pre-determined one year tour of duty

in the combat zone.

(vii) There was not the same sense of hopelessness that

prevailed in previous conflicts where death,

injury or peace became the only possible ways by

IX-7

which the soldier could extricate himself from

the battlefront.

(viii) Combat psychiatric casualties were far fewer

because morale was kept high through adequate

training, equipment. leadership and prompt

medical evacuation.

On the other hand, the relatively low rate of

psychiatric casualties in the combat zone was

more than offset by an exceptionally high degree

of adjustment problems upon return to the United

States.

(ix) Men rotating on individual schedules, lacked the

emotional support they might have received if

they had returned with other members of their

units. (Note that this did not apply to

Australians most of whom returned with their

units).

They did not return victorious at the successful

conclusion of a popular war, as occurred in World

War II, but were too often faced with resentment

and blame for an unpopular war over which they

had no control.

IX-8

(X) The magnitude of the adjustment problems was

extraordinary. The increasing unpopularity at

home of the Vietnam war, the increasing hostility

to soldiers returning from that war. the

increasing recourse to the draft, the increased

incidence of "fragging" (murder of officers) and

the increasing recourse to heroin and other forms

of drug abuse led to a stigmatisation of the

Vietnam veteran as unstable and unemployable and

as a potential drug addict. (Fragging and illicit

drug abuse were not significant problems in the

Australian Task Force.)

Dr. Victor J . De Fazio in his chapter in Fig ley1 s book

entitled "Dynamic Perspectives on the Nature and Effects

of Combat Stress" cites a number of complementary features:

1. The conflict was against an indigenous revolutionary

army.

2. The very special character of the war, its clandestine

nature, led to considerable brutalisation on both

sides.

IX-9

3. American troops were left with a sense of helplessness

at not being able to confront the enemy in set-piece

battles.

4. The spectre of being shot at and having friends killed

and maimed by virtually unseen forces, generated

considerable rage which came to be displaced on anyone

or anything available.

5. The dehumanisation of the Vietnamese was aggravated by

the striking differences in race, language, culture

and the recurrent threat that even the most gentle

looking person could, in fact, be the enemy.

6. The language of war was replete with references and

euphemisms which minimised the significance of events,

blunted affect and made everything sufficiently

unreal. The average GI, for example, became a

"grunt", a sort of sub-human, no longer capable of

thought or affection. People were "zapped", not

killed. The Vietnamese became "dinks", "slopes" and

"gooks", terms not confined to the enemy.

7. Being unable to distinguish friend from foe, troops

came to mistrust all Vietnamese.

IX-10

8. They also came to mistrust the representatives of

religion and mental health professionals who were

perceived as only interested in supplying "bodies" to

fight.

4.1 Homecoming

Veterans as children had observed the homecoming of their

fathers as heroes from World War II. Films and the media

emphasised the sacrifice and heroism and sympathetically

portrayed adjustment problems (e.g. The Best Years of Our

Lives).

By contrast Vietnam veterans were social lepers. They

were depicted in films and the media as psychopathic

killers. Their anger. grief and anxieties were treated

most unsympathetically (e.g. "The Stone Killers") .

The Vietnam war was one of the few from which American

soldiers did not return from an unqualified victory. In a

combat situation, the vindictiveness is often experienced

as a righteous wrath, while in peacetime it is felt as a

smouldering resentment directed at institutions and

individuals in authority. Minor rebuffs or oversights can

be met by the veteran with hints of retaliation and anger

IX-11

which seem all out of proportion to the initial act.

Mates or friends are at a loss to understand what they

have done to provoke such a response. The end results are

frequent rifts between the men. their friends or

families. It has been found that, regardless of the

veterans' professed view on the war (i.e. whether they

were hawks or doves), all had doubt about the morality of

the war.

The Commission had benefit of a lengthy consultation with

the head of the American Outreach Programme, Dr Arthur

Blank, a distinguished psychiatrist and a Vietnam

veteran. His understanding of the problems of US Vietnam

veterans is unequalled.

4.2 Arthur s. Blank, Jnr. M.D.

Dr. Blank has given perhaps the best description of the

stresses which veterans undergo in war-time and post-war 7

life. In "Stresses of War: the example of Viet Nam"

he has categorised the stresses in this way,

4.2.1 Stresses Typical of All Wars

(a) miserable living conditions (deprivation or denial of adequate food, clothing, shelter, cleanliness; exposure to the elements). (b) Fatigue.

IX- 12

(c) Sensory assault. (d) The fighting itself. (e) Wounds (suffered by self, mates, witnessing of civilian and combat horrors).

(f) Special Stresses of the Combat Situation (i) Capture and torture. ii) Isolation. (iii) Acute survivorship.

(iv) Authoritarian organisation. (v) Command incompetence. (vi) Observers (photographers, journalists, casualty clerks, psychiatrists, chaplains,

communications operators, intelligence officers).

4.2.2 Unusual Stresses Found in the Vietnam War

(a) Guerilla warfare. (b) Lack of clear objectives. (c) Limitations on offensive actions. (d) Terrorism. (e) Climate and topography. (f) Miscellaneous, bizarre physical dangers (flora

and fauna). (g) Tropical diseases. (h) Immersion in an extraordinarily poor Third World society. (i) Chaos.

4.2.3 Psychological Stresses Secondary to the General Political Character of the War

(a) The experience of absurd waste (including corruption, fraggings, avoidance of unnecessary or purposeless combat). (b) Government deceit and mis judgment. (c) Massive national conflict. (d) Defeat.

4.2.4 Atrocity

Defined as destruction going beyond the usual

boundaries of war, lying outside the requirements of military strategy.

(a) Atrocity directed against the land: Defoliation of forests and fields with herbicides.

(b) Meaningless destruction of human life: Captives pushed out of helicopters, shooting and napaiming of non-combatants, massacres, etc.

I X - 13

4.2.5 Additional Emotional Trauma

(a) Failure to live up to one's expectations. (b) Overwhelming fear reactions. (c) Self-inflicted wounds. (d) Accidental killing of comrades or civilians. (e ) Vietnamese left behind.

4.2.6 Stresses of the Immediate Homecoming Period

(a) Absence of sanction, presence of hostility. (b ) Absence of normal debriefing.

4.2.7 Long Term Factors Exacerbating the Effects of War Stress .

(a) Further fading of a sense of purpose. (b) Impossibility of further contact with Vietnam. (c) Unavailability of psychotherapeutic treatment. (d) Continuing blackout of the war as history.

4.2.8. Major Delayed and Chronic Stress Symptoms Seen in Vietnam Veterans

(a ) Type 1. Manifesting Primarily by Psychological Symptoms

(i) Classical traumatic neurosis symptoms. Flashbacks, nightmares, irritability, rage, dizzy spells, anxiety, insomnia, depression.

(ii) Depression. Without other symptoms, masking impacted grief about war

experiences and related conflicts (Shatan 1981).

(iii) Psychosomatic syndromes. Headache, low back syndrome, ulcer, migraine,

irritable colon, hypertension.

(iv) Violent paranoid states. Without

psychotic symptoms, or indicators of pre-war borderline personality disorder, these veterans manifest diffuse

hostility. suspiciousness, paranoia, irritability, and crowd phobia. This state represents a persistence of the paranoid, hyper-vigilant state that was

IX- 14

lifesaving for many participants in the terrorized guerilla atmosphere of Vietnam.

(v) Addictive disorders. Addiction to

alcohol marijuana, heroin. cocaine. thrills, risks. gambling - including gambling with fate as in chronic

high-speed driving.

(vi) Exacerbated_____ character_____ disorders . Dramatic exacerbation of character problems. such as impulsive behaviour or sociopathy, present in minor degree

before the war.

(vii) Suicides and homicides. These are

categorised separately for two purposes: to highlight them as problems. and also to indicate our lack of knowledge of the

diagnostic background of Vietnam

veterans who kill themselves or others. Fortunately, the number of homicides is quite small. That may not be the case for suicides; there is not a single

study of the incidence of suicide in Vietnam veterans; but there is a

persistent, almost universal impression among clinicians who work with this group, that the incidence of suicide is high and continuing. (Note that this is not so amongst Australian Vietnam

Veterans, see Chapter X).

(viii) Psychotic syndromes. This outcome, long-recognised in the literature from previous wars. has remained largely hidden in Vietnam veterans until

recently.

(b) Type II. Manifesting Primarily By General Alteration In Life Course

(i) Underachievement. Lacking significant symptoms, these veterans' lives are characterised by chronic underachieving or instability in education or work.

IX-15

(ii) Wandering____lifestyle. Though not

necessarily underachieving in any obvious way, the veteran goes from job to job, school to school, town to town without progression toward any goal.

(iii) Crime. Some veterans commit antisocial acts not as a result of pre-existing criminality, but as a part of stress disorder.

(c ) Type III. Problems Manifested Primarily in Relating to Significant Others

(i) Difficulties in intimacy with wife or lover.

(ii) Special interferences in relating to children.

(iii) Marked change in relatedness to the country and its institutions. Loss of political attachment may have occurred because the soldier in Vietnam felt himself sacrificed by military and civilian leaders who, out of ignorance or cynicism, did not allow him to win a

just war or, from the opposing

perspective, sent him to fight an unjust war.

(iv) General alienation. Affected veterans display a pervasive and generalised detachment from most processes of life - marriage, career, social and political

institutions, community, and friends. Some seem frozen at age 20, have not

learned more adult skills for living, and are unsophisticated in subtle and diverse ways.

(d) Type IV

Veterans in this group have experienced a profound shattering of images of self and humanity. These Viet Nam veterans have much in common with the survivors of Nazi death and concentration camps. They have lost some of

their basic faith in the capacity of humanity for goodness, as described in Holocaust

Survivors.

IX-16

5. THE NATURE OF READJUSTMENT

There are two major works on returnee readjustment after

World War II. The trilogy "The American Soldier" (1949) a

classic work of American military behavioural science

under the leadership of Stouffer, and "Men Under Stress"

(1945) by Grinker and Spiegel, which observed psychiatric

issues and practices in the Army Air Force, noted the

concern to maintain group unity, discipline and

cohesiveness of returnees who should be subjected to a

program of gradual transition to garrison life with a

thorough programming of conditions that they might expect

to encounter upon returning home. An emphasis on making a

good first impression upon return was satisfied by a

ceremonial greeting by bands at debarkation ports,

transfer to a reception centre close to home, the

provision of civilian clothes and money to begin a three

week furlough, and transfer to reassignment centres for

orientation to the nature of garrison Army life.

The general experience of the Vietnam returnee, by

contrast, was that within 48 hours of leaving the combat

zone he was immersed back in his total family milieu

without ceremony to mark the transition, orientation about

what to expect on return, or direction on where to go for

support if difficulties were encountered.

IX-17

In the United States. returning Vietnam GIs had to

re-enter an anti-war, racially tense, civilian society

with high unemployment under far from ideal

circumstances. Veteran unemployment rates, especially for

non-white returnees, were at astronomical levels and GI

benefits were unrealistically low in the then inflated

economy. As a group they shunned veterans' organisations

which they found irrelevantly still geared to the

interests of the World War II veteran.

Borus in his "Reentry: III. Facilitating Healthy

Readjustment in Vietnam Veterans" (Psychiatry. Vol. 36,

November 1973, page 428, at pp 429-430) cited the results

of a study defining the common adjustment issues facing

returning veterans. They were as follows:

(a) Military adjustment

(i) In contrast to Vietnam, these

combat-prepared returnees felt that their garrison units had no useful or productive mission for them to carry out and that their time was being wasted in the Army by performing meaningless and degrading jobs training.

unrelated to their

(ii) They missed the closeness and group support of the combat unit and felt that their present unit peers were neither supportive to their commitment to the Army, nor demanding of their affiliation

to the unit.

IX-18

(iii) They felt little confidence in the

leadership at the garrison post as

contrasted to great confidence in

leadership in Vietnam and, on the whole, felt it was difficult to adjust to the more formal discipline and military encountered on return to the garrison

post.

(iv) Universally, they said they had received no reorientation to the new demands of garrison life to help them through this transition.

(b) Family adjustment

Centered on the stress of the returnee’s

initial reunion with his family on arriving home from Vietnam, his adjustment to an often changed and disrupted family situation during his 30-day leave, and his attempts to

reintegrate into the family on a part-time (weekend) basis after return to active duty at the garrison. In each of these phases, the discrepancy between the veteran's fantasies about home and the reality of his return to the

family had to be resolved.

(c) Social adjustment

(i) The returnee had to deal with his

participation in Vietnam in the light of the society's anti-war, anti-military posture; defining his position on the war and the anti-war movement; and

readjusting to changed racial

relationships in garrison.

(ii) Most men had well-defined pro- or

anti-war positions about Vietnam, denied feeling sorry or guilty about their participation in the war and didn't feel slighted by society upon their return.

(d) Emotional issues

(i) Veterans had to work through changes in their emotional temperament related to Vietnam, and in keeping in touch with and expressing feelings in a socially

acceptable tens ion-reducing way.

I X - 19

( ϋ ) Some veterans also faced the more

serious adjustment tasks of resolving recurrent emotional disturbances about combat experiences, gaining control of violent feelings and behaviour, and gaining perspective and control over patterns of illegal drug use initiated or exacerbated in Vietnam.

(iii) Most men felt somehow changed by their Vietnam experience; the people who were having difficulty on return generally felt changed in a damaging way. while

those who were having little difficulty felt the experience either did not

change them or in some ways changed them for the better.

(i v) Most returnees felt more at ease

discussing and sharing their Vietnam experiences and feelings with other Vietnam veterans than with people who had not been to Vietnam.

5.1 American Studies

5.1.1 President's Commission on Mental Health; Mental

Health Problems of Vietnam Era Veterans8

The five principal mental health problems identified in

the Report, at page 1331, are:

(a) specific psychiatric disorders;

(b) drug abuse and alcoholism;

IX- 20

(c) stigmatization;

(d) failure of social integration;

(e) family breakdown.

5.1.1(a) Psychiatric Disorders; The Paradox of Vietnam

On the one hand. the Vietnam conflict produced a smaller

rate of neuro-psychiatric diagnoses in the combat zone

than any of the previous conflicts. On the other hand.

the incidence of psychotic disorders was far higher among

Vietnam soldiers and. unlike the reports of

neuro-psychiatric diagnoses, those of psychotic disorders

continued to rise after the fighting itself was reduced

and ended.

Thus the battlefield in Vietnam may well have produced

fewer immediate psychiatric casualties requiring

evacuation and discharge than did earlier conflicts, but

it left a far greater legacy of delayed and chronic

disorders which arise and persist long after the soldier

has returned to civilian life.

IX-21

5.1.1(b) Clinical Symptoms of War Stress

The most obvious and most commonly reported clinical

symptoms of war stress can be subsumed under the term

"acute combat reaction". This involves behaviour by a

soldier under conditions of combat usually interpreted by

those around him as signalling that he has ceased to

function effectively. The symptoms include loss of

appetite. irritability, jumpiness, disturbed sleep,

paralysis, blindness, aphonia, disorientation,

disorganization of thought. panic, apathy, choreiform

movements, tics, stammering, syncopal attacks, delirium

ana stupor.

5.1.1(c) Delayed Combat Reaction

What psychiatrists identify as delayed combat reaction is

no less serious or widespread, but it is much more

difficult to identify, report · and treat. Specialists

differ in their diagnoses. Some view delayed combat

reaction as consisting of a re-experience of the combat

situation minutes, weeks or years after the original

stimulus. This re-experiencing (or flashback) may occur

either during some period of stress in the veterans life,

or during a situation which closely resembles the

IX-22

environment of the combat situation. Other specialists

have included a more diffuse range of emotional

disturbances under the label of "delayed combat

reaction". Some of these are:

. affective muting - characterised by detachment

withdrawal and the diminished capacity to feel;

. guilt - characterised by a sense of failure to keep to

personal moral standards and a general expectancy of

punishment. The symptoms include painful feelings of

self-criticism, blame and remorse. Guilt among

veterans may also be manifested as survivor guilt - a

feeling that one's life was saved at the cost of

another's;

other disturbances - among them obsessional thoughts

of death, hyper-alertness and startle reactions, sleep

disturbances and nightmares, rage and aggression,

mistrust, paranoia and depression. These are often

reflections of hidden and repressed feelings of guilt

and anxiety.

The more delayed and diffuse the psychiatric

manifestations, the less likely it is that their

IX-23

connection with Vietnam service will be recognised.

Consequently, clinicians find it difficult to compile an

accurate aetiology; veterans suffering from the problem do

not receive adequate treatment; statisticians

under-estimate the true incidence; and government programs

fall short of meeting veterans' need.

5.2 Drug Abuse & Alcoholism (American Studies)

A common consensus among US Defense Department and law

enforcement officials is that heavy American narcotics and

marijuana use was limited to the war zone and that

veterans rapidly matured out of their drug use habit once

they had returned home.

However, the problems of alcoholism are rapidly increasing

in size and scope. The results of virtually all recent

research shows that the prevalence of alcohol abuse has

risen dramatically - a phenomenon related also to

increasing arrest rates for veterans, incarceration,

accidents, job loss, and medical problems. Even

researchers who differ in their findings regarding opiate

use are agreed on the high incidence of alcohol abuse.

IX-24

Public health service figures indicate perhaps that as

many as half a million Vietnam veterans (of 2.8 million)

are alcoholics; the Veterans Administration reports

107,000 inpatients and 323,000 outpatients treated for

alcoholism and their alcohol treatment facilities are now

growing by 13% annually (report dated 15 February 1978).

5.3 Stigmatization

One of the serious problems from which veterans suffer can

be defined by the stigmas imposed on them by the American

people themselves - stigmas which disadvantage them,

discriminate against them, and add to the severe mental

health problems which have already been identified.

Moreover, the stigmas which Vietnam veterans carry are not

so much their problem as the problem of society at large.

There is little foundation, in fact, for the majority of

negative stereotypes associated with Vietnam veterans.

All too often popular novels, films, television, and the

press, portray Vietnam veterans as losers, misfits, poor

soldiers physically or mentally unfit to fight, and as

drug addicts, homicidal maniacs and individuals who cannot

be relied upon to act in an emotionally controlled and

rational manner.

IX-25

Unemployment statistics in September 1977 showed the rate

of unemployment for veterans aged 20-24 was 20.1% versus

9.1% for non-veterans. (NB. USA not Australia).

There is a self-fulfilling prophecy in the stigmatization

process. Employers who fear instability of veterans often

underemploy workers who are veterans or offer low-skilled

and marginal jobs at wages well below the expectation of

returnees. This is discouraging to them and accelerates

job turnover and work dissatisfaction which, in turn,

convinces employers of the truthfulness of the stereotypes

in the first place. This cycle repeated for individuals

many times over lowers self-esteem, depresses morale, and

re-enforces whatever problems of health or psychological

disturbance may already be embryonic.

5.4 Failure of Social Integration

There is a sense of estrangement, of isolation from the

rest of society dominating the thinking of those suffering

many of the disabling psychiatric disorders and drug abuse

problems already discussed. Social stigmatization

aggravates feelings of alienation even among those without

the more obvious symptoms of maladjustment. At the

sub-clinical level, there are signs of negativism.

IX-26

distrust and loss of morale and self-esteem which

debilitate veterans.

5.5 Family Breakdown

Many of the mechanisms by which families of servicemen

learned to cope during their separation made the period of

reunion even more difficult and traumatic than either the

family or veteran could have anticipated. The dynamics of

this process are not well understood. Families of Vietnam

era veterans have been the subject of little systematic

study, but unusually high rates of separation and divorce

are indicative of the fact that Vietnam era veterans have

returned to face a range of problems in family adjustment

which they cannot really solve by themselves and for which

help is needed.

6. DEFINITIONS: THE CLASSIFICATION OF MENTAL ILLNESSES

6.1 International Classification of Diseases

The International Classification of Diseases (ICD)

is a manual of the international statistical

classification of diseases, injuries, and causes of

death. It is based on the World Health Assembly,

IX-27

and a manual is published by WHO providing details

of the categories and sub-categories. The current

version (I CD 9) is based on the recommendations of

the 9th Revision conference 1975. It endeavours to

deal in broader terms with specific subjects,

noticeably heart diseases, but the basic

classification as to mental disorders is that as

enunciated in ICD8.

The Department of Veterans' Affairs (DVA) has used

ICD9 since 1980 as the basis of its statistical

compilation of assessment.

Chapter 5 of ICDS classifies all forms of mental disorder,

even though associated with or secondary to physical

conditions. Psychoses are dealt with in categories

290-299, neuroses and abnormality disorders and other

non-psychotic mental disorders in categories 300-309, and

mental retardation in categories 310-315.

Neurasthenia is dealt with as a specific category in 300.5

and as a physical disorder in sub-categories 305.3 and

305.5.

IX-28

Postfebrile neurasthenia not elsewhere classified is

contained in sub-category 309.1, that is as a mental

disorder not specified as psychotic associated with the

physical conditions of drug, poison or systemic

intoxication, but excluding alcholism and drug dependence.

Toxic neurasthenia as such is given no classification.

Mental (non-psychotic) disorder due to or associated with

degeneration of the central nervous system is dealt with

at sub-category 309.8, particularly degeneration of

central nervous system, other or unspecified.

6.2 American Psychiatric Association Diagnostic and

Statistical Manual

6.2.1 Diagnostic & Statistical Manual - (DSM)

During the Korean War, the approach to combat stress

became somewhat pragmatic. Individual breakdowns in

combat effectiveness were dealt with in a very

situational manner.

Clinicians provided immediate on-site treatment to

affected individuals, always with the expectation

that the combatant would return to duty as soon as

possible. The results speak for themselves.

IX-29

During World War II, 23% of the evacuations were for

psychiatric reasons. But in Korea, psychiatric

evacuations dropped to only 6% (Bourne 1970) . It

finally became clear that the situational stresses

of the combatant were the primary factors leading to

a psychological casualty.

6.2.2 Promulgation of DSM I. II, III

There are three editions of the DSM as developed and

promulgated by and on behalf of the American

Psychiatric Association. DSM I was developed and

promulgated in 1952 , DSM II in 1968, and DSM III in

1980.

DSM I (1952)

This manual delineated an extensive class of "gross

stress reactions" characterised by individuals being

exposed to extreme emotional and physical stress

such as combat.

DSM II (1968)

DSM II deleted the category of "gross stress

IX- 30

reactions" and replaced it with a vague category

"Transient Adjustment Reactions of Adult Life".

Combat-related stress is mentioned in DSM II only in

the brief explication and illustration of "Adult

Adjustment Reaction" (fear associated with military

combat and manifested by trembling, running and

hiding.) The implication was that there could be

more or less appropriate resolutions of the stresses

of combat.

DSM III (1980)

DSM III provided a new category "post traumatic

stress disorder, acute, chronic and/or delayed".

The acute sub-type of disorder is synonymous with

the phenomenon previously labelled "shell-shock" or

"combat fatigue". This phenomenon decreased

immensely with the institution of various

behavioural manipulations of the combatants'

experiences in Vietnam. However, with recognition

that there were many long terms effects, the chronic

and/or delayed sub-types have special relevance for

the veterans of the Vietnam war.

IX- 31

Acute-traumatic stress disorder requires that there

be an onset of symptoms within six months of the

trauma and that the symptoms should have a duration

less than six months, i.e. the term of acute PTSD

should not exceed 1 2 months from the traumatic event.

Chronic or delayed PTSD requires either or both that

the symptoms extend for six months or more (chronic)

and that the symptoms manifest six months or more

after the event of the trauma (delayed).

6 .3 Post Traumatic Stress Disorder (PTSD)

Post Traumatic Stress Disorder (PTSD) is that

psychological condition most commonly associated

with the mental disorders of Vietnam veterans. It

Is a concept specifically recognised in DSM 111 and

is described at paragraphs 308.30, 309.81, and

300.00 at pp 236-239 of the Manual.

The essential feature is the development of

characteristic symptoms following a psychologically

traumatic event that is outside the range of usual

human experience. The characteristic symptoms

involve re-experiencing the traumatic event; numbing

IX-32

of responsiveness to, or reduced involvement with,

the external world; and a variety of autonomic,

dysphoric, or cognitive symptoms.

The traumatic event can be re-experienced in a

variety of ways. Commonly, the individual has

recurrent painful, intrusive recollections of the

event or recurrent dreams or nightmares during which

the event is re-experienced. In rare instances

there are states of disassociation lasting from a

few minutes to several hours or even days, during

which components of the event are relived and the

individual behaves as though experiencing the event

at that moment. Such states have been reported in

combat veterans. Diminished responsiveness to the

external world referred to as "psychic numbing" or

"emotional anaesthesia" usually begins soon after

the traumatic event. A person may complain of

feeling detached or estranged from other people,

that he or she has lost the ability to become

interested in previously enjoyed significant

activities, or that the ability to feel emotions of

any type, especially those associated with intimacy,

tenderness, and sexuality, is markedly decreased.

After experiencing the stressor, many develop

IX- 3 3

symptoms of excessive autonomic arousal, such as

hyperalertness, exaggerated startle response and

difficulty falling asleep. Recurrent nightmares

during which the traumatic event is relived and

which are sometimes accompanied by middle or

terminal sleep disturbance may be present. Some

complain of impaired memory or difficulty in

concentrating or completing tasks. In the case of a

life-threatening trauma shared with others,

survivors often describe painful guilt feelings

about surviving when many did not, or about the

things they had to do in order to survive.

Activities or situations that may arouse

recollections of the traumatic event are often

avoided.

Symptoms of depression and anxiety are common, and

in some instances may be sufficiently severe to be

diagnosed as an "Anxiety or Depressive Disorder".

Increased irritability may be associated with

sporadic and unpredictable explosions of aggressive

behaviour upon even minimal or no provocation.

Impulsive behaviour can occur such as sudden trips,

unexplained absences or changes in lifestyle or

residence.

IX-34

Symptoms may begin immediately or soon after the

trauma. It is not unusual. however, for the

symptoms to emerge after a latency period of months

or years following the trauma. When the symptoms

begin within six months of the trauma and have not

lasted for more than six months the acute subtype is

diagnosed and the prognosis for remission is good.

If the symptoms either develop more than six months

after the trauma or last six months or more, the

chronic or delayed subtype is diagnosed.

Impairment may either be mild or affect nearly every

aspect of life. Phobic avoidance of situations or

activities resembling or symbolising the original

trauma may result in occupational or recreational

impairment. "Psychic numbing" may interfere with

interpersonal relationships, such as marriage or

family life. Emotional liability, depression, and

guilt may result in self-defeating behaviour or

suicidal actions.

6.3.1 Diagnostic Criteria for PTSD

A. Existence of a recognisable stressor that would

evoke significant symptoms of distress in almost

everyone.

IX- 3 5

One DVA consultant psychiatrist tended to place PTSD-type

disorders within I CD classification 308 and 309, being a

transient situation disturbance involving adjustment

reaction of adolescence or later life and evidenced by

combat fatigue.

The Commission understands that DVA now places PTSD-type

disorders in the nature of the category I CD 9 300-0 which

is more appropriate.

6 .4 Conclusion

The Commission is satisfied that Post Traumatic

Stress Disorder is a recognised mental illness

accepted by the scientific community.

7. AUSTRALIAN ARMY TESTING OF PSYCHOLOGICAL FITNESS

In the course of its inquiries. the Commission examined

psychiatric records and psychological records held by the

Army. The nature and reliability of the records are

comprehensively reported and analysed in the Australian 9

Veterans' Health Studies Mortality Report, Parts 1-3.

IX- 3 8

7.1 O n R e c r u i t m e n t

All recruits were subjected to careful psychological

testing and assessment. This included General

Service Battery of three tests conducted by or under

the supervision of a psychologist. (NB. not always

by qualified people). Literacy. numeracy and

intelligence were measured and unsuitable

personalities weeded out.

Results of tests administered at recruitment or

during basic training were recorded on the Service

Classification Record (SCR). Pre-service adjustment

difficulties (truancy, family mental health problems

etc) were noted.

A further psychological test was administered to all

members of the AATTV and those going as

reinforcements to units prior to departure for South

Vietnam. These were basically a repeat of the

recruit interview, designed to elicit the capacity

of the person interviewed to represent Australia and

to test their capacity to adjust on joining a

fully-formed unit.

IX-39

7.2 In V i e t n a m

The Array had no regular Australian psychiatrist

stationed in Vietnam during the whole of the

Australian Armed Forces presence, and any

psychological or psychiatric problems were dealt

with by psychologists visiting the Australian Task

Force areas at Nui Dat or Vung Tau essentially on an

ad hoc basis (except during 1969-70). Such

psychological testing as was undertaken in Vietnam

appears more to have been directed to testing

Regulars for career prospects and career changes.

Psychologists as such were posted to Singapore as

part of the Far East Land Forces (FARELF).

The nature of the treatment prescribed by

psychiatrists in the field is described below (see

Boman and Spragg).

7.3 On Discharge

There seems to have been no psychological or

psychiatric testing of National Servicemen upon

discharge unless they had been referred to medical

personnel, or had presented with psychiatric

IX-40

problems. If they were discharged on behavioural

grounds, a test or other form of attention most

likely preceded the discharge, although there seems

to have been no consistent pattern in this regard.

Moreover, there appears to have been no attempt made

by the Army to counsel soldiers as to the problems

associated with adjustment and fitting back into

civilian life. Such counselling as took place was

for the purposes of re-engagement and was more

directly aimed at keeping Regulars in the Army.

The Commission concludes that the psychological

health of the Australian veteran was of a high and

consistent standard. There appears to have been in

Australia less opportunity for evasion of National

Service by "draft dodging" or by "voluntary exile"

abroad, nor did the burden of service fall unfairly

or unduly on any one socio-economic group.

The level of instruction, of training, of peer group

support, of pride in one's corps and in one's unit,

of material comforts and - initially - societal

approval, produced a psychological/psychiatric

profile of a well-balanced and motivated serviceman.

IX-41

7.4 C o n c l u s i o n

The Commission is satisfied that such psychological

problems as may now manifest themselves in Vietnam

veterans can readily be explained by the nature of

the war in Vietnam and its aftermath in Australia.

A connection between psychological problems and war

service can reasonably be hypothesised.

8 . THE PSYCHOLOGICAL EVIDENCE

8 .1 Submissions relevant to this Chapter

1. The Returned Services League of Australia 1 0

2. The Royal Australian & New Zealand College of

Psychiatrists1 1

3. WAA's Case

IX-42

8.1.1 The Returned Services League of Australia

The RSL as an organisation claiming more than 12,000

Vietnam veterans categorised as "inaccurate" the

assertion that Vietnam veterans as a group are

unreliable employees, suffering widespread psychiatric

and physical disorders, alcoholics, prone to sudden

rage and violence and generally involved in family

breakups.

It was the experience of the RSL that many of the

relevant problems among Vietnam veterans are typical

of problems which have occurred with other groups of

ex-service personnel. It noted that war is a

stressful and damaging activity. It further noted

that there are. problems of adjustment back into

civilian life. There are post traumatic stress

effects on veterans which can have consequent effects

on families of veterans. There are the after-effects

of wounds and other disabilities suffered during war

and there can be alcohol-related effects as well.

The RSL did not doubt that some of the problems

affecting some Vietnam veterans may be linked with the

lack of overall community support of the Vietnam

12

IX- 4 3

conflict and the reception they received on return

after serving in Vietnam.

However, as a general point, the RSL enjoined this

Commission to emphasise the overall effects of war

service and not to seek to isolate individual causes

of problems in the absence of definite, scientific

evidence to support such conclusions. Finally, it was

of the view (representing a feeling among the

ex-service community) that the problems suffered by

Vietnam veterans are similar to those within the

ex-service community generally.

8.1.2 The Royal Australian & New Zealand College of

13

Psychiatrists

The recommendations of this College have received full

consideration.

The College approved and supported in broad outline

the recommendations and conclusions of the Senate 14 Report. In particular the College agreed with the

Committee's conclusion number 5. That conclusion is:

....on the available evidence, it is

unlikely that the psychiatric disorders

IX-44

reported by Vietnam veterans are caused by exposure to potentially harmful chemicals whilst in Vietnam. However. further

research is desirable. Although there are some similarities between the veterans' symptoms and those of toxic neuropsychiatric syndromes ... the level of exposure, even if at the level claimed by VVAA, is

insufficient to match the daily exposure over eight to ten years which is found in the literature on toxic psychiatric

disorders. The Committee has been impressed by the striking similarities of the

veterans' disorders to the psychiatric disorders found among the veterans of World War I, World War II, the Korean and the

Arab-Israeli Wars. These similarities include such symptoms as the rage reaction on which W A A has placed a great deal of

emphasis.

8.1.3 WA A's Case - Alleged Neurotoxicity of Chemical

Agents

8 .l. 3.1 As revealed from Issues of "Debrief" - The National

Journal of W A A

In "Debrief", Volume 3 No. 15 published in December 1982

it is stated that:

The Association, through its medical and

scientific advisers, has gathered an extensive library and research material suggesting the possibility that exposure to the toxic chemicals employed in Vietnam can cause toxic brain

dysfunction, a variety of cancers, genetic damage leading to malformations and certain disease in offspring. In the cases where the conception of a veteran's child occurred during (sic) or

immediately after his exposure, there is also the

IX- 4 5

possibility of malformation and certain diseases in offspring due to the presence of the toxic chemical.

The Minister (for Veterans Affairs) is

unimpressed by this evidence. He recently stated:

There is no credible evidence at this stage of the game that indicates that there is any connection between Agent Orange and any disabilities ... The key factor is war

experience.

The Minister is here referring to Vietnam

post-traumatic stress reaction. a psychiatric condition caused by Vietnam war experiences. It is the same syndrome which was called 1 shell shock' during the First and 'battle fatigue1 during the Second World War. Its symptoms are well known and documented and it is highly

likely, considering the nature of the Vietnam war, that many Vietnam veterans have been

affected by it. For Vietnam veterans, however, exposure to toxic chemicals in Vietnam has added a complication because evidence from research now being carried out in Holland and elsewhere suggests that such exposure may cause toxic brain dysfunction, the symptoms of which are similar of

those of Vietnam post-trauma stress reaction. Veterans displaying these symptoms are presently assumed by the Department of Veterans' Affairs to be psychiatric cases and no tests for toxic brain dysfunction are given. Their treatment may

therefore be inappropriate.

Dr C.J.M. van Tiggelen, a Dutch research

scientist at the forefront of research on this subject, examined a number of veterans who had been treated for post-trauma stress reaction and believed them to be suffering from toxic brain dysfunction. Dr van Tiggelen's conclusion is reinforced by the observations of a Macquarie Street Private Practitioner who noted his veteran patients' lack of response to certain psychiatric drug treatment. In 1980, while working in

Australia, Dr van Tiggelen was refused a small grant to further research the subject. (emphasis added) 1 5

IX-46

In "Debrief" Vol 4. No. 18, March 1983, it was stated that

It is ten years ago that the last of the 45,000 servicemen who fought in Vietnam returned to Australia.

Almost all of these soldiers, sailors and airmen had some trouble readjusting on their homecoming after a year away at a foreign war. Many

succeeded but many have not.

For those who have not, homecoming was the

beginning of a slide down a long dark tunnel. Successive bouts of intense irritability followed by withdrawal into himself signalled that the veteran had entered the tunnel. Communication with those around him became difficult and relationships with his family and friends began

to break down. The night offered no respite. To sleep became difficult and to sleep well,

imposeibile. crowded as it was with nightmares and anxiety.

Progressively, over several years, irritability developed into outbursts of verbal abuse and withdrawal deepened into depression. Even troubled sleep became a luxury. Skin rashes,

stomach pains or bronchitis may have developed or he may have been disturbed by moments of

dizziness or blurred vision. His own misery was matched only by that of his wife, who, at this stage, distraught at being unable to communicate with or understand him, and being intimidated by his unpredictable outbursts of rage, may have

left.

If she did not leave him then, it is likely that when, a couple of years later, his verbal abuse turned into outbursts of uncontrollable violence, she would have.

The final straw for her may have been another vicious physical attack on herself or the

children or the destruction of every breakable piece of furniture in the house. Even the

veteran's obvious confusion and contrition after such events may have ceased by this stage to be enough for her to endure her misery further.

IX-47

The loss of his first and perhaps second wife was accompanied by the veteran's depression

deepening, sometimes pulling him towards

suicide. In the absence of understanding and sympathy from his peers. from established

ex-Service organisations and often even from the Department of Veterans' Affairs. the veteran turned to alcohol to deaden his terror.

After about seven years in the tunnel the veteran lost his job for the first time. Soon after, he lost his second. A couple of years and perhaps five or six jobs down the tunnel, the veteran was

jobless, destitute and very sick.

There are people in our society who, whether past participants in a war or not, find coping with the stresses of life intolerable and follow a path of decline akin to that just described. Some have suggested. therefore, that the affected veterans would have developed their problems with or without their Vietnam war experiences.

But Vietnam veterans < do not represent a cross section of our society. The Vietnam force was a relatively small one whilst conscription made the pool of potential recruits enormous. Recruiters therefore could be very selective.

Potential recruits were thoroughly tested both medically and psychologically. Over fifty (50) per cent of those called-up for National Service were unable to meet the high standards required

and similar standards were required of those applying to join the regular army. Veterans. then, would not be expected, had the war not intervened, to be suffering even a low incidence of these problems. The incidence amongst

veterans, however, is very high.

Also. the results of research in the U.S. show that the symptoms suffered by Australian veterans are also common amongst veterans there. The research indicates that the condition is linked with the veterans' service in Vietnam and has

been titled Vietnam Post-Trauma Stress Reaction.

The cause of the phenomenon and its high

incidence amongst Australian veterans can be

IX-48

found in the special nature of the war in

Vietnam. Unlike the situation in W.W. II, there was no front line area in Vietnam to which the fighting and danger were confined. Wherever the soldier was, whether moving in a truck to or from

a rear area or in the heart of areas of contested jungle, there was the ever present risk of being blown-up by detonating a mine or mown down in a Viet Cong ambush. Support troops in rear areas whose location in previous wars made them

reasonably free from danger, now shared the daily fears and intense stress of those troops

searching out the enemy. There was no clear distinction between enemy soldier and neutral civilian. The civilian by day could be an enemy

soldier by night and often was. A soldier who left Australia with the 2nd AIF at the start of W.W. II and remained with them till his return to Australia at the war's end six years later, might

have, in that six years, been in a combat

situation in which he felt his life was in danger for four or five months.

Most Vietnam veterans spent one or two periods of twelve months in Vietnam, but for nine or ten months of each twelve-month tour they felt the stress of their lives being in jeopardy.

Brigadier Rodgers, a recent Director of Army Medical Services, spoke of the effects of these differences between the wars when giving evidence in 1982 to the Senate Standing Committee on

Science and the Environment. He said he had calculated that the infantry soldier in Vietnam endured up to two hundred times more stress than his W.W. II counterpart (Senate Inguiry hearings 4 February. 1982).

Another contribution to the veterans' problems was his reception on returning to Australia. Veterans learned not to speak of their

participation in the war after experiences of receiving verbal and sometimes physical abuse. When the war ended, those who were its staunch supporters, were unwilling to be reminded of the war not won or of the problems the lost war may

have caused those who they had fought. Those who opposed the war, continued to associate the soldier with the political decisions which committed Australia to fight in Vietnam.

IX-49

Surrounded by a community indifferent or hostile, an unresponsive R.S.L. and flawed Repatriation system, the veteran was often driven even deeper into depression.

By 1979, desperate veterans began to turn to each other. In 1980 the Vietnam Veterans' Association of Australia was formed which documented

veterans' problems and demanded government action. As a result. Senator Messner. then

Minister for Veterans' Affairs, agreed to the establishment of a Vietnam veterans' counselling centre in each capital city, centres quite separate from the unsuccessful Department of Veterans' Affairs.

The centres have been more helpful but there are more problems yet to be solved. There are an

alarming number of veterans who, because of their war-caused psychiatric condition, have lost their families, their jobs and their savings. They are homeless and destitute. There are disturbed veterans and their families in country areas on the brink of family break-up; break-ups which might be avoided with periods of professional counselling. Many veterans receive treatment in

the psychiatric wards of our Repatriation hospitals. On release from hospital they have nowhere to go to gather strength before facing the problems which have accumulated as a result of their years of illness. There are those, too. whose condition may not warrant hospital

treatment, but who are liable to occasional violent outbursts. These veterans learn to recognise the preliminary symptoms of such an outburst but can do nothing to stop it.

45,000 Australians served in the Vietnam war, and an alarming proportion of them are now suffering because of their service.

It is time those who supported Australia’s involvement ion the Vietnam War overcame their indifference and gave the same support as they gave to the war, to those who are now suffering because they fought.

It is time those who opposed Australian

involvement ceased blaming the soldiers for the

IX- 50

political commitment to the war. and recognised that Vietnam veterans, like Australian veterans of previous conflicts, were sent to a theatre of war by the Australian government and served there with distinction.

Let's give them recognition and support.

Let's finally bring the Vietnam veteran home.

Surely we can provide a bed and roof for homeless destitute veterans; provide accommodation in the capital cities for country families needing counselling; and provide a bush retreat, at which discharged psychiatric patients can gather

strength and where veterans, knowing they are unable to contain their rage much longer, can spend a few days calming down.

Let's provide these urgently needed services.

Let's finally bring the Vietnam veteran home.

Vietnam veteran's problems do not end there. The conflict in Vietnam was the first in the history of warfare in which huge quantities of toxic chemicals were sprayed from the air to defoliate forests, destroy crops and kill pests. Those used in the greatest guantities were herbicides made from various mixtures of 2,4-D, 2,4,5-T,

picloram and cacodylic acid. Depending on the combination, these mixtures were labelled Agent Orange, Agent White or Agent Blue.

Also used were the herbicides paraquat, diquat, bromacil, diuron, monuron, distillate-creosote and borate-chlorate. Insecticides used included DDT and malathion.

One possible result of veterans' exposure to these toxic chemicals is a condition known as toxic brain dysfunction, the symptoms of which are similar to those of Vietnam Post-Trauma Stress Reaction. The Department of Veterans' affairs refuses to recognise this possibility, so

that some veterans with these common symptoms. may be receiving the wrong treatment.

There is evidence, too, that veterans' exposure to these toxic chemicals may be the cause of some

IX- 51

of them contracting certain cancers and might also be linked with some of them fathering

deformed children. Many veterans are worried about these possibilities.

The government (some of whose members were

responsible for our participation in the war) and the Department of Veterans' Affairs. have a sorry record in dealing with the chemical issue. That is why the Vietnam Veterans' Association is demanding an enquiry separate from the

departmental and governmental arenas, a Royal Commission, into the possible effects on veterans and their families of the veteran's exposure to toxic chemicals whilst on war service in Vietnam.

Let's give veterans such an enquiry.

Let's finally bring the Vietnam veteran home. (emphasis added) 1 6

In "Debrief" Vol. 3, No. 21, July 1983 it was stated that:

All wars place great stress on those taking part in them but the nature of the Vietnam War ensured that the stress was unremitting. Additionally, because no area was safe in Vietnam, not only soldiers of combat arms but also those soldiers in a supporting role were continally under

threat. This stress has resulted in widespread psychiatric problems amongst Vietnam veterans causing mental torment. family break-up, sickness. alcoholism and poverty. (emphasis added) 1 7

8 .1.3.2 From WAA 's Submissions to the Commission

(i) From WAA's initial submission lodged in November 1983

- Alleged Neurotoxicity of Chemical Agents

In this submission it was stated that:

IX- 52

What is now seen in the veteran population namely the rashes, the problems of temperament,

neurological problems, bronchial problems, cancer and so on; the miscarriages by wives and their other problems, and the illnesses and deformities to be found are predictable given the exposure to

chemicals and the known toxic effects of those chemicals. (emphasis added) 1 0 . . . .

The World Health Organisation's publication, I ARC Monographs 1977, Volume 15: Exhibit 1157 reviews industrial exposure and the effects thereof.

The submission again is that the known toxic symptoms and the aftermath of the accidents reviewed are consistent with veterans'

complaints. 1 9

20

The reference to I ARC Monographs Volume 15: is

presumably a reference to Table 6 on Page 80 of that

monograph, the relevant parts of which are as follows:

IX-53

TABLE 1

(Extracted from Table 6 of Exhibit 1157) Toxic Effects of TCDD in Man

EFFECTS REFERENCES

W

polyneuropathies Goldman. 1972. 1973; Jirasek et al., 1973. 1974

lower extremity weakness Bauer et a1., 1961; Firestone. 1977;

Goldman, 1972. 1973; Jirasek et al.,

1973, 1974; Oliver, 1975; Poland et

a1., 1971

sensorial impairments (sight, hearing. smell, taste) Goldmann, 1972, 1973; Oliver, 1975;

Poland et al., 1971; Ton That. 1977

Psychiatric

neurasthenic or depressive syndromes Bauer et 31.. 1961: Firestone, 1977;

Goldmann, 1972, 1973: Jirasek et al..

1973, 1974; Oliver, 1975; Poland et

al., 1971

The submission then deals with, inter alia, the alleged

neurotoxicity of some of the chemical agents used in

Vietnam. It states:

Some of the known toxic effects of the chemicals

are:

2,4—D

Initially nausea, vomiting. muscular weakness. diarrhoea, swelling of the ankles, feet and legs

with malaise and headaches. Other symptoms are,

somnulence (sic). anorexia, gastritis, increased

IX—54

salivation. sensation of drunkeness (sic). heaviness of legs. hyporacusia (sic). weakness.

rapid fatigue, headaches and vertigo and damage

to the central nervous system — see L37 Page 41.

2.4.D is carcinogenic. ...

Document L37 is "Extracts from Literature on Certain Toxic

Chemicals, Their Use in Vietnam and Elsewhere, and Their

Reported Effects, as Supplied by Mr John Evans to the

Department of Veterans' Affairs".22 The material to

support the allegation of the neurotoxicity of 2,4—D is

found at pp 42~44 of L37 which reads (inter alia):

There has been some alarm (perhaps unjustified)

about the human toxicity resulting from the use

of 2,4—D and its derivatives. Some of the case histories of persons contracting neuropathy as a

result of 2.4—D treatment are presented here to

permit the reader to form his own 0 inion about

the magnitude of the hazard associated with the use of 2,4—D compounds. Goldstein et al 1959

in their report on peripheral neuropathy after

skin exposure to an ester of 2,4—D state that three individual patients. two farmers and a

female bookkeeper, suffered the disorder some

hours after exposure to the 2,4—D formulation

while attempting to kill weeds. The symptoms

progressed through a period of days until pain,

parasthesias and paralysis were severe.

Disability' was protracted and recovery was incomplete even after a lapse of years. They

concluded that there was little doubt that the

symptoms resulted from the percutaneous

absorption of the 2,4—D. The electromyographic

examinations supported the diagnosis of

peripheral neuropathy. Berkle and Ma ee 1963

report a similar case of neuropathy in a 30 year

old farmer four days after exposure to 2,4—D

dimethylamine salt; the symptoms included numbness and incordination (sic) of the hand and

finger muscles and a slow recovery. These

authors conclude that ersons who et eri heral

IX—SS

neuropathy from exposure to 2,4-D are very rare compared to the number of exposures there must be. They state that some individuals may have a predisposition to neuropathy and suggest that all users of these herbicides use protective clothing and wash immediately with soap and water in the case of accidental exposure. 2 3

A 38 year old woman with puerperal depression was admitted having swallowed, 1 hour previously, 40 ml. of 1Verdone' (I.C.I. selective weedkiller containing potassium salts of

2 .4- dichlorophenoxyacetic and proprionic acids)

... The fatal dose of verdone is reported as

greater than 45 ml. Ingestion of

2 .4- dichlorophenoxyacetic acid produces

epigastric pain, haematemesis, tremor,

convulsions, coma, renal failure, peripheral neuropathy, and severe skeletal muscle damage, while proprionic acid produces liver damage. Lung involvement has not been previously reported with verdone. We suggest that lung involvement may

occur with verdone but, unlike the lung damage in paraquat poisoning, it is reversible. (Davies & Jung, 1976) .

Severe sensory and motor symptoms necessitated hospitalisation of three patients, a 52 year old man, a 50 year old woman and a 65 year old man. In each case the disorder began some hours after the use of preparations of dichlorophenoxyacetic acid (2,4-D) to kill weeds; the symptoms

progressed through a period of days until pain, pares thesios (sic), and paralysis were severe. Disability was protracted, and recovery was incomplete even after a lapse of years. There was little doubt that the neurological damage was

done by the percutaneous absorption of spilled 2,4-D. The electromyographic examination supported the diagnosis of peripheral

neuropathy. Since there is no antidote or other specific treatment for 2,4-D poisoning, this herbicide should be used with caution.

(Goldstein et al; 1959 ).

It is probable that 2,4-D dimethylamine salt produced a primary sensory neuropathy in this 30 year old farmer. It is unlikely that a

IX-56

contaminant could be present in sufficient quantities to produce a neuropathy, but even admitting this possibility, it seems likely that preparations containing 2.4-D may produce neuropathy. Therefore, the recommendations of Goldstein, Jones and Brown are emphasised:

shorter periods of exposure, frequent washing of the skin after exposure, and changing of clothes when they become wet with the solution.

Despite the extensive use of 2,4-D preparations. resultant peripheral neuropathy is very rare. and an afflicted individual probably has some predisposition to neuropathy or susceptibility to the toxin. Nevertheless, as it cannot be

determined who is predisposed or susceptible, and as no antidote to 2.4-D intoxication is known, prevention is simpler than treatment. (Berkley & Magee, 1963).

Many cases of peripheral neuropathy are reported at page 128 of the I .A.R.C./W.H.O. Publication No. 15 of 1977, (Exhibit 1157) at page 289

highlights the neurological symptoms being associated with 2,4-D and chlorophenols. (pp 128 and 289 of IARC Monographs Vol 15, 1977: Exhibit 1157) state:

Similar case reports of poisoning in

agricultural workers have been reported following spraying of 2,4-D (Monarca & Di Vito. 1961; Paggiaro et al., 1974; Todd, 1962). The main initial symptoms were

muscular weakness, vomiting. diarrhoea. fever, hyperthermia and tachycardia. In two cases, neurological symptoms occurred, which continued for 40 days to 2 years after

exposure and included loss of deep-tendon reflexes and paralysis of thigh and leg muscles.

Assouly (1951) reported that workers

employed in the fabrication of 2.4-D

developed symptoms of somnolence, anorexia and gastralgia, increased salivation, a sweet taste in the mouth, a sensation of drunkenness. heaviness of the legs and hyperacusia.

IX-57

Subjective clinical symptoms reported among workers using various esters and salts of 2,4-D included rapid fatigue, headache, loss of appetite and pains in the region of the

liver and stomach. Sensitivity to taste and smell was lowered (Fetisov, 1966).

Bashirov (1969) examined 292 persons (248 men and 44 women) engaged in the manufacture of the amine salt and butyl ester of 2.4-D, with exposure ranging from under 5 years to

6-10 years (for 194 and 98 persons,

respectively); 63% of these workers

complained frequently of weakness, rapid fatigue, headache or vertigo. About 20% had disturbances of the cardiovascular system (mainly hypotension and bradycardia) and of

the digestive organs (dyspeptic symptoms and gastritis). The various liver dysfunctions that were found were more pronounced in workers with longer exposures to the

herbicides. (At page 128).

Chloracne and liver impairment, formerly thought to be caused by chlorophenols, were shown essentially · to be due to TCDD

(Hofmann, 1957; Kimmig & Schulz, 1957a,b; Schulz, 1957); the actual aetioloqical cause of porphyria cutanea tarda has not been identified (Poland et al, 1971), and the origin of certain other symptoms,

particularly the neurological ones. may also be other frequently associated substances such as 2,4-D or chlorophenols.

An outbreak of chloracne affected 60 workers at the 2,4,5-T factory of the Dow Chemical Company in Midland, Michigan in 1964

(Firestone, 1977).

Of 29 subjects with features of chloracne working in a 2,4-D and 2.4,5-T-producing factory of the Diamond Alkali Co., Newark, New Jersey. US, 11 had increased excretion

of uroporphyrins. In 3 cases, a diagnosis of porphyria cutanea tarda was

unquestionable; 2 of these had raised serum glutamic-oxaloacetic transaminase levels. Many of the workers, whether or not they had uroporphyrinuria, had hirsutism.

IX-58

hyperpigmentation, increased skin fragility and vesicobullous eruptions on exposed areas of skin (Bleiberg et al, 1964); Firestone. 1977) .

Poland et al (1971) re-examined all of the employees of the same factory in 1969, after the level of TCDD in the

2,4,5-trichloropheno1 had been reduced from 10-25 mg/kg to less than 1 mg/kg and found chloracne in 13/73 workers. A number of subjects had hyperpigmentation or facial hypertrichosis, but no definite diagnosis of porphyria could be made, and only one worker had mild uroporphyrinuria. The authors suggested that chloracne and porphyria cutanea tarda are essentially independent

syndromes. About 30% of the workers

suffered from gastrointestinal symptoms (nausea, vomiting, diarrhoea, abdominal pains or blood in the stools); about 1 0 % of the workers had other systems, such as lower extremity weakness, headache and/or

decreased auditory acuity. (emphasis added at page 289 ).

Because the I.A.R.C./W.H.O. Publication is an international agency document, it is written in such a way as to repeatedly advise the reader that he has to draw his own conclusions. Thus, the contents in the body of the document must be studied, rather than the summaries. (John Evans Personal Observation).

As, however, the changes that may be produced in the central nervous system after sublethal doses seem to be irreparable, though in mild cases a compensatory reduction to the point of freedom from symptoms may be obtained, it is perhaps

timely to urgently advise caution in dealing with and using the chlorinated phenoxyacetic acids. Should the skin become contaminated, the

substance should be removed immediately to avoid percutaneous absorption. (Nielsen et al, 1965). (At pp 42-44) .

IX-59

2,4,5-T

WAA's initial submission does not allege any

neurotoxicity associated with 2,4,5-T on its own. It next

deals with TCDD and states:

TCDD

Its neurological effects: polyneuropathies. lower extremity weakness, sensorial impairment.

Its psychiatric effects: neurasthenic or

depressive syndromes - see page 1555, Transcript of Senate Inquiry and references given. (Page 1555 of the Senate transcript reproduces Table 6 from Page 80 of Exhibit 1157, the relevant parts of which were set out above).

In addition to the properties set out above the neurotoxic potential has to be considered. Certainly 2.4-D has neurotoxic potential. 2,4,5-T with TCDD contaminant can cause

neurasthenic syndrome.

Whilst it may be arguable that these chemicals alone are not shown conclusively to cause all the symptoms certainly the solvents even at sub-toxic levels do cause toxic encephalopathy.(emphasis added) ^ 4

Cacodylic Acid

Sodium cacodvlate and cacodylic acid Carcinogen (or co-carcinogen) and can cause chromosomal damage and chronic illness - see L9, Page 23 et seq and L37. 2 5

The L9 document, the so-called "Report, Dr Fleming and

Summary of quoted material". Is a refinement of document

IX-60

L37. and so the following extracts from L9 summarise

WAA's allegations as to the neurotoxicity of these

compounds, as presented in WAA's initial submission,

namely:

1. Ansul Chemical Co., makers of Agent Blue, state that when an individual is exposed (to cacodylic acid) daily for extended periods, the inspection of skin sensitivity should be supplemented by monthly urinalysis for arsenic. Symptoms of acute poisoning from cacodylic acid are headache, vomiting, diarrhoea, dizziness, stupor convulsions, general paralysis and death. The dosage

reguired to cause these symptoms may be as little as one ounce (28 gramh) of cacodylic acid per human adult. (Orians and Pfeiffer. 1970) .

Cacodylate is converted to the toxic,

inorganic, trivalent arsenic in the body. Sodium cacodylate. Sodium dimethylarsenate; ' Arsecodile; Arsicodile; Arsycodile. An organic compd. of arsenic yielding

inorganic, trivalent arsenic in the body (is excreted partly unchanged, ...) (Merck Index 7th Edition 947).

Pentavalent inorganic compounds -

derivatives of arsenic acid, H3ASO4 , are not in use as medicaments; so it is not

surprising that no case is known in which arsenical medicinal cancer has been observed on this basis; but, as it is known that

pentavalent arsenicals are reduced in the body into trivalent ones (see p. 230), it can be understood that they play a role in occupational cancer (see p. 217).

Some pentavalent organic arsenicals as cacodylates, atoxyl and arsacetine are - or were - frequently used as medicaments; but it seems that they never have proved as

carcinogens; only in case 135 possibly cacodylates were used. (Neubauer, 1947).

IX- 61

Sollman (1950) describes cacodylic acid as a material which has medical properties similar to those of inorganic arsenic "to which it is partly reduced in the body".

Since the reduction is slow the toxicity is reduced but the effects last longer ...

Cacodylic acid, especially when given by mouth, imparts a garlic odor to the breath, sweat and urine. (House et al, 1967:

Exhibit 101). (At pp 24-25).

2. The subjective observation of the workers that forestry areas which have been recently treated with cacodylic acid have an

extremely strong odor of garlic should not be taken lightly. This may indicate

transformation of the compound to arsine gas, a chemical reaction that is already documented . . . since the toxic properties of arsine gas are much more severe than and markedly differ from those of the arsenic

salts. In dealing with forestry workers, or other agricultural workers exposed to organic arsenicals, one should also be alert to the development of either central nervous system or hematological toxicity... (Wagner et al. 1974). (At p 26).

3. During the two months of intensive exposure to cacodylic acid, none of the workers

complained of symptoms or had signs

suggesting arsenical intoxication. This would indicate that the compound is safe to use when proper safety precautions are taken... At the present time, it would

appear that workers exposed to cacodylic acid should be monitored regularly for increased arsenic excretion... The

importance of safeguards, such as the proper clothing during application. cannot be overemphasized. p 32) . ...

(Wagner et al. 1974). (At

4 . Evans considers the paper by Roth. "The

Sequelae of Chronic Arsenic Poisoning in Moselle Vintners" (1957)(Exhibit 692) to be the most fundamental one in relation to Agent Blue (John Evans. Personal

IX- 62

Communication). It is possible that the accidental defoliation of Nui Dat in 1966 from the air was caused by Agent Blue. It is most likely that the amount of trivalent arsenic exposure in Vietnam was more than

that in the Moselle spraying as it was more circumscribed (John Evans Personal

Communication). Between March 1971 and March 1972, only the chemical defoliants Agent Blue and Hyvar were used by the

Australian Force in Vietnam (Hansard, House of Representatives, 15 May 1980: 2790). (At P 44).

To the extent that it is possible to deduce WAA's case on

the neurotoxicity of cacodylic acid from the above

material, it would appear to be that cacodylic acid (an

organic arsenic) is converted in the body to inorganic

arsenic and consequently the neurotoxicity of inorganic

arsenicals is applicable. This must be the allegation

as, otherwise, there would be no justification for the

inclusion in both L9 and L37 of a considerable amount of

information concerning the toxicity and neurotoxicity of

inorganic arsenicals.

The only basis for the case is that cited, namely the 7th

Edition of the Merck Index. Later Editions omit the

reference. It relies on outdated work done at a time when

methods of analysis did not permit distinction between

types of arsenic. The process suggested would be contrary

to the established metabolic fate of arsenic compounds in

mammals.

IX-63

It should be remembered that cacodylic acid is a major

product of the detoxification of arsenic in humans and

that it is readily excreted and not stored in the body.

There is nothing in the literature to suggest that

cacodylic acid is degraded to inorganic arsenic in vivo;

indeed the reverse is the case.

There is an ill-informed fear of arsenic compounds amongst

the general population which probably stems from the well

known uses of toxic arsenic compounds such as arsenic

trioxide as homicidal agents.

Expert toxicologists reject the suggestion out of hand as

does the Commission. 2 6 See further under Cacodylic Acid

infra.

Malathion

The submission next deals with the alleged neurotoxicity

of malathion. It states:

Malathion

(3) Central Nervous System - uneasiness,

restlessness, anxiety, tremulousness, tension, apathy, giddiness, withdrawal and depression, headaches, sensation of floating, insomnia, excessive dreaming and nightmares, ataxia

(involuntary muscular antiox), slurred and slow

IX-64

speech with repetition, drowsiness, difficulty in concentrating, confusion, emotional lability, coma with absences of reflexes, Chegne-Stokes respirations (rhymethic waxing and waning of respiration), convulsions, hyperpyrexia

(excessively raised temperature) depression of respiratory and circulatory centres with hypoprea (slow or shallow breathing) or aprea (cessation of breathing) and fall in blood pressure - see L37 p. 34. (At pp 57-58).

At pp 34-35 of document L37 is a Table that simply sets

out, inter alia, the " CNS manifestations" of "Acute and

Sub-acute Exposures to Malathion".

Paraquat

The submission makes no allegation as to the neurotoxicity

of paraquat.

Chlordane

The submission continues as follows:

Chlordane

Enters by skin, inhalation, absorption, liver poison - L6. In animals: skin irritation, nervous system, liver damage, inarition (sic) atoxia and collapse - L6. It is carcinogenic.

(At p 58).

Document L6 "Pesticides. A Review of their Uses,

Proper ties and Hazards" Department of Health

(Commonwealth) Information Service, November 1951, insofar

IX-65

as it deals with the neurotoxicity of chlordane. states

that:

Chlordane may enter the body by skin absorption, inhalation, and ingestion. It is principally a liver poison and there is also some indication that it is stored in some form in the tissues, especially in the fat. The fatal dose for man has been estimated at 5-60 grams. The

physiological effects noted in animals are moderate skin irritation, central nervous system manifestation, particularly relating to optic centres, liver damage, inanition, ataxia, convulsions and collapse. The onset of symptoms

is 45 minutes after ingestion ... (At p 41).

Dieldrin

The submission next deals with the alleged neurotoxicity

of dieldrin. It states:

Dieldrin

Nervous system neurological: Muscular pains; weakness in legs; general tiredness; increased sleep requirements; paranthesia; headaches; vertigo; orthostatic; paresis (slight paralysis, weakness of limb); co-ordination disorders;

hypes thesia (impairment of variation); reflex variations; vegitive (sic) (functioning involuntary or unconsciously, pertaining to autoromic (sic) nervous system);

overexcitability; EEG abnormal findings. Nervous system - psycholopathological (sic) Reduction in initiative and interest;

hyperesthetic - emotional tendencies; pronounced fluctuation in intensity; memory and

concentration disorders; libido and potency disorders; alcohol intolerance; moments of depression psychosis; reduced drive; affectivity disorders in the narrow sense; impaired mental faculties; See L37 p. 38. (At pp 59-60).

IX-66

Document L37 deals with the possible neurotoxicity of

dieldrin in the following terms:

Weight-loss leads to release of dieldrin from fat The following case history is of interest showing as it does the relationship between the storage of dieldrin in the fat and its release into the system when weight loss developed as a result of symptoms from over exposure.

... the operator developed a severe frontal

headache. He became nauseated and vomited on several occasions and his appetite deteriorated. He felt dizzy, was sweating quite profusely and developed diarrhoea. Over the next four or five days following this epidose (sic) he lost 6.3 kg

in weight as a result of diarrhoea, excessive sweating and loss of appetite. He said he became irritable particularly with the headaches and that he was not normally an irritable person. He also said his memory had deteriorated...

Toxicology of dieldrin In the Shell booklet on the Safe Handling and Toxicology of Dieldrin, 11 symptoms of poisoning are listed with the following comment and I quote:

1A person at risk of absorbing dieldrin, who complains of several of these symptoms, present at the same time, should be regarded as suffering dieldrin poisoning and removed from further exposure. Symptoms which may be present are:

(1) Headache - this is usually frontal and tends to be most severe in the

mornings. Analgesic drugs, such as aspirin and codeine, frequently have no effect. (2) Dizziness. (3) Blurred vision or diplopia. (4) Abnormal sweating. (5) Loss of appetite. (6) Nausea. (7) Insomnia, with nightmares when sleep is

achieved.

IX-67

(8) Changes in personality - eg depression, irritability and loss of memory. (9) Involuntary muscle movements. (10) Unexplained falls without loss of

consciousness. (11) Blackouts or convulsions. (12) Physical examination frequently reveals: (a) Muscle twitching.

(b) Altered deep tendon reflexes, usually exaggerated.'

... Paul (1959) reported a case of dieldrin

poisoning which involved a 29-year-old farmer who consulted his doctor because he was overweight. The doctor gave him some weight reducing tablets and he lost 3.1 kg in a week. He then began to

feel ill, attributed it to the treatment and stopped the tablets. However, the symptoms increased with violent headaches, frontal in nature, drowsiness, and lack of appetite with some twitching of the arms and legs ... (Glass, 1975: Exhibit 650).

Evans suggests that symptoms occurring in

veterans following weight loss are more likely to be due to dieldrin release from fat than dioxin release. (John Evans Personal Observation).

E.E.G. Changes Intoxication by aldrin, dieldrin, endrin, and isodr in may cause convulsions; these convulsions are sometimes preceded by subjective complaints, but quite frequently they occur without

forewarning or without any prodromal symptoms or signs. Occasionally convulsions are preceded by symptoms of myoclonic epilepsy. Therefore myoclonia is considered highly indicative of immediate danger of forthcoming epileptiform convulsions.

Fourteen patients with convulsions caused by intoxication with the abovementioned insecticides all showed specific anomalies in the E.E.G. consisting of bilateral synchronous theta-wave activity and occasional bilateral synchronous spike and wave complexes. believed to be

associated with brain stem injury.

These specific disturbances in the E.E.G. may persist for some time after apparent clinical

IX- 6 8

recovery, but they almost always disappear spontaneously after discontinuation of exposure. (At pp 38-39) .

Lindane

No allegation is made in WAA's initial submission as to

the neurotoxicity of lindane. (See p 61).

WAA' s initial submission makes no other allegations as to

the neurotoxicity of any of the other compounds that are

the subject of this Inquiry. However, it does state:

The world-wide recorded information on chemicals used in Vietnam is enormous and beyond the scope of this submission to attempt to deal with it and draw conclusions which form the W A A submission. Dr John Poliak, Mr John Evans and Dr van Tiggelen

have been engaged to prepare detailed reports ....

W A A relies for its submission upon the above reports when available. All three are being prepared and will be made available to the

Commission as soon as they are received. (At p 53).

8.1.3.2(H) From WAA 's Toxicology Submission dated 31 May

1984: Exhibit 1878

In this submission W A A states:

IX-69

In Vietnam the possibility of chemical poisoning was not considered. The classical symptoms of most chemical poisons being considered are nausea, headaches, fever, dirrhoea (sic). etc were lumped under the all embracing terms of fever of unknown origin (f.u.o.) These illnesses were very common in Vietnam some of short

duration, some of long, but considered all part of a soldiers lot.

The following case reports and articles show just how toxic the chemicals used in Vietnam are known to be. It is emphasised that the effect upon service personnel can be expected to be

compounded by the failure to recognise exposure to toxic substances and to treat them. Civilians are removed quickly from exposure but that just

did not happen in Vietnam. (At pp 29-30).

2,4-D

The submission then deals with the following studies that

are alleged to support the neurotoxicity of 2,4-D:

(i) Metcalf (1957) "Control of Hazards in Use of Agricultural Chemicals - California Experience", American Medical Association Archives of Industrial Health, Volume 15, October 1957 (Exhibit 1878A-T1) at pp

337-352. It is worth noting, however, that Metcalf does not deal with 2,4-D in the text of his article and the only

reference to this compound is found in a question and answer exchange between a conference participant and a Doctor Frank Princi in the following terms, namely:

Is 2,4-D absorbed through the skin? Can 2,4-D cause peripheral neuritis? 2,4-D is not an insecticide; it is a herbicide, at least in this country, although, interestingly enough, it has been used in England as an

IX-70

insecticide. To do so they have had to use far greater quantities of the technical material than we do here. To mv knowledge it does not cause

peripheral neuritis. They have had some cases in England. I know of none in this country. (At p 3 52);

(ii) Goldstein et al "Peripheral Neuropathy After Exposure to an Ester of

Dichlorophenoxyacetic Acid", Journal of the American Medical Association Volume 171, No. 10 (1959) at pp

130/1306-133/1309: Exhibit 77. This article reports on three cases of exposure to a derivative of 2,4-D that apparently

caused prolonged and serious neurotoxic symptoms including peripheral neuropathy. It should be noted, however, that the authors only stated that "the time

relationship was such that it seemed reasonable that the herbicide caused the neurological disease" and later (J.A.M.A. Volume 173, No 1 at page 87) agreed that

they could not rule out the possible role of the petroleum solvent and the

emulsifier mixed with the 2,4-D that the "cases" were exposed to, in the causation of the peripheral neuropathy;

(iii) Todd "A ' Case of 2,4-D Intoxication", Journal of IOWA Medical Society, October 1962 at Pages 663-664: Exhibit 1580, which was a report of a case study of a

man who was exposed to a derivative of 2.4- D that caused nausea, vomiting, fever, limb weakness and loss of sensation in the toes, and rendered him unable to walk for

two years;

(iv) Berkley and Magee "Neuropathy Following Exposure to a Dimethy lamine Salt of 2.4- D", Archives of Internal Medicine, 111. Pages 351-352 (1963): Exhibit 21 which was a report of a case study of a

man exposed to a derivative of 2,4-D that resulted in a pricking sensation in the fingers and toes and then in the other parts of the body; numbness, aching and

IX-71

stiffness in the hands and knees and loss of control in the hands. The diagnosis was primarily sensory peripheral

polyneuropathy. It is important to note that the authors commented that, "Despite the extensive use of 2,4-D preparations, resultant peripheral neuropathy is very rare, and an afflicted individual probably has some predisposition to neuropathy, or susceptibility to the toxin". (At p 352);

(v) Fetisov "Occupational Hygiene in the

Application of Herbicides of the 2,4-D Group", Hygiene and Sanitation, 31 at pp 383-386 (1966): Exhibit 1606. That was a report of an investigation of the effect of 2,4-D on the state of health of persons engaged in its production or its use in agriculture. These persons complained of rapid fatigue, headache, pains in the

liver, poor appetite etc. It is

significant to note that WAA's submission (at p 35) acknowledges that the Fetisov paper does not look at long term effects;

(vi) Fullerton "Toxic Chemicals and Peripheral Neuropathy" Proc. Royal Soc. Medicine Volume 62 February 1969, pp 201-204: Exhibit 681, which is a review of much of

the scientific material on this topic, including many of the papers referred to above. This paper will be dealt with at some length below;

(vii) Berwick "2,4-Dichlorophenoxyacetic Acid in Man: Some Interesting Clinical and

Laboratory Findings", Journal of the American Medical Association, Volume 214, No. 6 (1970): Exhibit 22 which is a

report on a man who accidentally ingested a mouthful of 2,4-D (estimated to be

approximately 30 mis) who then exhibited fibrillary twitching and paralysis of intercostal muscles. It is significant to note that this paper only deals with the acute toxic effects of oral ingestion of 2,4-D as acknowledged by WAA's submission

(at p 37);

IX-72

(viii) Prescott et al "Treatment of Severe 2,4-D and Mecoprop Intoxication with Alkaline Diuresis", British Journal of Clinical Pharmacology. (1979), 7, 111-116: Exhibit

439, which is a report of a self-poisoning with a selective weed killer containing 2.4- D and mecoprop that led to prolonged

deep coma. pyrexia. hyperventilation, hypoxaemia, myotonia, skeletal muscle damage and electrocardiographic changes consistent with cardiomyopathy. Suffice

it to say that this man deliberately

ingested the contents of a lemonade bottle half full of a weed killer which was later shown to contain 10% 2,4-D and 20%

mecoprop;

(ix) Nielsen et al "Fatal Poisoning in Man by 2.4- Dichlorophenoxyacetic Acid (2,4-D): Determination of the Agent in Forensic Materials", Acta Pharmacologica and

Toxicologica, 1965, 22, 224-234: Exhibit 138, which is a report of a fatal

poisoning of a man by an amine salt of

2.4- D. Suffice it to say that the total amount of the poison in the body was set at not less than 6 grams. corresponding to at least 80 mg/kg;

(x) Dudley and Thapar "Fatal Human Ingestion of 2,4-D, a Common Herbicide", Arch. Path., Volume 94, September 1972, Pages 270-275: Exhibit 57, which was a report

on an elderly man with senile dementia who died six days after ingestion of a large amount of 2,4-D;

(xi) Assouly "Desherbants selectifs et

substances de croissance", Achives des Malades Professionnelies, 12 (1951) at pp 27-30 (Exhibit 1878A-T10) which reports that workers engaged in the manufacture of

2.4- D and its ester form suffer drowsiness with a sensation of heaviness in the legs, irritation in the upper airways. loss of appetite, sweet taste in the mouth,

hypersalivat ion, sensation of inebriation, hypersensitivity to noise. digestive problems, anorexia, ptyalism (salivation), vertigo, "asthenie" and "cephalus".

IX-73

(xii) Amirov et al "The Health Condition of Workers Producing the Herbicide 2,4-D", Biological Abstracts 51 (1970) which reported on examinations performed on 292 workers producing 2.4-D for 5-10 years. The examinations revealed complaints of dyspeptic symptoms, general weakness„ easy fatigue, vertigo, headache and insomnia in 31.3%. Furthermore, under clinical examination 50 persons showed moderate functional changes in the peripheral circulation often with a tendency to

hypertension, functional disorders of the nervous system of a neurasthenic character with symptoms of autonomic-vascular variability and asthenic syndrome. The

abstract does not disclose the level of exposure to 2,4-D or whether they were exposed to any other chemicals during the period;

(xiii) Desi et al "New Evidence Concerning the Nervous Site of Action of a Chemical

Herbicide Causing Professional

Intoxication", Acta Physiologica Acad. Sci. Hungarieae. 22 (1962): Exhibit 47, which reports the results of experiments performed on cats given 100 mg/kg of 2,4-D daily for at least a week. The authors conclude that. "On the basis of the

results obtained it is believed that DCPA acts primarily on the central nervous system, paralysing its function. The functional disorders in different organs are merely secondary to the central

nervous effect." (At p 80);

(xiv) Desi et al "Nervous System Effects of a Chemical Herbicide", Archives of

Environmental Health, 4, pp 95-102 (1962): Exhibit 46, which reports the results of experiments performed on rats, cats and dogs following acute (a dose of 200 mg/kg of body weight administered

intraperitoneally) and chronic (the same amount was given daily in the chronic experiments until the death of the

animals) exposures to 2,4-D. The authors concluded that 2,4-D had a damaging effect

IX-74

on the function of the central nervous system in the experimental animals and consequently suggested that, "it must be assumed that human subjects exposed to the action of 2,4-D also may suffer via

smaller dose milder disturbances in function of the nervous system and of higher nervous activity respectively". (At p 102).

The paper by Fullerton "Toxic Chemicals and Peripheral

Neuropathy" (1969): Exhibit 681, referred to above,

reviews much of the data on peripheral neuropathy and puts

in perspective. It states:

Although there are many known toxic substances, it is easy to exaggerate their clinical

importance for it must be remembered that in a substantial number of patients who__ develop peripheral neuropathy no cause is discovered, o w n after extensive investigations have been carried out. When this happens any chemical in

the patient's environment can be a useful scapegoat; but some of the reports of neuropathy alleged to be caused by a particular chemical are not very convincing and once a substance has been

blamed for a particular toxic effect the case against it may be self-perpetuating. Without denying the importance of reporting suspected toxic effects, even if not absolutely proven, it

is vital that, from time to time, the evidence should be critically reviewed.....

The substances which mav be met in industry_and which may cause peripheral neuropathy__may__be listed as follows: I . I I . I I I .

I. Peripheral neuropathy predominant: Lead, acrylamide, organophosphates, thallium; I I . CNS involvement prominant: Carbon

disulphide, methyl mercury, methylbromide; I I I . only__after gross_____overdose: ___ Arsenic, trichloroethvlene. tetrachlorethane,___2,4-D (dichlorophenoxvacetic acid),____penta -

chlorophenol. DDT;

IX-75

IV. Other systems more affected: Carbon

tetrachloride, carbon monoxide.

These substances are surprisingly few in number. (At p 201). ...

The time of onset of symptoms may give an obvious lead to their cause, particularly following accidents. For example, there are in the

literature reports of 7 patients who developed neuropathy which seems reasonably attributable to dichlorophenoxyacetic acid. or2,4-D as it is commonly called (Goldstein et al 1959, Monarco & di Vito 1961, Todd 1962, Foissac-Gegoux 1962, Berkley & Magee 1963). This substance is a

herbicide and poisoning in all instances followed exposure of the skin to the liquid for many

hours. A general illness developed within twenty-four hours and neurological symptoms a few days later, (emphasis added) (at p 202-203).

2,4,5-T and TCDD

WAA's toxicology submission next deals with the alleged

neurotoxicity of 2,4,5-T and TCDD. It states:

2.4.5- T and TCDD In Archive for Industrial Pathology and

Industrial Hygiene 18. 538-555 (1961) (T16) Bauer and Ors: (Exhibit 719) report upon 1 Occupational Poisoning from the Manufacture of Chlorophenols Compounds.

Three groups of exposed workers were referred in the report. The first group of 17 were engaged in the manufacture of pentachlorophenol. The other two groups, one of approx. 60 cases and the other of 31, were engaged in the manufacture of 2.4.5- T.

In both the latter groups it is reported, page 1 1 . . . As with the patients from a third group in the Hamburg area...these trichlorophenol workers suffered additional damage to their health often

IX-76

a long time after occupational exposure had ceased... 1

The health effects for the latter two groups were (p . 2) - 'serious dermal manifestations', residual acne, persistent neuromuscular weakness of the leg muscles, vasovogetative lability and pyschopathological disorders. On page 5 the authors report the workers having pain and weakness in legs, paraesthesis, abnormal

electroencephalogram, headaches. vertigo and tendency to collapse, abdominal pains, gastric secretion disorders and on page < 7

psychopathological changes. Complaints madq by exposed workers were polyneuropathic-like complaints in the extremities, cardiovascular and abdominal symptoms. Other complaints are weakness, tiredness, indisposition, insecurity, disturbed and ill.

It is significant to note that not only are the above complaints frequently made by Vietnam veterans but the following might be said of very many veterans (page 7, 0.5).

...they complained of affectivity changes in the narrow sense in the form of increased emotional excitability, irritability, a tendency towards furious outbursts and also a certain apathy.

Other complaints made by the exposed workers which correspond' to veterans' complaints are p.7, 0.7 - '...reduction in potency, mostly a decrease in libido...', sleep disturbances and alcohol

intolerance.

Page 8 under Discussion 2. refers to liver

damage, chronic bronchitis and myocardium damage.

It is important to note that symptoms and

complaints listed above are some years after exposure. It is also important to note, as is to be expected, not all workers are affected in the same way and to the same degree.

Initial symptoms of the exposed workers were eye, respiratory tract irritation, headaches, dizziness, nausea, severe skin irritation, chloracne, fatigue, nervousness and intolerance to cold, (emphasis added at pp 46-48). ...

IX-77

A report by P.J. Goldman from the Medical Dept, of Baden Aniline and Soda Factory Ltd (BASF) was published in 1972 (T20) . The report is of an accident which occurred on 17th November 1953, during the manufacture of 2,4,5-T.

Initially 42 workers were exposed which resulted in a mass poisoning - see Figure 3. page 4.

Half this number had initial dermatitis only but the cases of six are noted on page 5. Cases A

and B were examples of the transfer of the toxic chemical to others who were not directly exposed. Case B is a dramatic example of

exposure. The son of an exposed worker had not been at the site of the accident. Cases D, E and F demonstrate the long term dermatitis effect.

The other cases reviewed show severe but

differing symptoms which affected workers. Case H hung himself. Case I died from a number of

possible causes related to the poisoning.

Under discussion p. 11 is noted that, in

accordance with the literature, the result was not only chloracne but 'serious dermal damage, liver diseases and damages to other internal organs as well as changes in the nervous system.1

A further report by Goldman in 1973: (Exhibit 75) refers to the same accident (T21) at BASF in 1953 (T21). (At pp 50-51). ...

The next paper referred to published in

Ceskoslovencka Dermatologie, 48 No. 5. 306-317 (1973), (T-24) is by Jirasek and Ors and is entitled "Acne Chlorina and Porphyria Cutanea Tarda During the Manufacture of Herbicides": Exhibit 105. Again the report is of an

industrial accident whilst manufacturing 2,4,5-T.

Page one reports two deaths from the poisoning and 1 hepatic lesion disturbance in porphyrin lipids and protein metabolism and neurological and psychological changes'. ...

Symptoms complained of were 'tiredness, weakness of lower limbs, muscular pain, insomnia and excessive somnia, excessive sweating, loss of

IX-78

appetite, headaches and a number of mental and sensual disturbances', (p 12).

At the foot of the page is a reference to the

fact that after eight years of treatment there was no improvement, a dismal prognosis for at least some exposed veterans.

Then on page 13, of the total 78 exposed persons 70 had damage to the nerve system verified by EMG tests and the majority had psychological

disturbances. Three more of the exposed persons died, one suffering 'porphyria, extremely fast cerebral aterosclerosis with atypical

morphological finds and dementation took place'. Two of the patients died due to bronchial

carcinoma.

The authors (page 14) believe that T.C.D.D. caused the detrimental effects. (At pp 52-53).

The Jirasek et al 1973 paper: (Exhibit 105) does not (at

page 12 or elsewhere) suggest that the symptoms of

"tiredness, weakness of lower limbs, muscular pain ...

etc" persisted for 8 years as suggested in the above

extract from W A A Toxicology Submission. The authors make

it very clear that it was the condition of "acne chlorina"

that had persisted in some cases for 8 years without

improvement. It is also worth pointing out that the

authors prefaced their list of complaints, ie "tiredness"

etc, with the words "our patients had a number of

subjective complains" (sic) that W A A did not refer to in

the above extract from its toxicology submission.

The submission continues as follows:

IX-79

01iver in British Journal of Industrial Medicine 1975, 32. 49-53: (Exhibit 143) reviews the case histories of three scientists who had minimal exposure to TCDD.

On p . 50, Case A suffered initially chlorine and elevated blood cholesterol. Case B suffered chloracne and after some two years, abdominal pains, weight loss, headaches, loss of vigour and fatigue, irritability, periods of anger. hirsutism difficulties, difficulties with mental and muscular co-ordination and blurred vision. He also had raised serum cholesterol. Case C had

symptoms similar to Case B but without skin complaints (no chloroacne)(sic) or headaches.

Under conclusion p .52 is the following:

1 The history of these three patients

emphasises that dioxin must be regarded as a highly toxic chemical and even those working with laboratory quantities with normal precautions are at significant risk.

Intoxication may occur in the absence of abnormal liver function tests, and urinary porphyrinas and even chloracne and more fundamental physiological effects may be apparent after a long interval extending to two years or more after initial contact1.

It has often been suggested that veterans who were said to be healthy upon discharge could not be suffering from chemical toxicity. Scientist B and C who had minimal exposure would almost certainly have been discharged, if they had been

in the army, as healthy and had the same

arguments as have sometimes been applied to veterans, applied to them. (At pp 54-55).

It is significant to note that in the Oliver paper

(Exhibit 143) his conclusions section goes on to say:

The evidence presented above, although far from conclusive, suggests those accidentally exposed

IX-80

to dioxin may be subject to long delayed toxic effects. Clearly these findings need

confirmation from larger numbers of cases. Unless specifically looked for. symptoms could readily be missed, as could their possible

relationship to earlier dioxin absorption, (emphasis added) (at p 52).

Cacodylic Acid

The submission next deals with the alleged neurotoxicity

of cacodylic acid. It states:

Agent Blue (Sodium Cacodylate/Cacodylic Acid) The literature, which extends for over a century, refers to organic and inorganic arsenical combination. Cacodylic acid is an organic acid whilst sodium cacodylate is an inorganic salt (of an organic compound).

28 Ed. Martingale (sic) at p. 1754: (see Exhibit 774) says that cacodylic acid is reduced to an inorganic acid in the body and that it has the same effects in the body as arsenic trixoide.

(sic) When considering the literature in

relation to arsenical poisoning the effects of organic, inorganic forms of arsenic must be considered as well as arsenic trioxide.

To reiterate, this reference itself relies upon the 7th

Edition of the Merck Index. The only basis for the case

is that cited, namely the 7th Edition of the Merck Index.

Later Editions omit the reference. It relies on outdated

work done at a time when methods of analysis did not

permit distinction between types of arsenic. The process

suggested would be contrary to the established metabolic

fate of arsenic compounds in mammals.

IX- 81

It should be remembered that cacodylic acid is a major

product of the detoxification of arsenic in humans and

that it is readily excreted and not stored in the body.

There is nothing in the literature to suggest that

cacodylic acid is degraded to inorganic arsenic in vivo;

indeed the reverse is the case.

There is an ill-informed fear of arsenic compounds amongst

the general population which probably stems from the well

known uses of toxic arsenic compounds such as arsenic

trioxide as homicidal agents.

Expert toxicologists reject the suggestion out of hand as 27 does the Commission.

The submission continues:

In addition to the above, arsine, an extremely toxic gas produced in the atmosphere by

transformation by microfungal action on cacodylic acid - see The British Medical Journal V3, 24 th August, 1974 p. 487 (T38) . Further, sewage fungi can have the same effect - see Bulletin of

Environmental Contamination & Toxicology Vol 9, No. 2. 1973 p. 84 (T39).

The result is therefore, in addition to the possibility of exposure by inhalation, ingestion and/or dermal contract, those soldiers who passed through recently sprayed areas could have

breathed in the decomposition gas, arsine.

IX-82

Acute signs of poisoning reported by Martingale (sic) p . 1754 are severe gastric pain, vomiting, profuse watery diarrhoea proteinuria (presence of protein in the blood) numbness and tingling of extremities, thirst and muscular cramp. (At pp

65-66) .

The article "Arsenic Makes A Comeback", referred to above

as document T38, is not as firm on the "transformation"

point as the above extract from W A A submission suggests.

The authors state that:

After application for its intended purpose this compound may be transformed into arsine by microfungal action. Fortunately none of the American foresters experienced the burning skin,

acute dysphagia or respiratory distress caused by exposure to arsine. This degradation into arsine by biological action is a process to which

attention was forcibly drawn in Britain 30 years ago when some arsenical residues from a chemical works accidentally entered a public sewer, with alarming results at the local sewerage treatment

plant. A close watch is still needed on the fate of any other arsenical compounds used in industry or agriculture. (emphasis added) (at p 487).

The submission continues as follows:

The effect of inorganic arsenic upon 57 patients was studied and reported upon by R.B. Jenkins in Brain, 1966. 89 p. 479 (T40) under the hearing "Inorganic Arsenic and the Nervous System": Exhibit 1625.

Thirty seven patients suffered from neuropathy and "a history of preceding gastro-intestinal illness was obtained from 27 of them".

On page 483 the author says "The prognosis of recovery from neuropathy depends upon its

IX-83

severity. Complete recovery occurred in purely sensory and the mildest sensorimotor case". Gastro-intestinal illness was. of course, very common in South Vietnam.

It is significant to note that the various

symptoms and ultimate result of those persons reported upon in the Appendix - Selected Case Reports p. 492. (emphasis added) (at pp 66-67).

The Jenkins paper: Exhibit 1625 referred to as document

T40 reports on the examination of 57 patients (11 of whom

were children under 6 years of age) following their acute

poisoning by various forms of inorganic arsenicals.

The authors indicated that the probable sources of arsenic

in the adults were: attempted homicide, 11; attempted

suicide, 13; accidental ingestion, 5; medicinal arsenic.

1; illegal alcohol, 6; and unknown. 10. The sources of

the arsenic for the other 8 patients is not discussed, the

arsenic poisoning only being identified by excessive

guantities of arsenic in their urine, hair or nails.

The submission continues as follows:

The next paper referred to is to be found in

Archives of Environmental Health Vol. 24, April 1972 (T41) page 277. (Tarrant et al 1972:

Exhibit 701). Forestry workers were required to wear protective clothing whilst using arsenical herbicides (cacodylic acid). The study shows that the workers absorbed quantities of arsenic and point out how careful it is necessary to be

to prevent absorption. As has been pointed out

IX-84

previously, servicemen in Vietnam were

(generally) not required to wear protective clothing, nor warned of the possible damages of exposure to herbicides. (At p 67).

The Tarrant paper: Exhibit 701, was a study of forestry

workers exposed to cacodylic acid on a daily basis over a

9 week period. Although the authors indicate that no

evaluation of the health effects of this level of exposure

can be made from their study they nevertheless stated that:

No health problems were encountered in the study group that could be classified as arsenic

poisoning. There were 136 man weeks of exposure to arsenical silvicides recorded for study members. During that exposure period, 14 men complained of headaches, six of abdominal cramps, five of weakness, four of nausea and one of skin

rash. The controls, observed for 27 man weeks had one episode of nausea and one of weakness. The number of persons, especially controls. under observation was small; and no firm conclusions can be drawn, although the large number of

reports of headache may have some significance. The crew members were aware that they were part of a health study of an arsenic compound and, as a result, may have overreported symptoms. They did not, however, have an increased rate of sick

leave over other Forest Service employees, (emphasis added at p 280).

W A A submission continues as follows:

A further such report is to be found in the .. . (Annals of Internal Medicine) Vol 28, February 1974, Page 77 (T43). (Wagner et al, 1974:

Exhibit 709). Again cacodylic acid was the herbicide used. At page 79 a warning is given as to the seriousness of the possibility of arsine gas being present by transformation. (At p 68).

IX-85

The Wagner et al paper: Exhibit 709, was a survey of

forestry workers exposed to cacodylic acid on a daily

basis during a two month period. It was calculated that

the average exposure to cacodylic acid (dry weight) was

870 grams per man per week. Significantly enough, the

authors stated that:

During the entire period of exposure, none of the individuals lost any time from work. One worker did complain of a two day episode of mild nausea, diarrhea and generalized aches. However, he did not seek medical attention for this and took no

type of medication or time off. (At p 78). ...

Although occupational studies on workmen

chronically exposed to arsenic salts have been performed, these compounds, with the exception of the study by the Ansol Company, have been based on workers exposed to inorganic

Occupational studies do indicate that the salts. worker

chronically exposed to inorganic salts; will excrete an average of 70 micrograms per liter without symptoms of arsenic intoxication and at levels as high as 5 milligrams per liter may be

reached. However, it should be emphasised that these figures reflect exposure to inorganic arsenic and a considerably different toxic effect mav theoretically occur as a result of the

organic compounds with which this report deals.

During the two months of intensive exposure to cacodylic acid, none of the workers complained of symptoms or had signs suggesting arsenical intoxication. This would indicate that the compound is safe to use when proper safety

precautions are taken. ...

The subjective observation of the workers that forestry areas which have been recently treated with cacodylic acid have an extremely strong odor of garlic should not be taken lightly. This may

IX-86

indicate transformation of the compound to arsine gas, a chemical reaction that is already-

documented . If this reaction does occur,

observations of the urinary excretion of arsenic may have little meaning since the toxic

properties of arsine gas are much more severe than and markedly different from those of the arsenic salts, (emphasis added) (at p 79).

However, it must be realised that neither the Tarrant et

al study: Exhibit 701 nor the Wagner et al study: Exhibit

709 found any health effects suggestive of arsenical

poisoning amonst the workers exposed to cacodylic acid on

a daily basis for periods ranging from two through to nine

weeks. Consequently, the two studies cited by W A A

provide no evidence of any toxic effects from exposure to

any such arsine gas.

W A A submission continues as follows:

Turning then to the transformal product of Agent Blue, arsine.

Eight sailors were affected by this gas upon a ship, Asia freighter. Symptoms were fever, weakness, nausea, vomiting, diarrhoea, abdominal pain, haemoglobinuria - British Medical Journal

6th September, 1975 (T54) p. 559.

The symptoms are consistent with those described as fever of unknown origin or pyrexia of unknown origin.

Possible consequences of such poisoning are peripheral neuropathy, fragmentation of myelin, disintergration (sic) of the axis cylinder, neurotoxicity. Residual disability is said to be not uncommon - see page 562. (At page 70).

IX- 87

Document T54 "Arsine Toxicity Aboard the Asia freighter"

by Wilkinson et al reports a study of sailors acutely

exposed to arsine gas in a confined space for between 1

and 3 3/4 hours following the leak of an arsine gas

cylinder, so the severe symptoms referred to above are

hardly surprising.

Finally, in connection with Agent Blue W A A 1s submission

concludes:

Agent Blue, (including its metabolites and decomposition products) toxic characteristics are that it is a carcinogen, mutagen, it affects skin, blood, jus neurotoxic. is a respiratory poison, effects (sic) liver, kidney, heart, brain, lymphathic system and testicles, (emphasis added) (at p 71).

DDT

The submission then turns to the toxicity of DDT and, in

connection with its alleged neurotoxicity, states:

In animals DDT 'produces varying degress of gross and histologic damage to the liver and other organs and signs of central nervous system toxicity1 see Deichman: 1 Toxicology of DDT and Related Chlorinated Hydrocarbon Pesticide1 in Journal of Occupational Medicine April 1973, Vol.

14. No. 4 (T59).

IX-88

Ά NIOSH Publication No. 78 - 200 under the

heading "Special Occupational Hazard Review of DDT (T60) reviews the toxic effects of DDT. Commencing at p. 117 is a summary of the known effects.

On that page is reported the earliest symptoms of the poison as being paraesthesia and tremor of the extremities, confusion, malaise, headache, fatigue and delayed vomiting.

On page 118 is reported neurologic dysfunction, polyneuropathy, paraesthesia, tumors and convulsions.

Page 119 at 0.4:

1 Sanchez - Medal et al (1963 ) presented circumstantial evidence that implicated DDT as a· cause of aplastic anemia (failure of cell production in the bone marrow) and thrombocytopenia (decrease number of blood pablets). However, the association of these conditions with B.H.C. and other chlorinated hydrocarbons is on firmer ground.

On pp 120, 121, 122 are a list of known effects of DDT poisoning. (At pp 73-74).

The Deichmann paper referred to as document T59 states:

Chronic exposure of experimental animals to toxic doses of DDT produces varying degress of gross and histologic damage to the liver and other organs and signs of central nervous system

toxicity.

Also, significantly enough, the author states:

More recently, it occurred to us that patients with liver or central nervous system diseases may have elevated tissue retention of these

pesticides. ...

IX-89

Out study presented no evidence that the diseases were responsible for the elevated retention of DDT and other organochlorine pesticides, nor did our investigation present evidence that the

increased retention of pesticides caused or contributed to the severity of the diseases (Deichmann & Radomski. 1968; Redomski et al 1968). (emphasis added) (at pp 285-286).

The NIOSH publication "Special Occupational Hazard Review

- DDT" referred to above as document T60 discusses the

neurotoxic symptoms referred to in the above extract from

the W A A submission, in the context of either high doses

of DDT taken orally or prolonged occupational exposure to

this compound. Significantly, it then goes on to consider

at some length the volunteer studies and studies of

occupationally exposed workers. Those studies failed to

disclose any evidence of the neurotoxicity of DDT in spite

of, in some cases, heavy doses over several years. (See

pp 119-127). The Report concludes:

Although several incidents of poisoning after accidental ingestion have been reported. DDT is of relatively low toxicity for humans. The estimated LD50 is about 250 mg/kg and the median dose for clinical effects is about 10 mg/kg. Workers exposed for long periods to technical DDT

and absorbing 18-42 milligrams per day, as reflected by residue concentrations up to 1.1 ppm in blood and 650 ppm in fat, showed only minor or equivocal clinical signs ... (At p 147).

W A A submission concludes in connection with DDT that:

IX-90

DDT is, in addition to other toxic effects, a carcinogen and neurotoxic. (At p 75).

Dieldrin

VVAA's submission then turns to the toxicity of dieldrin

and, in connection with its alleged neurotoxicity, states:

Reference to this insecticide is to be found in 28 Ed. Martingale (sic) p. 836, and in 'Clinical Toxiciety (sic) of Commercial Products Acute Poison1, Section III (Therapuetics (sic) Index).

... on page 122:

'In contract (sic) to acute poisoning after repeated exposures several spraymen developed a syndrome undistinguishable (sic) from idiopathic epilepsy, except that it ceased upon the exposure was terminated (Hayes 1957). A motor

polyneuropathy resembling the Guillain - Barre syndrome is a rare complication of exposure (Jenkins and Toole, 1964)... Mild and transcient (sic) injuries of kidney (edema (sic) of tabular epithetuim) and liver . . . have been described

... In one case evidence of liver damage

persisted for more than one year'.

Another publication of significance is the Bulletin of World Health Organisation, 1959, 20, 891-892 (T61) Dr Wayland J. Hayes reports that illness has recurred moths (sic) after the last

exposure. On page 904:

'It is true that after having a fit, some

sprayman have continued their occupational exposure to dieldrin without disasterous (sic) effects. However, the recurrence of symptoms in men and animals after exposure has stopped raises

the possibility that dieldrin produces a

morphological and/or bio-chemical lesion which persists for some time and may give rise to

recurrent illness...

IX-91

O n the s am e p a g e :

'Many of the cases which have been recognised as dieldrin poisoning have involved serious illness... Recurrent convulsions have been observed in experimental animals and occasionally persist until the animal dies at an old age. In addition to sudden falls, unconsciousness and convulsions, another disturbing signs (sic) in some cases of dieldrin poisoning in man and animals is mental disorder. In man the trouble has taken forms ranging from loss of memory,

insomnia and nightmares to mania. It is reported that two men have died in convulsions following exposure to dieldrin ...

Dieldrin is. in addition to other toxic effects, a carcinogen and neurotoxic. (At pp 76-78).

Malathion

W A A 1 s toxicology submission next deals with the alleged

neurotoxicity of malathion. It states:

Malathion This insecticide is one of the organo phosphate group.

A NIOSH publication of June, 1976 deals with 1 Occupational Exposure to Malathion1 (T62).

Pages 20-49 deals with effects upon humans. It is to be noted that the symptoms of malathion poisoning are reported in Table 111-2 on p. 36 et seq. At p 37 are set out the symptoms of CNS

manifestations. They are uneasiness,

restlessness, anxiety. tremulousness, tension, apathy, giddiness, withdrawal and depression, headache, sensation of "floating", insomnia with excessive dreaming (nightmares), ataxia, slurred and slow speech with repetition, drowsiness, difficulty in concentrating, confusion, emotional

lability, coma with absence of reflexs, (sic)

IX-92

Cheyne-Stokes respirations, convulsions, hyper-pyrexia, depression of respiratory or aprea and fall in blood pressure.

Archives of Neurology 14 (1966) 611-616 (T63) describe a near fatal case of malathion

poisoning. At page 615 under the heading of Summary:

... Respiratory muscle weakness, the

muscarinic manifestations of cholinesterase inhibitions, pneumonitis created by the hydrocarbon carrier of the insecticide and pre-existing pulmonary illness combined to create severe the prolonged pulmonary

insuf ficiency....

This chemical is a neurotoxic and alligen (sic) in addition to its other toxic properties. (At pp 79-81).

The NIOSH paper "Occupational Exposure to Malathion"

referred to as Document T62 sets out "CNS Manifestations"

associated with acute and sub-acute exposures to

organo-phosphate insecticides. The cases relied upon all

referred to in this paper to support the CNS

manifestations set out therein, either involved accidental

or intentional ingestion of large guantities of

organo-phosphate insecticide (not always involving

malathion) or long-term exposure to organo-phosphate

compounds in an occupational setting. It should also be

realised that the CNS manifestations set out in the NIOSH

publication are drawn from a paper by Namba et al

"Poisoning Due to Organo-Phosphate Insecticides - Acute

and Chronic Manifestations" (1971): Exhibit 671, which

concludes that:

IX-93

Although studies have indicated neurotoxicity in some organophospha te insecticides in certain species of experimental animals, persistent neuropathy in man by poisoning due to

commercially available organo-phosphate insecticides seems exceptionally rare,

considering the large number of incidents of acute poisoning. Manifestations were variable among reported patients and not comparable to the

results in experimental animals. (emphasis added) (at p 487).

The Archives of Neurology Paper "Accidental Malathion

Poisoning" referred to above as Document T63 deals with a

case of the accidental ingestion of a large amount of

malathion with nearly fatal consequences. It would appear

to have no relevance to either short or long term exposure

to low levels of malathion by either the dermal or

inhalation route.

W A A 1s toxicology submission continues as follows:

Chlordane

Chlordane is in addition to other toxic effects a carcinogen and neurotoxic. (At p 82).

Dapsone

28 Ed. of Martingale (sic) page 1489 reports Daprone (sic) to cause anorexia, nausea,

vomiting, headache, dizziness, tachycardia, nervousness, insomnia, skin disorder ... (At p 83).

IX- 94

Picloram

The WAA 's toxicology submission makes no allegation as to the neurotoxicity of picloram (see page 84).

The W A A submission continues. as follows:

Lindane BHC

A review of the toxicity of gamma benzene

hexachloride toxicity is to be found in Archives of Dermatology, Vol 113, March 1977, p 353 (T65).

Page 354 deals with human use. Symptoms of

toxicity are reported at the foot of the centre column as 1 nausea, vomiting, convulsions, repsiratory (sic) failure with cyanosis and sometimes death'...

Symptoms of poisoning are vomiting, restlessness, muscle spasm, atoxia, convulsions, central nervous depression, pulmonary edema, headaches, irritation in the eyes, nose, throat, dermatitis and urticarisa occasionally. (At pp 84-85).

The Archives of Dermatology paper "Gamma Benzene

Hexachloride Toxicity" referred to as document T65 makes

it quite clear that the symptoms referred to. as set out

in the above extract from W A A submission, are the

symptoms following acute poisoning after oral ingestion of

this compound. The paper does not reveal any evidence of

neurotoxicity of this compound following low level

exposure even over long periods of time.

WAA's toxicology submission makes no allegations as to

IX- 9 5

the possible neurotoxicity of paraquat. diquat. bromacil.

diuron or monuron. The submission merely states that.

"these chemicals appear to have been used in small

quantities in South Vietnam." (At p 87).

Further the toxicology submission makes no allegation as

to the neurotoxicity of pyrethrins (see page 88).

9. EVIDENCE IN SUPPORT OF WAA'S NEUROTOXICITY ALLEGATIONS

9.1 Dr van Tiggelen

There is no doubt that W A A relies heavily upon the work

of Dr van Tiggelen to support its allegations of

neurotoxicity.28

9.1.1 "Organic Neurasthenic Depressive Syndrome"

29

The report by Dr van Tiggelen states, "a sub-group of

Vietnam Veterans with neuro-psychiatric complaints is

suffering from an organic neurasthenic - depressive

syndrome with demonstrable objective signs of

encephalopathy and neuropathy" and that "exposure to

potentially neurotoxic chemicals has been a major factor

IX-96

contributing to the development of neuro-psychiatric

pathology."30

Dr van Tiggelen defines "organic neurasthenic depressive

syndrome" in terms of symptoms identified from various

sources„ namely:

(1) The work of Ross et al, especially "Specificity

of Psychiatric Manifestations in Relation to

Neurotoxic Chemicals", Acta Psychiat. Scand

(1983) 67. supplement 303. 100-104. Dr van

Tiggelen states:

Ross (1983) puts forward that any toxic chemical affecting the nervous system produces a non-specific syndrome: a non-specific neurasthenic syndrome of organic base, consisting of complaints such as asthenia, fatigue, weakness, headaches, dizziness, insomnia, nightmares, indecision, anxiety, tension, depression and forgetfulness.

He shows that apart from this

non-specific syndrome. other symptoms can be found, being specific for the neurotoxic chemical involved. As such he presents "erethism" ie irritability, excitability, temper, quarreling (sic) and xenophobia (shyness and

sensitivity), caused by

mercury-exposure.

In workers, exposed to organo-tin, known limbic neurotoxin (Walsh 1982, Valdes 1983) he reports as a specific

IX-97

symptom " bouts of depression" and "attacks of rage and temper", (emphasis added)31

(2) Dr van Tiggelen's own "clinical observations in

1980", based on "incidental observations" of

"younger members of the farming community" (some

of whom came because " they were concerned about

their failing health, which they related to a

possible effect of herbicides") and "not on hard

32

scientific epidemilogical data" Dr van

Tiggelen states:

In some twenty patients I found an

organic__________ neurasthenic-depressive syndrome:

- fatigue„ apathy. lethargy. loss of energy, loss of libido, problems with memory and concentration, personality change, irritability, attacks of uncontrollable rage and anger, followed by bouts of deep depression and

remorse, lasting for some days.

- neuritis-like complaints: numbness, pins and needles, tingling, itching.

- vague complaints like hyperhidrosis, hypersalivation, gastro-intestinal symptoms of nausea. diarrhoe (sic), constipation, sleeping problems.

A very common complaint was intolerance for alcohol.

At the end of 1980 I saw some (20)

Vietnam veterans. presenting with similar complaints ("claiming exposure to chlorophenoxv herbicides during the Vietnam War), (emphasis added).

IX-98

(3) Dr van Tiggelen's own "clinical observations" in

1983 when he was consulted by forty Vietnam

veterans, mostly referred by WAA. Dr van

Tiggelen states:

In view of the self-selected group of veterans, the brief period involved, the limitations of private practice in the broadest sense of the word, I like

to stress that this report is in no way a scientific document, but rather an cumulation (sic) of clinical

observations.34

The general pattern of complaints, noticed over the last few years, is increasing fatigue, apathy and

lethargy, reduced libido and vague neuritis complaints. The symptoms that seem to cause most concern are the

increasing problems with meory (sic) and concentration. These cognitive complaints, in combination with the excessive irritability, alternating with periods of severe depression and

remorse, are perceived as a threatening condition for which help is sought.35

Having defined the "neurasthenic depressive syndrome"

apparently as a combination of all or any number of the

symptoms set out above from three sources. Dr van Tiggelen

expresses the opinion that: I

I suggest that this neurasthenic-depressive syndrome can be considered as the non-specific symptomatology caused by exposure to neurotoxic chemicals (Ross 1983), reflecting an organic base

in an abnormally low level of vitamin B12 in cerebrospinal fluid ....

IX-99

The strong similarity in symptoms, signs and response to treatment in Vietnam veterans on the one hand and in the other groups on the other

hand, seems to indicate that the common factor of exposure to chemicals is a decisive one,

(emphasis added).·16 . . . .

Apart from this non-specific syndrome the Vietnam Veterans appear to have as a specific symptom the presence of attacks of rage and anger, sometimes uncontrollable and resulting in physical

violence, followed by bouts of severe depression and remorse. As rather specific symptoms

sleepiness and muscle twitching are mentioned, (emphasis added).37

W A A clearly based their general allegation that many of

the chemical agents that were used in Vietnam can and have

caused neurotoxic and neuropsychiatric problems in

Australian Vietnam veterans, on the opinions of Dr van

Tiggelen.

9.1.2 REJECTION OF DR VAN TIGGELEN1S VIEWS - REASONS

However, for the reasons that follow, the Commission finds

that Dr van Tiggelen1 s thesis and opinions are of very

little, if any, probative value and are certainly not to

be preferred to the other contrary thesis and opinions on

neurotoxicity and on possible causes of veteran health

problems.

The reasons for the rejection of the van Tiggelen1 s views

can be summarised as follows:

IX-100

(1) Dr van Tiggelen is a general medical practitioner

with no specialist qualifications. He is not a

psychiatrist, a neurologist nor a toxicologist.

He bases his opinions upon a selective and biased

review of scientific literature and his limited

experience in private practice38;

(2) Apart from his "clinical impressions". the data

upon which he relies deal with chemical agents

which were not used in Vietnam and with human

exposure to those agents in high doses and/or

over long periods of time.

For example. reliance is placed upon the work of

Ross et al. That work deals with "neurotoxic

chemicals" namely. tetraethyl lead, inorganic

lead, inorganic mercury and inorganic tin

compounds. Particular reference is made to

dimethyltin dichloride, methyl chloride and "the

most toxic" trimethyltin chloride. Furthermore,

the "non specific syndrome" identified by Ross is

discussed in the context of heavy acute

occupational exposure to the stated chemicals

with no indication as to whether "the effects are 39 long standing"

IX-101

(3) The only chemical agents referred to by Dr van

Tiggelen that were used in Vietnam were 2.4-D,

2,4,5-T (contaminated with TCDD), DDT and the

solvent n-hexane. The evidence cited to support

the neurotoxicity of these compounds is at best

limited; what exists related to acute neurotoxic

effects following heavy accidental, occupational

or experimental exposure;

(4) No attempt is made to demonstrate an association

between disability and any specific chemical.

(5) The submission contains no evidence that the

characteristic syndrome results from exposure to

chemicals used in Vietnam;

(6) Dr van Tiggelen himself qualifies his thesis and

opinions in his report to such an extent that he

is effectively saying nothing of probative

value. He states:

(a) In view of the self selected group of veterans, the brief period involved, the limitations of private practice in the broader sense of the word, I like

to stress that this report is in no wav a scientific document, but rather an (ac)cumulation of clinical

manifestations.40

I X-102

(b) To what extent (if any) a direct

neurotoxic effect of the chemicals on the central nervous system is possibly involved or to what extent (if any) an indirect neuro-toxic effect, involving subclinical liver dysfunction and or estrogenising effects of chemicals, is possibly involved. is at the present state of knowledge unclear.

To what extent chemical-induced

psychological and emotional impairment contributes to the development of a delayed stress syndrome seems to be a very relevant question.

To what extent exposure to chemicals in combination with other factors can contribute to the development of

sub-clinical liver dysfunction, increasing the individuals

vulnerability for neurotoxic effects of alcohol, seems____to____be____equally

relevant.(sic)4i

(c) Circumstantial evidence is presented that the neurasthenic-depressive syndrome in Vietnam Veterans shows remarkable similarity in symptoms, signs and response to symptomatic

treatment with the phenomena observed in people with a history of

occupational long-term or accidental short-term exposure to chemicals including dioxins ....

Far more efforts have to be made in

basic research into this matter: too much is unknown about the effects of chemicals on health. Such research will not only be important for the

Vietnam Veterans, but also for society as a whole, who (sic) is gradually

going to be exposed to as many

chemicals as people in Vietnam have been exposed to.

However. at the same time, pending the results of more research, the people in need should be provided for. (emphasis added throughout).42

I X-103

(7) Dr van Tiggelen also made the following

admissions and concessions during his oral

evidence:

(a) That reduced psychological coping capacity

can be related to non chemical events and 43

could occur without any "events";

(b) That his whole thesis rests upon

44

"circumstantial evidence";

(c) That he was not before the Commission to

present any case against particular chemical

agents used in Vietnam and that he was not

interested in the cause of neuropsychiatric

problems. During questioning by Mclnnes Q C

(for W A A ) the following exchange occurred:

On the assumption that a person had been exposed to chemicals in

Vietnam, can you express any opinion as to what was the most likely cause of soft neurological signs? --- There are a couple of restrictions that have to be brought in. I do not

know to what extent people have been exposed, and that is what I have

emphasised yesterday. I do not even care. I am not really concerned

about what has caused the problem. I have a patient in front of me who obviously has a problem, where I

I X - 104

find some objectivation (sic) with soft neurological signs. Secondly, a restriction to be brought in. in

no way should it be suggested that those limited numbers are indicating - and I think that 80 per cent of

the Vietnam veterans have problems because this is a group coming

through_____ self-selection. For example. I know now that from the patients that I saw in 1980 the

majority had a history of severe alcohol abuse, far more than the second group I am reporting on here, 50 per cent, half of this group, the second group of 40, had a history of alcohol exposure. But taking those remarks into account what I found

was that I found a similar

neurospsychiatric syndrome, listed again on page 21, with similar soft neurological signs in patients in Holland, farmers, tulip growers, and

people with history of industrial exposure, women with estrogen exposure developing post-natal depression. I found exactly the same complaints and the same soft neurological signs as I found in a group of farmers - again a

self-selected group here in Victoria - had similar symptoms syndrome, soft neurological signs in a certain percentage of Vietnam veterans that

I saw in 1980 and in 1983. Taking

into account that similarity, plus the abundant information in the literature on the development of a similar syndrome in people after exposure to a variety of chemicals - and I repeat most of it exposure to mixtures of industrial solvents. I

really have the opinion also

supported by the effectiveness of the treatment that I have been

giving resulting in the

disappearance in a certain

percentage of the soft neurological signs that we can speak of a similar chemical etiology. and I stress

I X - 105

again - and I would like to get it

very clearly across - 1 am not here because I think thisί or that

chemical in Vietnam did it. I am

primarily here because I think with more research something can be done about the problems of the people. and I really think the problems are very real. (emphasis added).

(d) That his theory or hypothesis is not

validated. During cross-examination the

following exchange occurred:

So we are still in the realm of

hypothesis and the need to validate the hypothesis, correct? -- That is certainly correct.

And it is not your claim, as I

understand it, that your submission or the work that you have done

validates the hypothesis? -- Not at all.46

(e) That a "non-specific s'ign is one which could

relate to one or more of a number of

47

disorders or to no disorder" at all;

(f) That the syndrome that he sees can be

explained on the basis of a neurosis.

During cross-examination he said;

In fact, those sort of symptoms are the classic complaint made by people

suffering from post-traumatic neurosis. are they not? -- Amongst other

syndromes, yes.4ti

IX-106

(g) That the symptoms associated with PTSD and

his "neurasthenic depressive syndrome" are

"identical"; are also fairly catagorised as

symptoms of a generalised anxiety disorder;

and "consistent" with a tension deficit 4 9

disorder residual type.

(8) The following internationally recognised

toxicologists who were asked to review the van

Tiggelen Report totally rejected the thesis put

by him:

(a) Professor Holmstedt simply stated that "it

does not contain sound science";50

(b) Professor Aldridge, a specialist in

neurotoxicity dealt with the Van Tiggelen

report in his written statement to the

Commission. He stated:

The basic problem before us is:

1. Is there an increased incidence of neuro-psychiatric disorders in Vietnam veterans? 2. If there is. can this be linked to

exposure to chemicals used? 3. Is it possible to provide some

rational hypothesis how exposure

I X - 107

to chemicals for one year

producing no acute signs, followed by a long silent period leads to neuropsychiatric disorders?

The report by Dr van Tiggelen does not address these questions.

The review of experimental work is selective and ranges over a wide range of chemicals, solvents, herbicides, metals. etc. These are known to be neurotoxic and to produce acute neurotoxicity. It

is possible that an acute

poisoning leading to neuronal loss might lead to later behavioural changes but an acute episode(s) would be essential.

For example, on page 17 and page 18 he refers to the effects of

trimethyltin on animals and man. The experimental work leading to the discovery of the morphological correlate for this toxicity was carried out in my laboratory (my name is on the paper) and was

published in a long paper in 1980 in the American Journal of

Pathology. The facts about this disease are as follows.

The major neurobehavioural changes occur before and during the

demonstration of neuronal neurosis in selective areas of the central nervous system - the hippocampus, amygdaloid and piriform cortex. Recovery in animals and man is said______to______be______complete;

neurobehavioural change in animals can only be found by sophisticated techniques even though they will have considerable neuronal

deficits in the areas stated

above. I must emphasise - late

and minor neurobehavioural changes result from an acute episode of gross neurobehavioural change due to death of neurons in particular

areas.

IX-108

This example illustrates a general critisism (sic) of the paper by Dr van Tiggelen. As our knowledge increases it is clear that most

chemicals are toxic in very

specific wavs. They affect

particular organs, particular types of cells and by different mechanisms.

This report brings together a wide variety of chemicals and tries to link their effects to a single

neuropsychiatric entity. I do not find this useful and indeed may be a disservice to research and the Vietnam Veterans. The report adds

unproven hypothesis to unproven hypothesis and provides no

evidence to link exposure to

chemicals to this disease entity. The only common link between the case histories appears to be the improvement provided by

Dr van Tiggelen's medication. This treatment would require

careful evaluation before it could be accepted but as far as I can

understand Dr van Tiggelen does not provide any hypothesis why it should work, (emphasis added). =>1

It is significant to point out that Senior Counsel for

W A A did not challenge Dr Aldridge on his criticism of the

van Tiggelen Report.

9.2 Dr John Poliak

Dr Poliak's submission52 to the Commission made only

brief reference to "the effect of 2,4,5-T on the central

nervous system". He stated:

I X-109

The effect of 2,4,5-T on the central nervous system has been recorded by two groups of workers, one in Sweden (Sioden and

Soderberg. 1972. 1975, 1978: (Exhibit 184)) the other in Australia (Sanderson and Rogers, Rogers,

1981: 1983 :

patterns of

significantly administration 2,4,5-T, given

(Exhibit 741) Crampton and (Exhibit 1291). Behaviour rats and chicks were

affected after the

of a single low dose of

to the mother during

pregnancy or to the egg during the early stages of the incubation period.

The improved methods for the detection of aberrant behaviour patterns, devised by Crampton and Rogers (1983) (Exhibit 1291). showed that a single dose of 2,4,5-T (6

mg/kg containing 0.03 ppm TCDD) given to the mother on day 8 of gestation. led to

excessive movement. excessive grooming,a decrease in food intake, aversion to the usual foods and increased fear reflexes when the rats were 65 days and 5 months old.

These are behavioural teratogenic effects.

Sioden and Soderberg (1978) (Exhibit 184) correlated the changes in behaviour patterns with some biochemical changes. Tryptophan (an essential amino acid) and serotonin (a neurotransmitter substance in the brain and a muscle constrictor in arterioles,

intestines and bronchioles) decreased in offspring of 2,4,5-T injected rats and were implicated in the "deficits in behavioural and learning functions." Sioden and

Soderberg (1978) (Exhibit 184) also showed that 2,4.5-T increased the thyroid activity of rats at birth. but subsequently these rats developed permanent hypothyroidism (an underactive thyroid) leading to lassitude,

lack of energy and lowering of body

termperature. Sanderson and Rogers (1981) (Exhibit 741) found that the injection of 2,4,5-T (7 mg/kg, TCDD content 0.03 ppm) retarded learning functions and increased fear-related functions in the hatched chicks.53

IX-110

This evidence from Dr Poliak is of no probative value

because:

(1) The Sjoden and Soderberg experiments and the

Crampton and Rogers experiments involved the

administration of 2,4,5-T to pregnant female rats

on days 7, 8 or 9 of gestation and the

experiments of Sanderson and Rogers involved

injecting 2,4,5-T into chicken eggs. The report

of those experiments as referred to in Dr

Poliak's submission seeks to draw conclusions as

to alterations in the behaviour patterns of the

offspring born following the treatment. Even

apart from the fact that the methods of the

studies have been criticised they can have no

relevance to the possible neurotoxic effects on

adult humans.

(2) Professor Aldridge in a personal communication

stated that there was no evidence that 2,4,5-T is

likely to be associated with the neuropsychiatric

disorders seen in some Vietnam veterans and that

there was no evidence of sensitivity of the adult

human brain to conceivable doses.

IX-111

9.3 Dr Shearer

WAA , in i ts

54

final submission placed a great deal of

reliance on

55

Dr Shearer's written statement and her

oral testimony.She is a nurse with post-graduate training

in molecular genetics, but no training as a toxicologist.

Although not a neurotoxicologist she expressed opinions as

to the neurotoxicity of many of the chemical agents used

in Vietnam based on her reading of some of the available

scientific literature. In her written statement she

states:

9.3.1 2,4-D

Nearly all of the listed symptoms can be

attributed to the herbicides in Agent White and Agent Orange, and particularly to 2,4-D. From both published papers any (sic) my own review of medical records of people poisoned by 2,4-D - effects include extreme fatigue, tingling, numbness, dizziness, headache, depression, suicide attempts, irritability, inability to concentrate, lapses of memory, nausea, vomiting, diarrhoea, abdominal pains, miscarriages. low sperm counts, hematuria (sic), blurred vision and severe allergies: (She cites Goldstein: Exhibit 77; Berkeley: Exhibit 21; Todd: Exhibit 1580; Wallis: Exhibit 1581; Bezuqlya: Exhibit 1582; Radlonov: Exhibit 1583 ; Singer: Exhibit 1584.56

The published papers cited by Dr Shearer do not refer to

depression, suicide attempts, miscarriages. low sperm

I X - 112

count. haematuria and severe allergies and are, in any

event, of limited value when considering the neurotoxicity

of 2,4-D because they deal with the symptoms of acute

toxicity following high oral doses or exposure to unstated

doses; or exposure to various doses in combination with

other unstated chemicals. The inadeguacy of the data in

the papers cited by Dr Shearer is pointed out by Fetisov,

1966 who stated that:

Reports concerning the toxicity of 2,4-D

derivatives when acting through the

gastrointestinal tract and on contact with the skin, though fairly numerous. are controversial and inadequate for the toxicological

characterization of the preparations. 57

Dr Shearer also dealt with the alleged neurotoxicity of

some of the other chemical agents used in Vietnam, in her

supplementary written statement58 to the Commission. She

stated:

9.3.2 Cacodvlic Acid

Cacodylic Acid: . . . there is evidence for contamination (Stevens. 1979: Exhibit 1619) and interconversion (Exon: Exhibit 1622; NAS: Exhibit 1623) with trivalent inorganic arsenic which has been strongly correlated with human cancer (NAS: Exhibit 1623). (Trivalent inorganic arsenic) is

a suppressant of the immune system (Wagner: Exhibits 709 & 1627) and causes crippling neuropathy (Chhut tani. 1967: Exhibit 1624; Jenkins 1966: Exhibit 1625). Cacodylic Acid is

IX-113

converted in the environment to volatile and highly toxic arsine gases (Sandberg: Exhibit 1626; Wagner: Exhibit 709 and 1627).b9

This allegation as to the neurotoxicity of cacodylic acid

rests on the premise that cacodylic acid is "converted" to

trivalent inorganic arsenic in the body and to volatile

and highly toxic arsine gas in the environment.

It is sufficient to say that the papers cited do not

support the theory of conversion. Exon and Harr (Exhibit

1622) for example postulates that MMSA "may be converted

to a more toxic state in vivo." Recent animal work (e.g.

Stevens et a 1 Exhibit 724, Yamauchi et al (referred to in

Exhibit 731)) is to the contrary of such conversion. It

would, as stated above, be the reverse of the probable

process of detoxification.

It should be remembered that cacodylic acid is a major

product of the detoxification of arsenic in humans and

that it is readily excreted and not stored in the body.

There is nothing in the literature to suggest that

cacodylic acid is degraded to inorganic arsenic in vivo;

indeed the reverse is the case.

IX-114

9.3.3 Malathion and Diazinon

Dr Shearer next deals with the alleged neurotoxicity of

malathion and diazinon. She states:

Malathion and diazinon are organophosphate insecticides which primarily inhibit

cholinesterase enzymes necessary for proper functioning of the nervous system. Subclinical enzyme inhibition is common in exposed persons (Grech. 1964: Exhibit 1628; Elliott. 1963:

Exhibit 1629) and may be associated with

measureable neuropathy (Stalberq. 1978: Exhibit 1630) or neuropsychological dysfunction (Korsak. 1984: Exhibit 1631; Metcalf. 1969: Exhibit 1632). Chronic exposure can lead to psychiatric illness of suprisingly long duration (Gershon: Exhibit 1633; Dille. 1984: Exhibit 1634). 60

As all Vietnam veterans were exposed to malathion

regularly, these studies are dealt with in some detail.

(1) The Grech et al study does not provide support

for any risk. The enzyme levels of heavily

exposed agricultural sprayers of the compound

were not different from the controls. The paper

notes the acknowledged safety of malathion (LD50

4,000 mg/kg) and its "big margin of safety."

(2) Elliott et al report fenthion and malathion and

DDT trials in Western Nigeria. Most of those

IX-115

sprayed with malathion suffered no fall in

cholinesterase levels: the levels which fell

reversed to normal quickly and there was no

detectable illness.

(3) The Stalberq (1978) paper was a study of spraymen

working daily with solutions of 4% lindane, 0.2%

pyrethrum, 0.125% piperonylbutoxide, 2.5%

malathion or 2% bromophos in kerosene. The

workers were also intermittently exposed to 0.5%

diazinon and dursbane. The exposure period

ranged from between 1 and 24 years. So, not only

was the exposure not confined to malathion or

diazinon or even a combination of these two

compounds but also the exposure period was over

several years.

Furthermore, the authors state that exposure to

the chemical mixture referred to "may be"

associated with measureable neuropathy, although

they found that:

None of the examined subjects reported clinical symptoms of intoxication indicating a reaction to

organophosphate exposure. Apart from occasional headache, sometimes related to work, the subjects had no symptoms or signs of any neurological

disturbance.61

I X- 11 6

(4) Korsak et al62 studies people highly exposed

occupationally to a variety of pesticides for

years. The subjects were quite asymptomatic.

Some slight association with marginal

neurological deficits were shown. Exposure data

were self reported estimates and unrealiable.

(5) The paper by Metcalf and Holmes (1969) displays

many of the same inadequacies. No particular

organophosphate compound is identified. No

adequate evidence is presented as to the likely

exposure. It does appear, however, that the

unspecified and unquantified exposure extended

over many years. The authors found that:

Neurological examinations have been given to an approximately equal number of highly exposed and minimally exposed workers. There is no difference

between the groups in terms of such hard neurological signs as sensory or motor deficits.63

There is no increase in the incidence of hard EEG abnormalities such as spike activity of focal slowing.(at p 363.)

(6) The Gershon and Shaw (1961) paper is a study of

psychiatric sequelae in 16 people exposed to

various organophosphorus insecticides for long

I X-117

periods (18 months to 10 years). Some of the

cases had been exposed to high doses of at least

one organophosphorus compound and most of the

cases were exposed to a considerable number of

those compounds over time. The authors

themselves state that:

It may be objected that our results are due purely to chance and that exposure and mental change are not correlated. It is true that our results have not been analysed statistically and that

they are drawn from the community at large.64

(7) The Gershon and Shaw (1961) paper was reviewed by 65 Stoller et al (1965) and the authors stated:

The population at risk was not analysed fully; and the field survey, based on the questionning of 16 physicians as to 'whether they thought mental ill health had increased and, if so. whether those

in the country were more affected than the town dwellers' could not provide an objective answer.66

As a consequence of the perceived inadequacies with the

Gershon and Shaw work, Stoller et al undertook an

epidemiological study that:

Produced no evidence of schizophrenia and depressive states arising from the use of

organophosphorus insecticides. Neither is there

I X-118

any evidence that psychoneuroses or personality disorders are commoner in high usage areas than elsewhere.67

Clearly the studies cited do not support Dr Shearer's

conclusions.

9.3.4 Lindane

Dr Shearer next dealt with the alleged neurotoxicity of

lindane. She said:

Lindane is a neurotoxic insecticide. Persisting alteration in neurological and psychological function of exposed workers have been reported (Ecobichon and Joy (1982): Exhibit 1647.68

The Ecobichon and Joy (1982) text is a review of

literature covering, inter alia, the neurotoxicity of

lindane. It does refer to reports indicating that high

acute doses of lindane or chronic exposure to lindane can

result in "persisting neurological sequelae". However.

the following points should be noted:

(1) The authors state that:

The period over which these (persisting neurological sequelae) occur appears highly variable but does seem to bear a relationship to the severity of

symptoms occurring in acute

intoxication or to the duration of exposure in more chronic ones.69

IX-119

(2) The authors also state that:

Schuettmann has implicated lindane as a responsible factor in the development of hematopoietic, hepatic and nervous system pathologies. He observed

polyneuritis in workers exposed to lindane. Psychological disorders including anxiety, irritability, insomnia and motor pathology were also detected.70

(3) Although temporarily persisting neurological

sequelae are reported, there is no evidence

presented of permanent neurological damage

following exposure to lindane. Even the most

severe effects are reported to resolve

completely, usually well within a year of the

exposure;

(4) The literature reviewed by Ecobichon and Joy

discloses no evidence of long term neurotoxicity

in the absence of symptomatology of acute lindane

poisoning.

9.3.5 Dieldrin

Dr Shearer next dealt with the neurotoxicity of dieldrin.

She stated:

I X- 12 0

Dieldrin is a neurotoxic insecticide which causes changes in the electro-encephalogram tracings of exposed humans which may take up to a year to normalize (Ecobichon and Joy, 1982: Exhibit

1647).71

The comments (supra) on the literature reviewed in the

Ecobichon and Joy text apply equally here. Note also the

authors also comment that "occupational exposures to

dieldrin a t levels a thousand times higher than the

exposure of the general population have been tolerated

without obvious effect

72 for up to 15 years" and that

even in those cases of chronic exposures where symptoms

have appeared, complete recovery takes place within, at

most, a year.

9.3.6 N-Hexane

Finally, Dr Shearer dealt with the alleged neurotoxicity

of N-hexane. She said:

A major component of petroleum distillate is N-hexane, which has been shown to induce

peripheral neuropathy in humans and animals (Takeuchi, 1975: Exhibit 1657; Buiqatti, 1978: Exhibit 1658; Takeuchi. 1980: Exhibit 1659; Finkel, 1983: Exhibit 1660).73

The papers cited by Dr Shearer do support the proposition

that daily human and animal exposure to high doses of

IX-121

N-hexane over prolonged periods of time (years), is

associated with an increase in peripheral neuropathy. The

humans studied were healthy and working.

It is significant to note that in her "summary of long

term-effects", (Exhibit 1615) Dr Shearer makes no

reference to any long term neurotoxic effects.

The relevance of this association to the minimal exposures

(if any) of Australian personnel in Vietnam escapes the

Commission.

9.4 Dr Silbergeld

Dr Silbergeld was called by WAA. The opinions that she

expressed on the neurotoxicity of the chemical agents used

in Vietnam have received close consideration,

notwithstanding the Commission's reservations about her

qualifications and her obvious bias.

74 In her written statement to the Commission Dr

Silbergeld dealt with the alleged neurotoxicity of some of

the chemical agents used in Vietnam.

I X- 12 2

9.4.1 TCDD 2.4.5-T

In connection with the alleged neurotoxicity of TCDD and

2,4,5-T contaminated with TCDD, Dr Silbergeld stated:

It is my opinion that TCDD receptors exist in human cells and in their various organs which are similar, if not identical, to the TCDD receptor described in rodents. Based on this, it is my opinion that it is appropriate to extrapolate mechanistic studies in animals to humans. In

support of my opinion, I refer to the work of Hudson & Rice, (1983: Exhibit 1680) and to the annexed list of papers and laboratory research work under the heading of 1Silbergeld -

Receptors/TCDD1.

It is my opinion that TCDD causes toxic effects in several different ways ... In respect of

neurotoxicology it has an effect on

porphyrin-related aspects of neuro-psychology including demyelination and neural receptor changes. By the mechanism of the induction of mono-oxygenase____enzymes , ____TCDD can cause

porphyrinopathies and porphyrin related disorders of the nervous system. A metabolic product of TCDD is thought to inhibit a uro-decarboxylase enzyme, which has its own effect upon the

integrated system of haem synthesis. TCDD also can cause immuno dysfunction through its effects on the thymus gland and its derived cells.

In some sense almost all of the toxic effects of TCDD involve structural genes and translational events at the nuclear level related to changes in the protein synthesis directed by messenger RNA.

In the area of porphyrinopathies, cancer, reproduction, neurotoxicity and immunotoxicity there is ample evidence in my opinion to suggest this mechanistic connection to be scientifically valid. (emphasis added).75

IX-123

The above opinions by Dr Silbergeld are of little

probative value in this inquiry for the following reasons:

1. Dr Silbergeld attributes a wide range of biological

effects to TCDD because of its ability to induce

certain enzymes. She postulates that the toxicity of

TCDD, is mediated by a binding with the cytosolic

"receptor". However:

(a) Poland and Knutson (1982) relied upon by Dr

Silbergeld, states that:

It has been suggested that the

induction of monooxygenase activity and other coordinately expressed drug metabolising enzymes and the consequent enhanced metabolism of steroids

(Gustafsson and Ingelman - Sundberg, 1979; Arneric et al 1980) and other endogenous substances (Thunberg et al, 1979) may play a role in mediating the toxicity of TCDD. However, there is no direct evidence to support this

hypothesis. (emphasis added).76

(b) TCDD has been shown to induce a wide variety of

enzymatic activities in addition to those

referred to by Dr Silbergeld but the significance

of such a complex pattern of enzyme induction and

its relationship to the peculiar acute and

chronic toxicity of TCDD in animals is not known;

IX-124

I

(C) Poland and Knutson (1982) 77 also state that:

The similarity of the structure -

activity relationship for toxicity and that for receptor binding suggests that the halogenated aromatic hydrocarbons exert their toxicity through the

cytosol receptor. However, many

tissues in vivo and cell lines in

culture that contain the receptor and respond to TCDD with the induction of AHH activity show no evidence of a

toxic response. Thus, while the

cytosol receptor may be essential for toxicity. it is not sufficient,

(emphasis added).

(2) Dr Silbergeld seeks to correlate clinical signs with

laboratory investigations via hypotheses or

speculation when she attempts to link neuropathies

allegedly associated with TCDD exposure with an

unspecified form of porphyria which is, in turn,

allegedly related to TCDD enzyme induction. She

suggests that TCDD adversely affects porphyrin

biosynthesis leading to demyelination; that it

disrupts haem synthesis producing an acquired

porphyria; and causes changes in transmitter

receptors.78 She specifically attributes the

clinical signs (in animals) of "loss of neuromuscular

control, weakness, fatigueability, loss of sensation

and decreased nerve conduction" to these assertions79

IX-125

However, in her oral evidence:

(a) Dr Silbergeld's answers

that this was a theory.

Q C she stated:

to various questions indicated

During questioning by Mclnnes

So that the requirements at a molecular basis for dioxin toxicity are the entrance of dioxin into the cell and the presence within the cell of a receptor which

recognises dioxin. On a molecular basis, if those two conditions occur - and we know that they occur in certain human cells and in many animal cells - then the rest of the cascade of biological. biochemical and eventually toxic effects is indeed

inevitable.80

(b) She did not produce any data or express any opinion

about the level of dose required to produce the

"cascade" of effects (presumably including neurotoxic

effects), nor did she provide any data to support the

alleged "inevitability" of those effects;

(c) She indicated that her opinion about the production of

neurotoxic effects depended upon porphyria being

induced. The Commission simply notes that no case of

porphyria cutanea tarda has been found amongst

Australian personnel and that Ranch Handers were

porphyrin normal.

I X-126

from the (d) She indicated, in answer to a question

Commissioner, that "this kind of damage" (to the

nervous system) only occurs "if porphyria persists for

a long time".81

Dr Silbergeld further states, in her written statement

that:

In my opinion the clinical literature - ranging from case studies by Suskind and others to

epidemiological studies (Seveso and Ranch Hand 11: Exhibit 1394) - provides evidence that dioxin and 2,4,5-T with dioxin contamination are neurotoxic. Signs (clinical impressions and self-reported symptoms) of CNS toxicity and peripheral nervous system polyneuropathy have been confirmed by objective psychometric tests

(Ranch Hand II) and electromyography (Pazderova et al, 1981: Exhibit 1738; Singer et al. 1982: Exhibit 1584). In Suskind1s Reports (see Exhibit 1550) of the 1949 and subsequent exposures at Monsanto. neuropathy is persistent and

significant; it is considered by him to be one of the characteristic signs of intoxication.82

The probative value of this evidence is negligible,

because:

(1) The study of Suskind et al83 was conducted following

a chemical explosion at Nitro West Virginia in 1949.

This involved massive exposure to TCDD. Immediate

toxic symptoms included eye and respiratory tract

irritation, headache, dizziness and nausea and a

IX-127

severe irritant reaction of the exposed skin followed

by the development of chloracne, severe pains in

muscles of upper and lower extremities, shoulders and

thorax on exertion; fatigue, nervousness and

irritability; decrease in libido; dyspnea; vertigo and

intolerance to cold.84

(2) Soon after the 1949 explosion Suskind expressed the

opinion that the workers were suffering from "systemic

intoxication" categorised by acneform skin lesions,

hepatitis, disturbed lipid metabolism, peripheral

neuropathy and probably mild central nervous system

involvement.85 However, in 1953:

Four of the six workers examined in 1949 and 1950 were re-examined and six additional workers involved in the accident were also examined. The findings in this later

examination indicated a general regression of both the cutaneous and non cutaneous symptoms which had been present earlier. All of the workers showed a marked

improvement in their skin lesions - there were residua of the acne and a few active lesions. In a few cases, workers continued to complain of aches and pains of the lower

extremities and back, nervousness. excessive fatigue and dsypnea. No clinical

explanation for these complaints could be made based on the results of the physical examination, (emphasis added)86

(3) In a recent report87 Dr Ray Suskind indicated that a

study of 418 current and former workers who were

I X- 12 8

involved in the production of 2,4,5-T between 1948 and

1969 revealed no effects on peripheral nerve

function.

Most of the workers in the exposed group had developed

chloracne. as a result of the reactor accident in

1948.

The Commission had a two day consultation with Dr

Suskind. It is clear that his 30 year follow up study

of these workers satisfies the Commission that there

were no long-term health consequences of this heavy

exposure other than a small number of persistent

chloracnes. In particular no neurological or

psychological consequences were shown.

(4) In oral evidence. Dr Silbergeld conceded that the

workers in the Suskind studies were exposed to

"relatively heavy" levels of a mixture of

chemicals.88

(5) The Ranch Hand II study89 concluded that:

.... it appears at this time, that there are no neurological abnormalities in the Ranch Hand group that can be attributed to

herbicide exposure in Vietnam.

IX-129

90

Dr Silbergeld disagreed with that conclusion.

When confronted however she reluctantly admitted that

the nerve conduction tests, which should have shown a

deficit .if her demyel [nation theory was correct, were

91

normal in the Ranch Hand group.

(6) The Czechoslavakian workers studied by Jirasek et al,

92 93 1976 and by Pazderova et al, 1981 suffered "mass intoxication" whilst producing herbicides

including 2,4,5-T over periods ranging from 2 weeks to

3 years. The exposure level was such that test

rabbits placed in changing rooms adjacent to the work 94 area soon died. Furthermore, Pazderova notes that:

The mass occurrence of psychic disturbances, predominantly anxiety and depression, was in the first years of illness mainly due to exogenous influences: fear of death;

disfigurement; invalidity; marital problems; and in young individuals, the difficulty of entering intimate close relationships because of the disfigurement resulting from chloracne.95

(7) The evidence supports a conclusion that the TCDD

exposure at Seveso has not resulted in significant

neurological effects.96 The International Steering 97

Committee on Seveso (1984) reviewed all the Seveso

neurological studies at its sixth meeting in 1984 and

concluded that:

I X - 1 3 0

Initial reports of a decrease in motor nerve conduction velocity (without clinical neurological effects) in some individuals apparently have not been confirmed in late evaluations. A correlation of those

findings in a few persons with a possible exposure to TCDD seems unlikely although the evaluation of the data is still going on and a sufficiently detailed report still has to be presented to the ISC.98

In Rome in October 1984, Dr Pocchiari confirmed that

no neurological deficits were now being found.

(8) Moses et al, 1984 reviewed the health status of

workers with past exposure to TCDD in the

manufacture of 2.4,5-trichlorophenoxy acetic acid

and found that:

Exposure to TCDD in 2.4,5-T production may result in apparently permanent changes in the skin. Sensory changes in peripheral nerves and possible changes in liver metabolism in those with current or past chloracne are

suggested by the data as well. Based on worker histories, even severe acute toxicological effects of TCDD were reversible or markedly improved over

time. While the cross-sectional nature of the study, the low participation rate, and the highly select nature of the population limit the conclusions that can be drawn, it is unlikely that permanent. severe and debilitating

toxicological sequelae are inevitable after exposure to TCDD sufficient to produce chloracne. It must be noted, however, that individual susceptability may make certain workers with heavy

IX-131

exposures more vulnerable, which may have been the case with former worker with severe neuropathy described in this study.(emphasis added). 99

It should be noted that at the International Symposium on

Chlorinated Dioxins and Related Compounds, which was held

October 25-29, 1981, in Arlington, Virginia, a panel of

leading experts on TCDD reviewed, inter alia, human

neurological problems resulting from TCDD exposure and

coneluded:

Peripheral neurotoxicity has been observed in workers exposed to high levels to TCDD, PCBs and pentachlorophenols. There are no objective clinical signs of central nervous system damage in individuals exposed to chloracnegens; however, many have complained of a wide range of subjective symptoms in severe poisoning. Some of these symptoms have also been reported in cases of low

exposure and the significance of this is not understood, (emphasis added).100

The panel consisted of Drs Grow and Reggiani (Chairmen)

and Drs Austin, Cook, Gaffey, Hay, Honchar, Kimbrough,

Lathrop, Barclay Shepard and Allan Smith. This group was

both expert and balanced.

W A A tendered a document, "Health Assessment Document For

Polychlorinated Dibenzo-p-dioxins", eminating from the US

EPA in 1984, asserting it to be the result of a review,

inter alia, of neurotoxicity data on TCDD.

I X - 13 2

VVAA relied on a passage at 8-83 as follows:

There seems to be general agreement that exposure to 2,3,7,8 TCDD, whether acutely or chronically leads to chloracne, altered liver function, hematological abnormalities, porphyria cutanea tarda, hyper-pigmentation, hursutism and some peripheral neuropathy, (emphasis added).101

This document is endorsed "REVIEW DRAFT: (DO NOT CITE OR

QUOTE)."

This does not surprise the Commission since the passage

cites no authority or scientific paper other than Stevens

102

et al (1981). That author concludes at page 31 that

the quantitive aspects of TCDD dosage in Vietnam on a

worst-case basis, indicated, "that the dioxin sprayed with

Agent Orange in Vietnam cannot have caused systemic

illnesses in Vietnam veterans or birth defects in their

children".

Asserting a "general agreement" without reference to dose

is lacking in rigour. The Commission finds that there is

no such general agreement unless rigorous dose criteria

are applied. The effects noted have been found only after

doses very much higher than worst-case possible exposures

in Vietnam.

IX-133

Stevens estimates a mimimum toxic dose, extrapolating from

a series of animal studies, at 0.1 ug/kg 1.

He estimates the dose of a soldier directly sprayed at 7 x

- 5 -1

10 ug/kg or l/1750th of the minimum toxic

dose. 103

9.4.2 2,4-D

Dr Sibergeld in her written statement to the

104

Commission, then proceeded to deal with the alleged

neurotoxicity of some of the other chemical agents used in

Vietnam. In connection with 2,4-D she stated:

With respect to the chemical 2.4-D, on the basis of the only animal studies on mechanism, it is my opinion that there is sound evidence that 2.4-D adversely affects the liver; that it is a

membrane destabilising agent. particularly in neurons and may result in peripheral and central demyelinization (sic) particularly of the axonal processes. (emphasis added) 105

In her oral evidence Dr SiIbergeld expanded on this

opinion:

(1) Her opinion was based on a review of the

literature only. She had not done any research

on 2,4-D herself;106

I X- 13 4

(2) The human studies upon which she relied in

formulating her opinion included Dudley and

Thapar, 1972, Exhibit 57) which demonstrates

demyelination following suicidal ingestion of

2,4-D by a 76 year old man with senile dementia;

Goldsteie et al, 1959 (Exhibit 77) (supra);

Singer et al, 1982 (Exhibit 1584) (supra). She

also relied on Squibb et al, 1983 (Exhibit

1698).The rats in the first experiment were

injected with 15-160 mg/kg/day for 5 weeks, and

in the 2nd experiment with 10-40 mg/kg/day for 4

weeks - both huge dosages. In both experiments

their grip strengthened and there were no other

neurological signs. The effect disappeared upon

cessation of dosing. The relevance of this

escapes the Commission.

107

Dr Silbergeld also relies on Elo and Ylitalo

which relates to acute poisoning at oral doses of

250-500 mg/kg/day but slight impairment of

walking only at 100 mg/kg. This too is totally

irrelevant to the Vietnam context.

(3) Dr Silbergeld agreed that "putting it at its

highest 2,4-D and 2,4,5-T could only be described

as weakly neurotoxic".108

IX-135

9.4.3 DDT. Dieldrin, Lindane and Chlordane

Dr silbergeld next dealt with alleged neurotoxicity of

DDT, dieldrin, lindane and chlordane together. She stated:

All these chemicals are neurotoxic (see van Woert, 1982: EXHIBIT 1699; Woolley. 1982: EXHIBIT 1700; O'Brien) and can cause, upon high dose exposure. acute neurotoxic signs, including neuromuscular paralysis. loss of respiratory control, and seizures. (emphasis added).

Dr Silbergeld1s opinions as to the acute neurotoxicity of

these compounds is unobjectionable because there is little

doubt that high enough doses of any compound could

conceivably produce signs of neurotoxicity. However, this

inquiry is concerned with possible long-term neurotoxic

effects following exposure to these substances resulting

in no significant immediate neurotoxic signs.

In this regard, the following points should be noted:

(1) In connection with chlordane:

(a) Workers engaged in the manufacture and

formulation of chlordane for periods up to

15 years have exhibited no evidence of

harmful effects attributable to this

insecticide;110

I X- 13 6

(b) The International Program on Chemical Safety

expressed the same opinion in its recent

review of the toxicity of chlordane in

"Environmental Health Criteria: Chlordane"

(1984).111 It said that "no deleterious

effects associated with occupational

exposure to chlordane have been

- „ „112 reported;"

(c) Dr Aldridge in his written statement to this

Commission stated that "no permanent

neurological deficits have been seen" in 113

connection with chlordane

(2) In connection with lindane:

(a) Dr Aldridge in his written statement

indicated that in man and in animals the

first signs of poisoning with lindane are a

rapid onset of convulsions but that recovery

is rapid and that no permanent neurological 114

deficits have been seen.

(3) In connection with dieldrin:

IX-13 7

(a) A study of workers exposed for periods from

4-15 years of dieldr in levels of more than

50 times that of the general population

detected no adverse health effects either

clinically or by 20 biochemical and

haematological parameters.115

(b) Dr Aldridge in his written statement stated

that "in man and animals the first sign of

poisoning (was) a convulsion (but that)

recovery is rapid, probably by the reduction

of the concentration of dieldrin in the

nervous system by its partition into fat".

Dr Aldridge also indicated that permanent

neurological deficits have not been seen

even though changes in EEG may be seen for a

period after poisoning.116

Finally, in his oral evidence Dr Aldridge

indicated that in the absence of any acute event

including convulsion that he would not expect any

long-term neurological deficits to occur

117

following exposure to dieldrin.

I X - 13 8

(4) In connection with DDT Dr Silbergeld relies upon

the experiments conducted by Van Woert et al,

1982118 and Woolley, 1982119 These involved

the administration of high doses of DDT to

experimental animals and are concerned with the

acute. immediate neurological effects of such

doses. Both papers state that the DDT induced

neurological syndrome is reversible soon after

cessation of dosing which indicates that the

compound causes biochemical rather than

morphological changes and establishes that

long-term effects do not occur;

The World Health Organisation stated that:

In spite of the prolonged exposure of the entire population of the world and the heavy occupational exposure of a substantial number, the only reported poisoning cases were due to intentional or accidental ingestion. In most of

these cases only moderate nervous symptoms were observed and convulsions were rare.

Dr Aldridge in his written statement stated that

recovery from symptoms in the nervous system is

complete and there is no evidence of long-term

neurological effects. He also stated that except

I X - 13 9

for substantial accidental or intentional oral

ingestion of DDT little or no toxicity has

resulted even from rather gross occupational

121

exposure.

9.4.4 Malathion

Dr Silbergeld next dealt with the neurotoxicity of

malathion. She stated:

Malathion is fundamentally a neuromuscular poison which interferes with the enzymatic hydrolysis of acetylcholine, the chemical neurotransmitter which regulates nerve-muscle and nerve-ganglion communication. Acute high dose exposure causes neuromuscular dysfunction and loss of respiratory control; prolonged exposure at this level can have long term effects, possibly as a consequence of anoxic damage. (Exhibit 1676 at pp 10-11).

In other words if sufficient is absorbed to stop the

person breathing, brain damage may result. This is a

truism and irrelevant to neurotoxicity.

Dr Aldridge firmly asserts that no long-term neurological

122

would follow exposure to malathion in Vietnam. The

Commission accepts his evidence.

I X - 1 4 0

10. THE CASE PRESENTED BY ROSS LONNIE

Me Lonnie appeared before the Commission on behalf of some

400 Western Australian Vietnam veterans and their

families. He called some limited evidence of relevance to

the issue of the possible neurotoxicity of the chemical

agents used in Vietnam. That evidence was given by Dr

Peter Orris.

10.1 Dr Peter Orris

Dr Orris has no formal gualifications in the field of

neurotoxicity or psychiatry, and his experience is in the

field of occupational medicine. In his written

123

statement he states that:

Since 1978 we have seen over 110 Vietnam veterans at the Occupational medical clinic at Cook County Hospital. These veterans are self referred. through Veteran's Groups, occasionally through

the news media, and more recently from the

Veteran's Administration. Their universal request is for a dispassionate discussion and evaluation of whether their symptomatology and occasionally illness are likely to be related to

their claimed exposure to Agent Orange in Vietnam.

Amongst the more than a hundred patients, we have seen individuals with central nervous system toxic____dysfunction____which is____ clinically distinguishable from post traumatic stress

syndrome. These are two central nervous system

I X - 141

secondary to perceived or actual environmental exposures. Amonqst the veterans the syndromes have considerable overlap vet they are

characteristically quite different in

presentation.

The contrasting classic picture of the diffuse toxic neurologic damage produced by a variety of chemicals including the neuroasthenic syndrome associated with TCDD (24a). is one of initial symptoms of increased irritability, decrease in recent memory, decreased attention span, sleep disturbances, often sexual dysfunction and then secondary depression and frustration concerning the impediments these problems place upon daily living. This syndrome due to a variety of

compounds is now becoming a subject of intense research interest on the part of the scientific community and is now being studied by a working group of the World Health Organisation, Harvard University and others.

These two syndromes are quite different though in the veteran's population present often with degrees of overlap and occasionally severe forms may mimic each other if allowed to progress to chronicity. The importance of the differential diagnoses here is that post-traumatic stress disorder can be reduced in the severity of its manifestations through therapy so that the

individual may be able to function in his daily life. The second syndrome when recognised and described adequately to the patient may be coped with in a manner not engendering the same

depression and feelings of guilt that are the sequelae causing such additional social

dysfunction.

of the 110 plus patients that we have seen who came to us concerned about their exposure to Agent Orange, approximately 5% had histories and clinical syndromes which were probably related to

their exposure to TCDD, these included a patient with toxic central nervous system, dysfunction, peripheral neuropathy, hepatic dysfunction and sub-cutaneous leiomyosarcoma. Another with central nervous system dysfunction, peripheral

I X- 14 2

neuropathy, history of acneform rash and elevated liver enzymes, still another with acneform lesions in the characteristic facial locations for chloracne, central and peripheral nervous system dysfunction, and a carcinoma of the bladder. Further, one with elevated urinary uroporphyrins, history of acute post exposure photophobia and GI distress, and then the

development of chronic parasthesias and acneform lesions and cysts on the face.

An additional 10% demonstrated less

characteristic symptomatology and/or illnesses but with sufficient history and/or conditioning to suggest that they were possibly related to their exposure to TCDD in Vietnam, these included a patient with soft tissue sarcoma. ten patients with central nervous system dysfunction, nine

patients with peripheral parathesias and a number of patients with a history of rashes of less characteristic appearence (sic). We saw one patient that we felt had post-traumatic stress

syndrome and referred him for therapy, (emphasis added) 124

This evidence is of little probative value for the

following reasons:

(1) The evidence of Dr Orris is of a collection of

"clinical observations"; and provides no basis

upon which any conclusions about Australian 12 5

Vietnam veterans should be drawn.

(2) Dr Orris conceded that the cohort was small; that

it was self-selected; that exposure was not

documented; that the level and nature of exposure

to other toxic substances was uncontrolled and

I X - 14 3

unknown; that a number of the veterans in the

sample had been referred by veterans1

organisations; or inspired by the media; and that

almost every member of his "cohort" wanted to

link an asserted but unverifiable exposure to a

particular health problem or problems. 126

(3) Dr Orris agreed that distinguishing between "post

traumatic syndrome" and "central nervous system

toxic dysfunction" was "very difficult" and that

the two syndromes were in fact only

distinguishable by reference to the patient's

127

"perception of exposure".

In the Commission's view Dr Orris took the debate no

further.

11. THE FINAL SUBMISSION OF W A A 128

The introduction to the final submission states that:

The following submission is an outline of the main points made by the WAA. The preparation of a detailed submission covering all aspects of the evidence is not possible given the time allowed. No doubt the Commissioner will be seized of other aspects of the evidence which are in accordance with the submissions and will take them into consideration in his reports.

I X - 144

It must be said that this document makes no attempt to

come to grips with the problems posed by the evidence. It

asserts without argument that a neurotoxic response is

responsible for the syndrome and that "the psychiatric and

psychological symptoms exhibited by many Vietnam veterans

cannot be explained away by a diagnosis of post traumatic

stress".

12. WA R'S CASE ANSWERED

12.1 Dr Ellard

In evidence Dr J.H.T. Ellard rejected the proposition that

the syndrome could be attributed to exposure to chemical

agents. His reasons for rejecting the proposition may be

summarised as follows:

(i) The syndrome is not specific but is similar to

those described in returnees from other wars in

which herbicides were not used, and corresponds

with symptoms found in persons suffering stress

as a result of the rigours of ordinary life.

(ii) There was an absence of any "statistical

association between the syndrome and exposure

to herbicide".

IX-145

(iii) It was inherently "unlikely for a chemical

substance to produce a chronic reaction,

particularly a delayed chronic reaction,

otherwise than after an initial. clearly

recognisable, acute reaction".

He said of this group of symptoms:

It is a common grouping of symptoms seen in those who perceive themselves, probably correctly, to have been stressed, and who are discontented with things the way they are now.129

12.2 Dr Spraqq

Dr G.S. Spragg gave the following answers in response to

questions about the symptoms:

Do you think the 16 features are specific to veterans or are they characteristic or psychiatric disorders generally?--- The latter.

And found frequently amongst veterans of the Vietnam war and of other wars and in the

community generally?--- Yes.

And in particular, do you think that the rage reaction is specific and a cardinal

diagnostic feature of the Vietnam veteran syndrome?--- No. We find it everywhere. -*-30

IX-146

12.3 Displacement - Dr Blackburn and Dr Ellard

The role of Agent Orange in this context of stress-induced

neurosis was discussed by Dr Blackburn in "Review of the

Effects of Agent Orange: A Psychiatric Perspective on the 131 Controversy" as follows:

For some, the concern with Agent Orange represent a displacement from poorly understood awareness of mental disorder. The Vietnam veterans who believe they may have been poisoned by Agent Orange were usually exposed to the terrors and

tragedies of war. It may be more tolerable to perceive oneself as physically intoxicated rather than to recognize oneself as emotionally

vulnerable. It may be more acceptable for us, our society, and our leadership to believe that Agent Orange has damaged our youth, rather than to recognize and deal with the logical

consequences of warfare.

Dr Ellard at p 4605 agreed with the suggested role of the

mechanism of displacement in some veterans attributing

their problems to Agent Orange.

...they are people and it is a universal

mechanism, I am sure it operates in them.132

12.4 Drs Hall and MacPhee

Dr W. Hall and Dr D. Macphee in their paper entitled "Do 13 3

Vietnam Veterans Suffer from Toxic Neurasthenia?" ,

dealt explicitly with the speculation advanced by Dr van

I X- 14 7

Tiggelen that the syndrome described above and found in

Vietnam veterans was indicative of a neurasthenic syndrome

caused by chemical exposure while on service in Vietnam.

Specific criticisms of the van Tiggelen hypothesis as

summarised by Dr Hall are:

First, neurasthenia is a nonspecific syndrome: it is observed after a variety of chemical

exposures and after industrial accidents that do not involve any chemical exposure, and its symptoms are among the most commonly reported symptoms in surveys of psychiatric morbidity in the general community.

Second. there is no good reason to believe that neurasthenia is a common consequence of exposure to solvents.

Third. the claim that the linguomental reflex is a specific sign of cerebral damage is

unsubstantiated and highly implausible in the light of our knowledge of the nonspecificity of related reflexes such as the palmomental, which are positive in a substantial number of normals.

Fourth. toxic neurasthenia and the psychiatric disorders of Vietnam veterans differ in the pattern of chemical exposure. Workers who suffer from toxic neurasthenia experienced daily

exposure over a period of many years while

Vietnam veterans experienced intermittent exposure over the period of a year.

Fifth. toxic neurasthenia and the psychiatric disorders of the Vietnam veterans differ in their natural history. Toxic neurasthenia is reported to remain stable after exposure ceases while the disorders of the veterans are reported to worsen with time.134

To the fourth reason advanced there might be added the

words, "if at all".

I X-148

The two authors. as summarised by Dr Hall, proceed to

advance the alternative explanation:

There is also a positive case to be made for an alternative explanation of the veterans' psychiatric disorders. It derives from the literature on the occurrence of psychiatric disorders among the veterans of previous wars. Although the literature leaves much to be desired

from an epidemiological perspective it reveals that veterans of previous wars have suffered from a strikingly similar sydrome which includes symptoms such as depression, rage,

gastrointestinal symptoms, sleeplessness and irritability and shows the features that have been reported in the disorders amongst Vietnam veterans, namely, delayed onset and

persistence. - 1 -35

12.5 Professor J.G. Andrews

Dr J.G. Andrews and his co-authors, in the synopsis of the

paper prepared by them for the Commission136 stated that

they would "endorse" the position taken by Dr Hall and Dr

Macphee on this question.

12.6 Rejection of a Neurotoxic or Neurasthenia Cause

The Commission accepts Dr Ellard, Dr Spragg, Dr Blackburn,

Dr Hall, Dr Macphee and Professor Andrews.

It rejects a neurotoxic or neurasthenic cause for the

syndrome.

IX-149

13. DOES THE VIETNAM VETERANS' SYNDROME EXIST?

The Commission having concluded that there is no

neurotoxic effect operating upon Vietnam veterans the

question must still be asked whether there is a distinct

psychological or psychiatric syndrome which afflicts them.

It seems certain that it be so as the following analysis

of the evidence will disclose.

Brigadier Rodgers whose qualifications and experience have

been referred to earlier. said:

This post-war neurosis or exhaustion was not a neurotic thing. It was a psychological

problem.137

which he considered a normal reaction to the horror which

was Vietnam.

In the context of being asked about the "easy startle"

reaction he said that this was but one factor of "The time

honoured things that every soldier from every war has

suffered ... startle reactions, the insomnia, the

aggressive behaviour, over-indulgence in alcohol, physical

assault on a wife, lack of libido, dizziness, headaches"

and so on: all of these he described as "the

syndrome".138

I X - 1 5 0

Dr John Ellard to whom reference has already been made is

a consultant psychiatrist of high eminence in the Sydney

community. In addition to his basic degrees he is a

Fellow of the Royal Australian College of Physicians, a

Fellow of the Royal Australian and New Zealand College of

Psychiatrists, a Fellow of the Royal College of

Psychiatrists of the United Kingdom and as well a Member

of the Royal Australian Air Force Reserve and Senior

Consultant in Psychiatry to the Director General of Air

Force Health Services.

In his evidence Dr Ellard described a grouping of symptoms

caused by the dislocation and other features of war

service. That syndrome consisted of:

(a) Failure to maintain friendships;

(b) Fear of public places;

(c) Distress at being a stranger in one's own land;

(d) Inability to settle down;

(e) A feeling of anger and emptiness;

(f) Withdrawal of interest;

(g) Apathy;

(h) Bursts of uncontrollable aggression;

(i) Feelings of depression;

(j) Anxiety states;

IX-151

(k) Breathlessness;

(l) Headaches;

(m) Fatigue/lethargy;

(n) Indigestion;

(o) In rare cases. hysterical conversions.

Dr Ellard expressed the view that the antecedents of this

syndrome were seen not only in World War II veterans but

also in those who had been in other war zones and others

(non-veterans) who had been involved in life-threatening

events.

He made a most interesting analysis of the Agent Orange

phenomenon.

In his view the concentration of afflicted veterans on

Agent Orange is the result of a "displacement". This is

the mental transfer of the cause of a problem to a more

acceptable source. In order words the victim blames an

external cause, (chemicals). rather than accepting what he

perceives as some inadequacy in himself, a mental disorder.

Dr Ellard expressed the view that the cluster of symptoms

was not of a kind to be expected from the effects of

I X - 152

chemicals; it was of a kind classically associated with

returnees from war or prisoner of war camps; deriving from

stress.

Dr Wayne Hall, a lecturer in psychiatry and behavioural

science at the University of Western Australia, a member

of the Australian and New Zealand Association for the

Advancement of Science, the Australian and New Zealand

Society for Epidemiological Research and Community Health,

and the Australian Society for Psychiatric Research, gave

evidence. He has taken a particular interest in the

rehabilitative and readjustment problems of Vietnam

veterans and is a co-author of the most useful paper, "Do

13 9

Vietnam Veterans Suffer From Toxic Neurasthenia?"

This paper effectively rebuts Dr van Tiggelen's theories.

He concurs in a sense with the view expressed by Dr

Ellard. He perceives that the psychological disorder

producing the Vietnam veterans' syndrome is often

explained in terms equivalent to accusations of

malingering. He reminded the Commission of the long

standing difference between those who perceive the disease

as being one which afflicts only those who have some

predisposition towards it and those who see it as a result

of stress simpliciter.

IX-153

It must be firmly stressed that even if a veteran were

subject to predisposition and his stress produced

psychiatric consequences it does not follow that he is in

any way a malingerer.

Nonetheless the fear of being categorised as a malingerer

has led veterans to seek to blame Agent Orange and to seek

remedy or relief for that cause rather than addressing the

real problem. This is another way of analysing what Dr

Ellard calls "displacement".

Dr Griffith Spragg and Dr Bruce Boman are eminent

psychiatrists with considerable experience in treating

veterans of all wars. They agreed that the syndrome

exists and that it is unconnected with chemical exposure.

Associate-Professor Gavin Andrews. of the School of

Psychiatry at the University of New South Wales, a Fellow

°f the Royal Australian ,and New Zealand College of

Psychiatrists. a Member of the Royal College of

Psychiatrists. and Chairman of the Division of

Communicat ion Disorders at Prince Henry Hospital. gave

evidence.

IX-154

The Professor was requested by the Commission to review

and evaluate available literature on PTSD and its

treatment as it applies to Vietnam veterans, highlighting

where possible the Australian experience.

. 140

His review may be summarised as follows:

1. It discusses the value of making diagnoses, list

the types of anxiety and depressive disorders, their

distinctness and their overlap. It discusses the

prevalence in the general population by diagnosis, by

type of measure, by severity, by chronicity and by age

and sex. One would expect that some 8% of a group of

25-44 year old non-veterans would have a diagnostic

anxiety or depressive disorder, 16% would have shown

symptoms but not warrant a diagnosis, whilst in 4% the

disorder would persist for six months or longer and in

2% produce incapacity. Rates in veterans would have

to be shown to exceed these rates if Vietnam or the

post-Vietnam experience is to be regarded as a cause

of these illnesses.

2. It defines PTSD and outlines the history of the

concept. It describes its occurrence in survivors

from concentration camps, other wars, natural

I X - 155

disasters and personal calamities. It finds that the

symptoms form a specific cluster and that this cluster

allows the disorder to be differentiated from other

similar disorders. It finds evidence to support the

acute and chronic forms. but not the delayed form of

the disorder.

3. It looks at ways to discover whether social or

psychological disorders are a consequence of Vietnam

service and concludes that studies of large

populations of veterans and non-veterans offer the

most promise for research. It reviews six such

studies and notes that in the years immediately after

demobilization veterans seem to have an increased risk

of being depressed, discouraged and unemployed. Ten

years after discharge they are at an increased risk of

using too much alcohol, and experiencing symptoms

consistent with anxiety, depressive, and PTSD and

still show deficits in job status even though

unemployment may not be an issue. Those who sprayed

herbicides are also more concerned about their health

(e.g. Ranch Handers).

4. within the U.S. Vietnam group, heavy combat is

associated with drinking, arrests, and the symptoms of

I X - 15 6

anxiety, depression, and PTSD 10 years later: this

association lessens with time since combat, and some

of the association may be spurious.

5. The treatment outcome literature is primitive to

say the least. It concludes that treatments which

involve reliving, "working through", or graded

exposure to the traumatic experience appear to be the

treatment of choice for PTSD. The authors were

surprised at the lack of good research when, for many

psychiatric disorders, satisfactory treatment outcome

studies exist and treatment efficacies can be

established.

141

6. Data from the Legacies Study was reanalysed

in US at the Commission's request and the printout

arrived in Sydney on 16 September 1984. The report's

appendix reanalyses the comparative risks of white

non-veterans and veterans of occupational status,

education, drinking problems, psychological symptoms

and PTSD 10 years after service.

It found no data that was able to be analysed on the

effects of Vietnam service on Australian servicemen or

IX-157

their families. Therefore Australian general

population morbidity data and the American Vietnam

data are used to estimate the number of Australian

veterans likely to be afflicted because of their war

service.

An important aspect of Professor Andrews' evidence was his

establishing of a method for calculating the excess

psychiatric morbidity attributable to service in Vietnam.

He points out that psychiatric disorders are distributed

along a dimension from those who have transient symptoms.

to those who have sufficient symptoms to warrant a

diagnosis of a disorder„ to those whose disorder lasts for

six months or more, to those who are disabled by their

disorder.

He took the responses of a general population sample on a

symptoms check list and established the cut-off points for

the four levels listed above. He then corrected the

findings for the reduced prevalence of disorder in males.

It was then possible to move the distribution by the 0.25

standard deviation units shown to be the risk attributable

to Vietnam service. (See Appendix 1 of his report).

IX-158

This made possible a comparison of the percentage of

veterans scoring in each category with an expected

frequency in the general male population. The excess

could then be calculated. By applying this notional excess

to the numbers who served in Vietnam one can calculate the

number likely to be suffering and in need of treatment at

the present time.

The general health questionnaire is a symptom check list

which measures predominantly anxiety and depression.

Researchers took a random sample of. Botany Bay adults (a

total of 871) and found that on the 20 item version of the

questionnaire, 23. 5% reported more than 3 symptoms. At

this level if the responder had attended a doctor, the

doctor would have accepted that there was need for a

consultation with a psychiatrist.

12.2% reported more than 7 symptoms, and at this level

they would be likely to satisfy diagnostic criteria for an

identifiable psychiatric illness, listed in DSM III.

5.9% reported more than 11 symptoms and at this level it

is likely that the symptoms would persist for a median of

six months.

IX-159

3.2% reported more than 14 symptoms and at this level it

is likely that they would have found their symptoms

incapacitating.

In this study there were equal number of men and women and

the rates for males were lower. If these figures are

corrected in accordance with appropriate ratios by sex

then the male rates should be some 19% lower than the

population figures.

After correction, of males, 20% would be expected to show

symptoms, 9.9% to have a diagnosis, 4.9% to have a

diagnosis and symptoms which persist and 2.4% would in

addition be incapacitated.

The researchers adjusted statistically for the effect of

Vietnam, and found that 23.5% would be complaining of

symptoms, 12.2% would have sufficient symptoms to warrant

a diagnosis, 5.9% would have chronic conditions and 3.2%

would be incapacitated.

Thus, the excess attributable to Vietnam is 3.5% with

symptoms, 2.3% with a diagnosable condition, 1% with a

chronic condition and .8% incapacitated.

I X- 16 0

42,000 army personnel served in Vietnam and one can

conclude that 1,470 would have symptoms attributable to

Vietnam, 966 of this 1,470 would warrant a diagnosis and

420 of them would have a chronic condition because of

Vietnam whilst 336 of the 1,470 with symptoms would be

disabled.

The Commission observes that it is not an "either/or"

issue because whether the underlying condition was

actually caused by Vietnam or not the Vietnam factor would

come crowding in and exaggerate or worsen the present

state. The result is that approximately one quarter of

Vietnam veterans can be expected to be in need of

psychological or psychiatric help and in every case there

would be at least an exacerbation of their symptomatology

by reason of Vietnam service.

Dr Geoffrey Streimer is writing a thesis on the

psychiatric and social adjustment of Vietnam veterans for

a Doctorate. He is a member of the Royal Australian and

New Zealand College of Psychiatrists and Consultant

Psychiatrist to the New South Wales Institute of

Psychiatry.

IX-161

His research has established a substantial excess of PTSD

amongst Vietnam veterans. He considered that there was a

very clear relationship between that outcome and combat.

Mr William Davies, an Honours Graduate in Psychology is

employed as a counsellor with the W C S in Perth, Western

Australia.

His evidence is relied upon by W A A in its final

submission. This is puzzling because he makes no case for

chemical caused psychiatric difficulties and deposed that

the most appropriate diagnosis for the troubled veterans

seen by him was PTSD.

He was able to give a useful insight into the

effectiveness of counselling and treatment for troubled

veterans. He deposed that six to ten 90-minute

counselling service visits produced a dramatic improvement

amongst almost all the veterans seen by him. This is

indeed heartening.

The evidence of Dr Silbergeld and Dr Orris on this topic

has already been dealt with.

I X-162

13.1 Conclusion

There is a Vietnam veterans' syndrome, broadly

corresponding to PTSD. At this time about 25% of Vietnam

veterans will have psychological symptoms requiring

treatment, and this number may be expected to peak in

1988-89 and then gradually but steadily decline.

Treatment will produce dramatic improvement quite quickly

in all but the most recalcitrant cases.

Any mental health disorder in a Vietnam veteran should as

a matter of policy be accepted for Repatriation benefit

and entitlement purposes.

This is because on the balance of probabilities any such

disorder will be at least exacerbated by service in

Vietnam.

14. LITERATURE

14.1 Australian Literature

Appendix I to this Chapter lists a bibliography of

materials additional to the exhibits which were considered

IX-163

by the Commission. A striking feature is the relative

paucity of Australian literature on psychiatric disorders

of Australian personnel. During formal hearings expert

witnesses commented forcefully on the absence of research

particularly into the treatment in clinical practice of

PTSD in Vietnam veterans. This is indeed unfortunate.

Much of the available "Australian" literature, therefore,

borrows heavily from American sources. These are not

always appropriate to Australian conditions, having regard

to important socio-economic, racial, and recruitment

differences.

The pool of available research subjects in Australia is

limited. Much of the literature is anecdotal and

methodologically suspect. Selection bias and inadequate

testing for confounding variables are problems well known

to epidemiologists. In the absence of a morbidity study

of the type proposed by the Commission one can but take

note of the available literature.

The Commission finds it regrettable that the scientific

community and the body of practising psychiatrists, have

not addressed in scholarly fashion the mental health

problems of the Vietnam veteran community in Australia.

IX-164

14.2 British/Eurpoean Literature

Medical commentators have begun to address themselves to

the concept of PTSD and its treatment, particularly in the

context of war. Two articles by Brigadier Mostafa El

142 143

Sudany El Rayes and by David A. Kipper the Yom

Kippur and other Israeli-Egyptian conflicts presented

strikingly similar syndromes and treatments.

The British medical literature on PTSD has concentrated on

its development following bereavement. motor vehicle and

industrial accidents, rape and other disasters. R . J.

Daly in his "Samuel Pepys and Post Traumatic Stress

144

Disorder" asked if it had just appeared or if it had

always existed..

Nomenclatures prior to the use of PTSD - included

sub-categories such as "Acute Reaction to Stress" and

"Adjustment Reaction" and the emphasis was on depressive

reactions following acute stressors and on the brief and

reversible nature of these reactions.

I X-165

14.3 American/Canadian Literature

Canadian

The article by Dancey "Treatment in the Absence of

Pensioning for Psychoneurotic Veterans" (Exhibit 1504D)

(Nov 1950) (pp 347-349) is of historic interest only. The

Canadian Pension Commission decided to offer treatment to

any veteran with a neurosis regardless of his time or

place of service or of his income, provided that his

symptoms could be expected to fade after a brief period of

therapy.

Psychotics and psychopaths were excluded from the program,

and no financial allowances were permitted either to the

patient or to his family. This was thought to minimise

any desire that a veteran might have to remain more or

less permanently in hospital and at the same time created

a state of affairs where his family would urge him to return to work as soon as possible.

The average stay in hospital was usually less than two

months. No full-time psychiatrists were employed.

IX-166

14 5

The Articles by Marshall and Gauthier deal

respectively with "Failures in Flooding" and "The Current

of Status of Flooding Therapy".. "Flooding" is a generic

term for treatment techniques that have as their goal the

extinction of classes of maladaptive responses to aversive

stimuli by exposure to high-intensity subsets of these

aversive stimuli for prolonged periods in the absence of

actual physical injurious consequences.

For the client presenting with anxiety there is an

expectation of reduction in the client1s feelings of

anxiety. and less avoidance behaviour after the

intervention. If the client is also depressed, has poor

marital relations, sexual problems, or other dysfunctions,

there is no reason - in the authors' opinions - to

suppose that flooding, would have any effect on these

difficulties, unless specific additional precedures are

included in treatment. The authors dismissed the common

idea that flooding is potentially dangerous.

American

The Commission has relied on two reviews of current US

literature. The first is by Dr Bruce Boman "The Vietnam 14 6 Veteran Ten Years On" The other is Professor

„ . , _ _ 147

Andrews' Report.

I X - 167

It should be observed that the Commission has itself

studied all the literature referred to by them as well as

all that referred to in the Bibliography, Appendix 1 to

this chapter.

15. DR MICHAEL MAXWELL BARR

Dr. Barr graduated MB BS in 1974. His interest as a

private practitioner is looking at long-term toxic effects

of chemicals, particularly solvents, pesticides and

hydro-carbons. He believes that there is a close

relationship between Agent Orange and mercury, arsenic and

lead.

He considers it "possible" that veterans have been exposed

to a chemical which induces a metabolic disorder related

to mercury or thallium poisoning and acute porphyria is,

he thinks, the most likely candidate.

The Commission notes again that no porphyria has been

found amongst Australian personnel.

Dr. Barr in a letter to Medical Practice July, 1983 made

the following points:

I X-168

1. The delayed onset of effects of the mutagenic and

carcinogenic chemicals (allergies, depression, muscle

pains) is remarkably like that produced by viruses

such as myalgic encephalomyelitis;

2. The actual neurological deficits of the veterans

(dizziness, blurred vision, blackouts, parasthesia,

tinnitus) are extraordinarily similar to those

produced by poisoning by mercury and other heavy

metals;

3. The progressive nature of the peripheral (and central)

neuropathy mimics the effects of hydrocarbons such as

hexane and TOCP which induce a "dying back" neuropathy

of long myelinated fibres. Other related chemicals or

toxins (thallium or carbon disulphide, porphyria) also

induced psychosis and this could explain the rather

bizarre behaviour of the veterans when they have their

Vietnam flashbacks;

4. The Senate Inquiry ignored recent work on the high

level of urinary porphyrins in veterans which suggests

treatment may be possible for a porphyria-1ike

disease.

IX-16 9

Dr. Barr made a submission to the Senate Inquiry stressing

in his submission the similarity between the veterans

symptoms and those of heavy metal and organo-phosphate

poisoning.

Dr. Barr made a number of requests of the Commission to be

allowed to give evidence to this Commission, and supported

his requests with copies of some of his work.

Counsel for both W A A and Monsanto declined to call

Dr.Barr as a witness.

The Commission referred two abstracts of papers by Dr.

Barr, "Suppression of Pharmacobehavioural Effects of

Hydrocarbon Neurotoxins with Hepatic Microsomal Metabolite

Antagonists" and "Toxicologically Based Psychotic

Disassociative Disorders and the Vietnam Flashback

Phenomenon" for comment to Professor Aldridge, the world

renowned toxicologist whose qualifications have been set

out earlier in this Chapter.

In the first paper the behavioural effects of chronic

exposure to solvents, pesticides and hydrocarbons were

compared to those of mercury and porphyria involving

I X- 17 0

psychosis, depression, intolerance of alcohol, abdominal

pain, distal, axonopathy, and liver dysfunction (emphasis

added). Dr Barr claimed that it was becoming increasingly

clear that the neurotoxicity of industrial solvents

generally are due to the production of free radical

oxidants via liver microsomes.

Ά range of antioxidants originally used in mercury

poisoning were found to have a beneficial effect on

specific parameters of 20 patients suffering behavioural

effects of organic chemicals described above, for example,

blackouts, paraethesia, violence. headaches, stress

intolerance, and increased sensitivity to anti-depressants

and alcohol which are also metabolized by liver microsomes.

Professor Aldridge had this to say of that paper:

It is quite true that the hydrocarbons solvent hexane causes its neurotoxic effect by" dying back" neuropathy and this is brought about through a metabolite 25 hexane dyon. It is a big

jump from the hydrocarbon solvent hexane to the behavioural facts that have been seen in Vietnam veterans.....

This neuropathy is transient and the peripheral nerves repair themselves (emphasis added). There is in addition in a recent paper some suggestion that changes occur in the central nervous system

in the blood flow in various regions of the

brain. This is very recent work from a group in Edinburgh but it has not yet been assessed and is in fact being worked on in my laboratory in

England.

IX-171

It seems probable that this central effect is also produced by the metabolites produced largely, one expects, in the liver.

I think the most important feature is that there has not been much evidence of a peripheral

neuropathy except if I understand the documents it has seen in rather a few cases. For this

reason I think that the postulates in the

abstract by Dr. Barr are of doubtful significance to the Vietnam veterans syndrome.

The second paper gave the results of an intensive

neurological study of 130 veterans for severe behaviour

disturbances either described by the veterans themselves

(usually a situational reaction) and those not recalled by

the patient but only by observers, the second of which

categories had elements of automatism, fugue state,

twilight state. Oneiroid psychosis, and pathological

intoxication.

There was a linking of three classical categories namely,

temporal lobe seizures, paranoid psychosis and personality

disassociation states. Chemicals known to cause such a

syndrome were stated to be mercury, carbon disulphide and

thallium.

The porphyria induced psychosis of George III was also

identical. Most of the above disorders also caused a

"dying back" neuropathy according to Dr Barr who also

I X-172

claimed that the above are metabolized by hepatic

microsomes so that psycho-active drugs which are also

metabolised by the liver, for example. alcohol are

suspected of being one of the major triggers for these

episodes. Currently novel hepatic metabolite buffers

(anti-oxidants) have partially controlled the effect.

A strong link with complex partial seizures was postulated

by Dr Barr because of the high incidence of blackouts,

absences, alcinerte, drop attacks, memory lapses, and

transient disorientation depersonalisation, and lengthy

post-ictal stupor following rages.

Standard EEG1s in many veterans revealed focal slow bursts

over temporal lobes. However proof of the underlying

cerebal pathology was not the important factor but the

forensic and legal psychiatric implications for the

patient.

Professor Aldridge had this to say of the aspect of

metabolisation mentioned in the second paragraph of Dr.

Barr's abstract.

... In the second paragraph he mentions that

mercury, carbon disulphide and thallium are all metabolised by hepatic microsomes and suggests that psycho-active drugs which are also

I X - 173

metabolised by the liver, for example alcohol, might be one of the major triggers for these

episodes.

The Professor could not follow the logic of the argument

since he does not consider that mercury and thallium are

normally substrates for the hepatic microsomes.

The Commission also referred Dr Barr's views and papers to

a consultant neurologist. Professor G.A. Broe of Sydney

University, who thought that they were unworthy of

serious consideration.148

The Commission in all the circumstances decided that it

would not call Dr Barr. It rejects his theories.

I X-174

Crying in his sleep, screaming in the night. Lying in an ice-cold sweat, waking up in fright. Was that the click of a rifle, he just can't tell anymore, A sound of domesticity or a flashback to the war. With nervous shake movements his body sore and

aching...

Elizabeth McGrath, 1981

16. MENTAL AND PHYSICAL HEALTH AND WELL-BEING OF THE

SPOUSES OF VIETNAM VETERANS

W A A in its submissions made little reference to the

health effects on the wives of Vietnam veterans.

The manner in which the physical health problems of wives 14 9

were referred to in W A A 1 s initial submission

concerned miscarriages by wives and deformities in their

children (p. 12); it was claimed that "Wives who suffer

health problems arising from their spouses' exposure to

chemicals in South Vietnam should be entitled to

150

Repatriation benefits". .

Under the general heading of "Morbidity" complaints of

still births, miscarriages, urinary tract infection, and

. , 151

cervical cancer appear.

At page 35 of the submission reference is made to

"complaints found by Veterans Administration in Chicago."

IX-175

The reference given was checked and found to be to Maude

de Victor's claims in the WBBM T.V. Show! (as to which see

Chapter I).

No evidence was adduced by W A A concerning "Any effects on

the mental and physical and well-being of .. spouses"

resulting from "... the effects of any exposure to

chemical agents on the mental and physical health and

well-being of Australian personnel.." within the Term of

Reference (i) of the Letters Patent.

Evidence has been given of the stress undergone by

Australian personnel during the Vietnam conflict and

subsequently. While the major burden of mental ill-health

flowing from service in Vietnam has fallen on the veteran

himself, consequential results must have flowed on to his

wife and possibly his children.

The Commission needs to cite only the continuing media

controversy over Agent Orange. For example, the emotive

publicity alleging miscarriages and deformities must have

placed a heavy strain on the mental well-being of a

prospective mother.

I X-176

But the wives of troubled Vietnam veterans are subject to

psychological and perhaps physical burdens deriving from

the status of their husbands as Vietnam veterans. The

wife may acquire some part of the negative image which the

Australian community has developed - and still maintains -

in respect of the Vietnam veteran. Almost by osmosis a

negative community conception may be visited upon the wife.

But the matter goes beyond the image perception which

Vietnam veterans' wives may have of themselves.

As the wife of a veteran she may suffer second hand from

the terrors and the anxieties, the restlessness and all

the other negative factors associated with the "Vietnam

veteran syndrome". She may be subjected to unpredictable.

intemperate, or violent moods, and to sullen or estranging

behaviour. The children may need protection from erratic

and eccentric behaviour of a father . The recourse which

some veterans have had to drink, the inability of some to

maintain social relationships, restlessness and inability

to sleep, and changes in their patterns of employment and

residence, all must effect the wife of a veteran who is

disturbed.

IX-177

In the absence of the morbidity study proposed by the

Commission reliable figures are unavailable but a reading

of available (especially American) literature and the

informal sessions satisfy the Commission that the divorce

rate for Vietnam veterans is higher than in the community

„ n 152 at large.

Loss of libido is associated with feelings of alienation

and low self-esteem, associated with PTSD. This too must

have its impact.

The Commission is also aware that wives make many of the

initial contacts with the WCS. In those cases the wife

is often afraid that her husband will find out that she

has contacted the Counselling Service. That this is

common is clear from the informal sessions of the

Commission held throughout Australia.

In the absence of any submissions or other evidence

directly on the subject, the Commission is unable to make

a positive finding as to what precise mental and physical

effects Vietnam service has had on the spouses of

veterans. Certainly it is able to make a finding that

there is no chemical causation for such effects. However

it notes the consistency of the anecdotal evidence and a

commonality of experience.

IX-178

A common complaint of the wives has been that the veteran

"was not the person I married."

The Commission has no doubt that the wives of troubled

veterans are themselves suffering mental and physical

health consequences which it is unable to quantify or

qualify precisely.

If one accepts the premise that an impact on one part of a

family system may well affect the entire system,(and the

Commission has no doubt of it) remedial efforts ought to

be directed to the entire system. Treatment for the

veterans family, rather than just the veteran should

therefore be available. The paper of Charles Figley,

concerning the effects on the family system as a whole is

of relevance.153

As Dr T. Williams states:

It is clear that when the veteran exhibits

maladaptive patterns, these patterns are played out by those closest to him. In other words, if his family represents his closest and strongest affiliation - the system in which his

interdependence with others is greatest - then the family is usually also operating in a

maladaptive fashion.154

IX-179

It is crucial that the veteran, their spouses, their

families and the general population be provided with

information about PTSD amongst Vietnam veterans so as to

be sensitized to the issues involved.

17. PSYCHIATRIC AND PSYCHOLOGICAL TREATMENT OF VIETNAM

VETERANS

17.1 Repatriation General Hospitals (RGH1s)

In his evidence Mr Davies, of the of the Perth WCS,

expressed his opinion that the peak of veterans presenting

for treatment of some kind would be in about 1989 . This

coincides with the views of Dr.Arthur Blank,expressed to

the Commission in Washington.D.C.

Vietnam veterans initially are reluctant to seek treatment

for psychological illness. The chief requirement,

therefore, for any facility established to assist Vietnam

veterans is that it gain their trust. The atmosphere

created must be one which is non-threatening,

non-judgmental and in which the veterans will be assessed

155

in a "non-prejudicial and totally open way".

I X - 1 8 0

Dr Spragg, formerly Consultant Psychiatrist at the RGH

Concord (Concord) acknowledged that some Vietnam veterans

are so alienated that they need the reassurance of their

comrades.

He considered that a relatively small population required

group therapy and that it was more important that therapy

should be directed towards settling the veteran down,

getting him to have confidence in his therapist, and then

to try to get him back into the mainstream of the

population rather than remaining in a separate group.

often perceived by the veteran himself as a negative 156 elite.

Dr Boman, Specialist (Psychiatry) referred to the

treatment implications of the Vietnam experience for

returnees. The basis of treatment is the actual traumatic

experience of the tour of duty in Vietnam which should not

therefore be regarded as basically a neurotic problem due

to pre-military environment and influence. The veteran

may initially be very reluctant to talk about his

experiences because they are so unpleasant and painful

that he initially adopts an over-compensatory hostile

approach. He may feel guilt over events which occured in

Vietnam, including the death of friends, for which he

blames himself, or the guilt of the survivor.

IX-181

Dr Boman was, of the view that the person treating the

Vietnam veteran should be "much more of a real person

rather than hiding behind a screen, like some

psychoanalysts perhaps tend to do" (Transcript page 4700,

12 September 1984).

The two psychiatric wards, 24 and 34, at Concord were

visited by those assisting the Commission. It was not

possible for the Commission to visit every repatriation

hospital in Australia. But the Commission is aware that

there are from time to time differences in the quality of

treatment and staff attitudes within the repatriation

hospital system within Australia.

Dr Streimer, a consultant psychiatrist who had five years

experience at Concord whilst in psychiatric training, gave

evidence that high admission levels in 1980 continued in

1981 and 1982. He ascribed the high level to a change of

official policy towards letting Vietnam veterans into the

hospital but also to the concern generated by the toxic

chemical issue and an increased level of awareness amongst

Vietnam veterans of the "problems" publicised by the media

(Transcript pp 4978, 4978a).

I X - 182

The Commission notes especially Dr Streimer1s view that it

is dangerous to put all Vietnam veterans into the same

diagnostic mould.

The foundation stone of treatment is an accurate diagnosis

for that individual. The essential feature of treatment

is that the veteran must be allowed to ventilate his

disappointment and anger in an environment which is

understanding and accepting and in a situation which

avoids the perpetuation of his feelings of alienation and

separateness. Accordingly they should be encouraged and

allowed to help themselves to reintegrate and that they

not have the feeling of separateness reinforced by the

arrangements made for their treatment.

In further contrast to Mr Davies' evidence however. Dr

Streimer found that marital problems in the group surveyed

by him were no more frequent than among the controls. He

considered that family involvement and continuing support

were important aspects of treatment. For those suffering

PTSD the essential feature of treatment was to allow them

to relive their traumatic experiences and to work them

through so as to integrate those experiences into the 167 rest of their lives.

I X-183

RANZCP points out treatment of psychiatric war casualities

and Vietnam veterans is dependent on the diagnosis.

Disorders precipitated or exacerbated by war service,

organic mental disorders, and incidental psychiatric

disorders not related to active service will all receive

the currently accepted treatment for these conditions.

Even with the introduction of DSM III PTSD probably will

attract a wide variety of treatments depending on the

theoretical and training background of the therapist as

well as the diagnostic characteristics used. With chronic

or delayed PTSD some success has been reported with use of

anti-depressants but others have reported that

psychotropic drugs in standard dosage are ineffective. It

has also been reported that traditional

psychoanalytically-oriented psychotherapy is largely

ineffective. RAP groups in America have stressed the need

for the therapist to be a much more active participant in

the group rather than the uninvolved leader/therapist of

traditional therapy groups. and some therapists view

abreaction as either unnecessary or too "intrusive".

If a psycho-physiological basis for the condition is

accepted treatment might be expected to be directed more

at the immediate precipitating cause (in addition to any

co-existing disorder) and in preference to a focus on

I X-184

pre-service personality characteristics. In America in

addition to the untraditional RAP groups run largely by

the veterans themselves, traditional individual

psychotherapy, group psychotherapy, family therapy and

various behavioural techniques have been used.

With war veterans depending both on the severity of the

condition and the degree of patient repression of

traumatic memories (particularly the emotional component)

there is a range of treatments from fairly simple sharing

of the experience with sympathetic others through more

extensive exploration and desensitization procedures to

more dramatic abreaction and flooding. As might be

expected from the importance of group cohesion in

preventing Acute Traumatic Stress Disorder it is likely

that any and all such treatments will be more effective

within the overall safety of a peer group.158

The section on the treatment in the submission concludes

with a challenge:

The denial and avoidance which has been described as characteristic of Vietnam veterans are only matched by the denial and avoidance of mental health workers ...

Mental health professionals mirror the country's ambivalance toward the Vietnam war. In order to know how many need healing, they will have to risk 1 hearing' what these veterans have to tell us about themselves.159

IX-185

It is manifest that the treatment offered in the

Repatriation General Hospitals will depend largely upon

the diagnosis, the facilities available for such

diagnosis, and the outlook of the individual

professional. It is unlikely that any consistent or

uniform treatment will be prescribed, nor, for the reasons

given above. does it appear to be desirable that they

should. Individual problems require individual

treatment.

The evidence of Doctors Spragg, Boman and Streimer at the

one facility indicates a variety or diversity of approach,

and in the Commission's view this is appropriate. The

Commission reiterates its regret that, in the absence of a

morbidity study, it cannot do more than estimate the

extent of the problem.

17.2 Vietnam Veterans Counselling Service ("WCS")

By the end of 1980 the then Minister for Veterans' Affairs

had become aware of problems being experienced by Vietnam

veterans. Consultations had taken place with W A A and the

RSL and submissions for grants-in-aid to set up a

counselling service had been presented to the Government

by the W A A and the Vietnam Veterans' Family Association

of Western Australia.

I X- 18 6

In January 1981 the Minister anounced interim Departmental

arrangements to operate until a more permanent structure

was planned. In July 1981, the Minister had access to the

Outreach Program, an American program designed to reach

Vietnam veterans in what might be described as a "shop

front" setting, separate from the US Department of

Veterans' Administration. He was impressed and set about

establishing a similar system.

The first counselling service commenced operations in

Adelaide on 29 January 1982 and within six months

counselling centres were operating in all state capital

cities . and Darwin. Since then another W C S branch has

been opened in Canberra. Thus every capital city in

Australia possesses such a facility. Centres are now

located in Adelaide, Parramatta, Sydney, South Perth,

Hobart, Darwin, South Melbourne, Brisbane, Townsville and

Canberra.

An indication of the workload of the centres is that in

the four weeks ending 18 November 1983 there were a total

number of contacts of 1,828 in the centres. Those

contacts included contacts outside the centres and

contacts by telephone. A substantial number, however,

were of past clients, (754), and there were 150 new

clients in that four week period.

IX-187

The Commission had the benefit of an Informal Session with

the senior counsellors from the Perth. Townsville. Hobart,

Darwin, and Canberra offices of the W C S in Sydney on

Tuesday 13 December 1983. At the conclusion of the Formal

Session a communique from the senior staff of the W C S was

submitted to the Commission.1"60

A report by the W C S Brisbane Senior Counsellor (Mr Trevor

Fear) was also made available to the Commission.161

Each of the Senior Counsellors gave an account of his

centre's work. There were regional differences in

treatment and facilities but the outstanding feature was

the uniformity of clientele and description of the

syndrome. That communique solidly reinforced the

Commission's view that the syndrome exists, can occur in

delayed form and can be treated.

The session and the communique also displayed the skill

and concern of the counsellors themselves. Their success

has been prodigious.

Counselling Techniques

Practice

Although there is an abundance of professional

IX-188

literature from America on the problems and the

possible causes of the problems of Vietnam veterans,

there has been very little written as to the most

suitable methods of dealing with those problems.

Consequently, the Counselling Service has had to

develop its own treatment methods.

Some of the counselling techniques used include

individual psychotherapy, marital counselling, family

therapy and group therapy. Hence a wide range of

skills and expertise is required in W C S counsellors.

17.3 The Treatment of Vietnam Combat Veterans

The Combat Veteran as Survivor

There is a notable reluctance on the part of troubled

veterans to seek counselling assistance in general and

relief from combat-related stress in particular. Serving

soldiers actually fear disadvantage or even reprisal for

seeking help. Another factor is that a small percentage of

veterans feel contempt and mistrust for "the system".

Moreover, like other survivors of catastrophic events,

some veterans are fearful of authority and particularly of

being given psychiatric labels synonymous with being a

"psycho".

i X-189

1 7 . 3 . 1 P h i l o s o p h y

Efforts to understand and treat problems of war veterans

have a long history and a variety of causative factors

have been postulated. In the main these approaches have

worked from the assumption, sometimes only implicit, that

there is some inadequacy in the individual (coward, weak,

neurotic predisposition, unresolved childhood conflicts,

etc). The most recent formulation is PTSD. In this

conceptualisation, the veteran is viewed as not having

been able to adjust to an extreme stress situation.

War veterans are classed with victims of fire, earthquake,

assault, etc and are seen as having been unable to adapt

to the extraordinary stress, so they suffer from recurrent

intrusive thoughts and recollections of the event.

Pre-existing psychopathology is seen as pre-disposing to

development of the disorder.

This conceptualisation still maintains the "inadequate

individual" viewpoint, and fails to recognise that the

responses of hurt veterans to war and killing are totally

natural, normal responses to an unnatural, abnormal

situation - not the reverse. It is important that

society. Department of Veterans Affairs and those involved

in the treatment of veterans work from this standpoint.

I X-190

1 7.3.2 F a m i l y T h e r a p y I m p l i c a t i o n s

Many PTSD symptoms have implications for interpersonal

relationships. Those identified by Horowitz and

Solomon162 include

(i) difficulty integrating memories and fantasies of

the Vietnam experiences with past, present, and

future events;

(ii) impaired self-concept;

(iii) depersonalisation of interpersonal experiences;

(iv) depression;

(v) shame;

(vi) frustration and reactive rage;

(vii) general impairment of social relationships.

While such symptomatology as depression, shame and

impaired self-concept may be viewed as intra-psychic

phenemona, systems oriented therapists will quickly

recognise that they will have significant implications for

the family life of the veteran.

Many veterans and their families had high expectations for

post-war life that led to bitter disappointments when not

fulfilled or were marred, for example, by

unfaithfulness.163

I X - 191

1 7 . 3 . 3 T r e a t m e n t Issues

Because the problem presented to a therapist is likely to

go beyond combat stress per se it is not possible to

delineate a standard course of treatment. The problem

will probably be imbedded in the context of one of a

myriad of marital and family problems and should be

handled accordingly. There are however, specific issues

that should be addressed early in the treatment o’f PTSD:

(a) Intake Information about military service and

combat involvement should be included in the

routine intake procedure. For those who have

experienced combat the therapist should attempt

to identify the quality and quantity of initial

stress and the degree to which the veteran has

successfully coped with it.

(b) Co-therapy Where possible the therapist should

consider using a Vietnam veteran as a

co-therapist. (at least for a portion of the

therapy program.)

(c) The Unit of Treatment The primary unit of

treatment should be the veteran's family living

unit and all members of that unit should be seen

together early in the therapy program.

I X-192

17. 3. 4 " F l o o d i n g " as a T h e r a p e u t i c T e c h n i q u e

Dr James Quinn is probably best known in Australia for his

implementation of a "flooding" program for Vietnam

veterans at the RGH. Greenslopes. Brisbane. He is a

Doctor of Medicine. Member of the Royal College of

Psychiatrists (London), and Member of the Royal Australian

and New Zealand College of Psychiatrists.

He is a publicist of "flooding" as a behavioural

psycho therapeutic technique for Vietnam veterans.

The Commission has fully considered the contributions made

be Dr Quinn and regrets that time constraints precluded

his giving oral evidence.

The Flooding Technique has been defined above. Dr Quinn

in the course of making submissions informed the

Commission that the Department of Veterans' Affairs was no

longer providing any facilities for the continuation of

the flooding programs at Greenslopes.

His opinion was that almost all the PTSD patients in

Queensland could be treated over a period of three years

at a cost of $300,000, $50,000 of which would be needed to

IX-193

establish an appropriate physiological and video tape set

up and the rest of the money would be required for the

salaries of therapists. Patients could be treated on an

outpatient basis using either an exercise technique

(jogging, cycling with imaginal presentation) or the model

developed by Professor Keane.

A research proposal put by Dr Quinn jointly with Professor

P. Ley, Professor of Clinical Psychology, University of

Sydney, and another was rejected by the Department of

Veterans' Affairs. That study of attitudinal, behavioural

and psychophysio logical responses in Vietnam veterans

suffering from PTSD, and particularly of the relationship

between such responses and the process and outcome factors

of drug assisted graded exposure treatment would have

required the investigation of psychometric and

psychophysiological and behavioural features in distressed

and non-dis tressed Vietnam veterans. It would have

attempted to relate to such variables to process and

outcome factors in high dose and low dose diazepam

assisted graded exposure regimes.

The Commission finds that, on the basis of all available

evidence, the treatment known as "flooding" with or

without the use of drugs is a most useful technique and

IX-194

should be used in the RGH system where specialists

knowledgeable in its use are available and deem it

appropriate.

18. EVIDENCE OF TREATMENT OF PTSD

18.1 Review of Treatment Literature by Professor

* . 164

Andrews

The Report by Professor Andrews on the "Treatment of Post

Traumatic Stress Disorder" appears at pp 42-52 of his

Report to the Commission (Exhibit 1493). He concludes:

... the available empirical evidence is of such poor quality that it does not allow conclusive statements to be made about treatment efficacy. Indirect sources of evidence can be used to supplement the outcome literature, although conclusions reached from these sources must be

tentative. The indirect evidence indicates that common clinical practice which incorporates the reliving, "working through" or contact with the traumatic experience is at present the treatment of choice. To the present reviewers, the failure to attend to the usual methodological

requirements of scientific investigation in the treatment outcome literature stands in marked contrast to the size and quality of the

literature attempting to determine the cause and prevalence of the disorder in veterans (at pp 51 and 52).

The literature describing both the treatment and the

therapeutic process of recovery for PTSD can be divided

into four groups:

IX-195

(i) Narrative accounts of group treatment programs

which describe the theoretical basis of the

therapy and the presumed process of change

without giving data on the actual outcome

resulting from treatment;

(ii) Unsubstantiated observations and opinions

regarding factors claimed to be important in

effective treatment;

(iii) Reviews of treatment in which conclusions extend

beyond the available data; and

(iv) Treatment-outcome reports which describe

interventions for PTSD resulting from war and

from other trauma.

These studies were reviewed extensively by Professor

Andrews and have been read by the Commission.

18.2 Other Sources of Such Evidence

Three other sources of evidence are examined:

(i) Evidence from studies which report on the

treatment of components of PTSD;

IX-19 6

(ii) Evidence from reports of common clinical

practices;

(iii) Evidence from models which offer consistent and

empirically supported evidence for the aetiology

of PTSD.

These were examined in detail and the Commission found

that there is a common clinical practice in the treatment

of PTSD. This consensus exists despite different

theoretical positions which gives validity to procedures

which incorporate exposure to the traumatic experience as

part of therapy.

18.3 RANZCP Submission

The submission1 6 5 of the RANZCP ("the College") deals

with treatment at pp 22-23. Their basic conclusion is as

stated on page 24 (paragraph 10.5):

In the treatment and management of Vietnam Veterans, it is particularly necessary to differentiate carefully Post Traumatic Stress Disorder from Organic Mental Disorders.

In dealing with the concern expressed in the Senate Report

1 6 6 regarding the issues of "dependency" and the effect

IX-197

of compensation on persistence of chronic war neuroses

there is clinical evidence that those who have and are now

seeking help are more interested in coming to terms with

their difficulties than either wanting to assume the

patient role or pursue financial rewards.

Finally the Council noted a saying in America that RAP

groups "cure compensation" and - because of the nature of

the psychological problems of war veterans - the

identification of patients suffering from PTSD and

encouraging them to accept treatment is likely to be a

much bigger problem than malingering. This is certainly

confirms the Commission's strong impression that veterans

are unconcerned with monetary compensation and wish only

to be well.

It seems from the submission (Exhibit 1014) that the

College has no official policy as to the treatment of

veterans suffering from PTSD. There is also perhaps a

touch of irony in the concluding reference by the College

to an American article which observes that "Mental health

professionals mirror the country's ambivalence toward the

Vietnam war" (para. 9.8, p. 23).

IX-198

19. CONCLUSIONS

The Commission has been greatly impressed by the

dedication, concern and compassion of those whose

specialties have extended to the treatment of Vietnam

veterans and their families.

It is also apt to acknowledge that the aftermath of war is

keenly felt and all too often visited upon those who had

no direct part in its prosecution, particularly the

immediate families of those participants.

To the attributes of the courage displayed by Vietnam

veterans in a war that was. so far as Australia was

concerned, not officially "a war" but merely "a war-like

hostility" must be .added the devotion and courage and

determination and fortitude displayed in peace by their

spouses and their families.

It must also be recalled that members of the Australian

Task Force in Vietnam were highly trained,

well-equipped, and amongst the most competent

representatives of Australia's Armed Forces ever to have

served in any foreign theatre of war. They were carefully

selected for service and it comes as no surprise that the

IX-199

great majority have coped extremely well since their

return.

19.1 Initial Testing

Members of the services were subjected to psychological

testing on induction as described by AVHS in it's

Mortality Report. The Commission has no objection to the

tests devised, nor to their rationale.

However, what the Commission found disturbing is that the

psychological testing was conducted by a psychologist "or.

if not available, a clerk ...".

The evidence shows that in the course of one week a

qualified Army psychologist now occupying a Staff Officer

position, with two clerks. interviewed approximately

12,000 men! This is probably an exaggeration, and

possibly an extreme instance, but if true would indicate

one interview every nine minutes! This clearly would be

totally unsatisfactory.

19.2 Psychiatry in Vietnam

Adequate psychological back-up was also not provided

during the Vietnam conflict. Unless a serving Medical

I X- 20 0

Officer in Vietnam specifically requested a psychologist,

army specialists were sent to Nui Dat or Vung Tau only for

the psychological testing of members of the Regular army

in connection with the continuing of their careers in the

Army. The Army Director of Psychology. Colonel Arthur

Craig, for example, undertook 13 such trips to Vietnam

between March 1967 and March 1969.

Psychiatric help depended, in large measure. upon the

peripheral or ancillary expertise of doctors otherwise

concentrating on the mainstream of medical practice.

The evidence of Dr G. Spragg. himself a psychiatrist and

Medical Officer with the First Australian Field Hospital

and the Eight Field Ambulance in South Vietnam in 1970 is

illuminating. Dr Spragg1 6 7 stated that 50 per cent only

of his time was spent as a psychiatrist and the remainder

as a medical officer. He dealt with cases referred to him

usually by the RMO's.

Dr John Ellard who attained the rank of Group Captain in

the Royal Australian Air Force Reserve, visited Vietnam in

1966 in order to assess the stress involved in conducting

Airforce operations in Vietnam. It is clear from his

evidence that he, too, undertook psychiatric duties on an

ad hoc basis.

I X - 2 0 1

The overwhelming impression, then, is that psychiatric

facilities in Vietnam were limited, were ad hoc and were

designed to assist in the elimination or "weeding out" of

"elements" which might detract from the efficient

operational capacity and effectiveness of the Australian

Armed Services in Vietnam. American facilities were used

until the Australian Task Force medical facilities were

fully established, and it was only in 1969 that a

psychiatrist was posted to the field hospital in Vung

Tau. Overall there was a specialist psychiatric cover for

barely two of the ten years of the Australian involvement

in Vietnam. 1 6 8

The absence of adequate psychiatric facilities clearly

determined the implementation of official policy to

repatriate psychotic patients who were unable to respond

in the field to the treatments offered on the basis of

"immediacy, proximity, and expectancy".

19.3 Psychological Debriefing

The Commission was disturbed to learn of the failure to

provide any form of psychological debriefing or

re-adjustment counselling to Australian personnel on their

return to Australia. Numerous instances were cited during

I X - 2 0 2

the Informal Sessions of feelings of isolation,

indifference or apathy and of a lack of support upon

return. The Commission accepts that the average National

Serviceman wanted only to resume the threads of his normal

civilian life and would be unlikely to jeopardise an

early discharge by revealing any psychological disorder.

The Army should have provided adequate debriefing and

readjustment counselling and prepared proper Certificates

Of Discharge. The Commission has seen a number of

(isolated) instances where the Certificate of Discharge

bears the notation "Not suited to be a soldier". This

notation indicates either that tests reveal the subject to

be presently below standards considered acceptable for

Army service or that in the opinion of a psychiatrist the

subject is mentally unfit to continue to be a soldier, and

he was accordingly discharged on that ground alone.

This notation is pregnant with overtones of inadequacy

or lack of worth. The Commission considers it harmful to

employment prospects. If it is still Army practice it

should cease forthwith.

IX-203

19.4 Post Traumatic Stress Disorder and its

applicability to Vietnam Veterans

It is obvious that PTSD has been accepted by a wide range

of psychiatrists as an accurate and appropriate diagnostic

tool for a range of disorders involving a life-threatening

situation as then perceived by the individual.

PTSD is said to be more commonly related to the Vietnam

veteran in its chronic or delayed sub-type. The evidence

given before the Commission describes symptomatology which

is also referrable to traumatic events other than

Vietnam.

Anyone who has read Robert Graves1 "All Quiet on the

Western Front" will recognise features presenting in a

form which modern science now calls PTSD.

The Commission finds that PTSD is a valid concept

applicable to Vietnam veterans. The Commission, despite

the conclusion reached by Professor Andrews in his report

to the Commission (Exhibit 1493, page 22) that "claims of

a delayed onset of PTSD remain speculative" and that he

and his team "have found no hard evidence to support (the)

existence" of such a delayed form of PTSD, confirms its

I X - 2 0 4

finding set out above, that the Vietnam veteran syndrome

does exist and that on the evidence before it delayed PTSD

is the probable diagnosis for such syndrome.

19.5 The Results of Combat

The one- in- three veterans who reported experiencing

heavy combat in Vietnam also reported ten years later that

they were experiencing more stress symptoms, more angry

feelings and more drinking problems. The possibility of

these results being in part confounded is real.

The weight of available evidence, however, is such that

the Commission accepts the overall finding that combat,

particularly heavy combat, can conduce to the

symptomatology above described.

19.6 The Counselling Service

The Commission has been greatly impressed with the

dedication and the effectiveness of the W C S . It meets a

need perceived by the veterans and is closely identified

with the veterans. It suffers, if that be the appropriate

word, from too great an oversight by DVA of which it is

nominally independent, but on which it is for practical

IX-205

purposes (such as funding and administrative support),

totally dependent.

The Commission finds that the present level of funding and

of staffing is inadequate to meet the demands and needs of

the veterans themselves, let alone of family therapy and

other forms of counselling which the Commission

recommends.

The Commission also finds that the "charter" of the W C S ,

when compared with that operating in the "Operation

Outreach" program in America, is far too narrow. In

particular, despite the dedicated efforts of its members,

W C S has been unable to provide meaningful counselling

facilities not only to the more remote areas of Australia

but also to many major regional centres.

It simply is not good enough to expect troubled veterans

to travel thousands of kilometres when the need for

counselling is acute. It is a fact of life that a body

of veterans have settled in isolated or remote areas of

the country, often on mining or oil projects, far removed

from the metropolitan centres upon which the W C S is

centred.

I X-206

The Commission accepts the statistical expectation that

the peak period for those presenting with problems

requiring some input from the W C S will probably be

19 8 8 - 8 9. It is hoped that before those years are reached

this Report may have allayed some of the fears of veterans

and their families and so contribute to a speedier and

complete restoration of their sense of physical and mental

well-being.

I X - 2 0 7

"Peace hath her victories No less renowned than War"

John Milton in a letter to Oliver Cromwell

20. RECOMMENDATIONS

1. That all psychological or psychiatric testing of

members of the Armed Forces be performed by

professionally qualified personnel. Testing by clerks

should cease.

2. That any conflict requiring posting overseas of

Australian Personnel at battalion or greater strength,

a full-time psychiatrist be dispatched with other

medical facilities to provide appropriate treatment in

the field.

3. That the Armed Forces prepare and maintain a manual of

psychiatric practice in the field, including

principles of treatment such as "proximity, immediacy,

and expectancy".

4. That the practice of endorsing a Certificate of

Discharge "Not suited to be a soldier" cease forthwith.

IX-208

5. That wherever possible units travel and return to the

area of conflict together. After withdrawal from a

battle zone, prior to return for demobilisation,

personnel be placed in a military environment for a

period of at least two weeks. During this period

thorough de-briefing and demobilisation counselling be

given. A relaxed discipline should apply pending

return to civilian life.

6 . That after debriefing, the soldier be sent for a

further period of approximately two weeks to a

recreation facility with his or her primary partner

or spouse to permit adequate opportunity to

re-establish their relationship on "neutral" ground:

child care subsidies should be provided during this

period.

7. That under no circumstances should returnees be

returned to civilian life without appropriate

assistance, including money, civilian clothes and

adequate transport to their homes.

8 . That comprehensive psychological/psychiatric

assessment of every member of the Armed Forces be

undertaken prior to discharge.

I X - 2 0 9

9. That the Commission respectfully suggests that

thorough debriefing and "retirement" counselling

occur at the time of discharge of the " 2 0 year" man

from the regular forces. The re-adjustment problems

of these men have been brought forcefully(if

irrelevantly)to the attention of the Commission.

10. That the Vietnam Veterans' Counselling Service (WCS)

be established on a statutory basis, independent of

the Department of Veterans' Affairs, but responsible

to the Minister administering the Repatriation

Legislation. The enabling legislation should contain

a five year "sunset" clause.

11. That the W C S be available to visit remote areas with

known concentrations of Vietnam veterans.

12. That Senior W C S counsellors be permitted to issue

travel warrants to enable a veteran, with his spouse,

and family if necessary, to travel to the nearest

facility offering emergency psychiatric care, whether

or not that facility be within the RGH system.

13. That W C S forthwith be expanded to an extent adequate

to provide comprehensive family or group counselling

I X - 2 1 0

as required. It should also be expanded at an

administrative level to permit Vietnam veterans to

receive competent advice on repatriation

entitlements. The WCS, in this form, would therefore

act as mediator between the veteran and the

appropriate governmental agency.

14. That counselling services through W C S or otherwise be

available to any member of the immediate family of a

Vietnam veteran whether the veteran presents or not.

15. That W C S be given sufficient funds to perform an

educative role so that the veteran and non-veteran

community can be informed of the nature of the

problems actually facing the Vietnam veteran, and of

the rebuttal of the Agent Orange myth. It should also

publicise its own dual service.

16. That the pamphlet summary of the Commission's findings

and recommendations be made available free to all

members of the public from DVA, W C S , Post Offices and

all branches of the Commonwealth Bank.

17. That any PTSD-related disability pension be subject to

review by a professionally qualified person at least

once a year.

IX-211

18. That funds be provided to promote research, through

the NH & MRC, into the psychological problems of

Vietnam veterans, with particular emphasis on

treatment methods and differential success rates of

treatment systems.

19. That the Australian Government erect, in the National

Capital, a monument appropriate to the sacrifice of

Vietnam veterans living and dead. It should be

outdoors and readily accessible and should acknowledge

by name those who died on actual service.

20. That there be Government approval for the declaration

of a "Vietnam Veterans' Day" on an appropriate date to

be determined after consultation with Vietnam Veteran

groups. It is suggested that 18 August (the date of

the battle of Long Tan) might be an appropriate date.

I X- 21 2

ENDNOTES

1.

2 .

3 .

4 .

5.

6 .

7.

8 .

9 .

10.

11.

12 .

13 .

14 .

15 .

16 .

17 .

18 .

19.

20.

21.

22 .

23 .

24 .

Advancement of Learning , bk I.v8 .

Appel (1966) .

Bulletin of the US Medical Department 1943.

See Bib.

See Bib.

President's Commission on Mental Health 1978 pp 1331-1333 (See Bib).

See Bib.

Exhibit 1504Z.

Exhibit 1761.

Exhibit 1003.

Exhibit 1014.

Exhibit 1003.

Exhibit 1014

Exhibit 1448.

At pp 13-15.

At pp 9-17.

At p 45.

Exhibit 1040 at pp 12-13.

Ibid p 44.

Exhibit 1157.

Exhibit 1040 at p 54.

Exhibit 644.

Exhibit 101.

E x h i b i t 1 0 4 0 .

I X - 2 1 3

25.

26 .

27 .

28 .

29.

30.

31.

32.

33 .

34.

35.

36.

37.

38.

39.

40.

41.

42.

43 .

44.

45.

46.

47.

48 .

Ibid at p 56.

Exhibit 731, and the references therein cited.

Exhibit 731, and the references therein cited.

Exhibit 1040 p 53, Exhibit 1879, 77-78.

Exhibit 1343.

Ibid p 6 .

Ibid p 17-18.

Ibid p 20-21.

Ibid p 21.

Ibid p 29.

Ibid p 30.

Ibid p 33.

Ibid p 38.

See transcript pp 3382-3390.

Exhibited 1983 , Ross and Sholiton at pp 100. and 104.

Exhibit 1343 p 29.

Ibid p 38.

Ibid p 39.

Transcript p 3319.

Transcript p 3354.

Transcript at pp 3378-3379.

Transcript p 3392.

Transcript at p 3411.

Transcript at p 3430.

102

I X-214

49 .

50.

51.

52 .

53 .

54.

55 .

56 .

57 .

58.

59.

60.

61.

62.

63.

64 .

65.

66 .

67 .

68 .

69 .

70.

71.

72.

73 .

Transcript at p 1946.

Exhibit 1345 pp 9-10; see also Transcript p 3491.

Exhibit 1312.

Ibid pp 9-10.

Exhibit 1879.

Exhibit 1577A.

Ibid p 1.

Exhibit 1606 At p 383; see also Fullerton Exhibit 681 p 2 0 1 .

Exhibit 1615.

Ibid p 2.

Exhibit 1615 p 2.

Exhibit 1630. p 257.

Exhibit 1631.

Exhibit 1632. Ibid 361.

Exhibit 1633. pp 1373-4.

Exhibit 699.

Ibid p 1387.

Ibid p 1388.

Exhibit 1615, p 3.

Exhibit 1647 p 135.

Ibid p 136.

Exhibit 1615 at p 3.

Exhibit 1647 at p 132 and at p 136.

T r a n s c r i p t a t p p 3 4 3 5 , 3 4 3 8 .

E x h i b i t 1 6 1 5 a t p 4.

I X - 2 1 5

74 . E x h i b i t 1676.

75 .

76 .

77 .

78 .

79 .

80.

81.

82 .

83 .

84 .

85 .

8 6.

87.

88 .

89 .

90.

91.

92 .

93 .

94 .

95 .

Exhibit 1676 pp 3-5.

Exhibit 1701 p 526.

Exhibit 1701 p 537.

A paper by Eisen et al. 1983: Exhibit 1685 is cited to support this proposition: See Transcript at p 5564.

See Transcript at p 5559.

Transcript p 5564.

Transcript p 5561.

Exhibit 1676 p 8 .

Exhibits 250 and 1550.

See Exhibit 250 pp 11-12.

see Exhibit 1550, summary section.

Exhibit 250 p 12.

Exhibit 1984: Suskind (1983) "Long Term Health Effects Of Exposure To 2,4,5-T and/or its

Contaminants", Chemosphere 12: 769 .

Transcript pp 5664-5666.

Exhibit 1394 p XI1-15.

Transcript p 5671.

Transcript pp 5671-5671a.

Exhibit 547.

Exhibit 1738.

See English translation of Exhibit 547 p 8 .

See Exhibit 1738 p 10.

I X - 2 1 6

96 .

97 .

98 .

99 .

1 0 0 .

101.

102 .

103 .

104 .

105 .

106 .

107.

108 .

109 .

1 1 0 .

111.

112 .

113 .

114 .

115 .

See Boeri. 1978: Exhibit 25; Boeri et al, 1979; Reqqiani. in his statement to the Royal

Commission: Exhibit 1255 at pp 39-40, and

transcript at pp 2505-6 to the same effect.

Exhibit 1263.

Exhibit 1263 p 16.

Exhibit 1177 p 179.

See Human and Environmental Risks of Chlorinated Dioxins and Related Compounds edited by R.E. Tucker, A. L . Young, and A.P. Gray (1983) Plenum Press, New York at p 796.

Exhibit 1271a.

Exhibit 615.

Ibid p 31; as to dosages see Allen et al Exhibit 255; Kuratsune et al Exhibit 1727; Crosby et al Exhibit 345 ; Yoshimura et al; McConnell et al Exhibit 288.

Exhibit 1676.

Ibid p 9.

Transcript pp 5599-5600.

Exhibit 1579.

Transcript p 5671a.

Exhibit 1676 p 10.

See Exhibit 1976.

Exhibit 1902.

Exhibit 1902 at p 38.

Exhibit 1345 pp 5-6.

Exhibit 1345 p 6 .

See Jager, 1970; Versteeg and Jager, 1973; and Van Raalte, 1977, discussed in Exhibit 730 at p 5.

I X - 2 1 7

116 .

117.

118 .

119.

120.

121.

122.

123.

124 .

125 .

126 .

127.

128.

129.

130.

131.

132 .

133 .

134 .

135.

136.

137.

138 .

139 .

See transcript p 3467.

Exhibit 1699.

Exhibit 1700.

Exhibit 1980 at p 5.

Exhibit 1345 p 5. See also Transcript pp 3463, 3511-3511a to the same effect.

Transcript p 3478.

Exhibit 1740.

Exhibit 1740 pp 6-10.

Transcript pp 5858a. 5855-56. 5848-5852.

Transcript pp 5889-5891 and Exhibit 1740. Para 15.

Exhibit 1740 para 18 and transcript pp 5867-5870, 5873.

Exhibit 1879.

Transcript pp 4595-7.

At p 4853 of the Transcript.

Exhibit 1452 p 339.

Transcript p 4605.

Exhibit 1462.

Exhibit 1463. p 2.

Ibid, pp 2 and 3.

Exhibit 1493 at p 4.

Transcript pp 338-9.

Transcript pp 338-9.

E x h i b i t 134 5 p 6.

E x h i b i t 1462.8.

I X - 21 8

140. E x h i b i t 1493.

141.

142 .

143 .

144 .

145 .

146 .

147.

148 .

149 .

150.

151.

152 .

153 .

154 .

155 .

156 .

157 .

158 .

159 .

160.

161.

Exhibit 1497.

Exhibit 1464.

Exhibit 1465.

Exhibit 1504G.

Exhibits 1504E and F.

Exhibit 1472.

Exhibit 1493.

Personal communication to Counsel Assisting - August/September 1983.

Exhibit 1040.

At p 13.

At p 64.

Vietnam veterans in America are reported as having a divorce rate 26% higher than their peer groups.W. Davies W C S , Personal Communication.

C. R. Figley and D. H. Sprenkle "Delayed Stress Response Syndrome: Family Therapy Indications", Journal of Marriage and Family Counseling. July 1978. ....

See Bib.

W. Davies, Transcript p 5048.

Transcript pp 4851-2.

Transcript pp 4989-90.

Exhibit 1014 pp 22-23.

Ibib p 23.

Exhibit 1459.

E x h i b i t 1460.

I X - 219

162 . Exhibit 1504T.

163 . Exhibit 1472.

164 . Exhibit 1493 .

165 . Exhibit 1014.

166 . Exhibit 1448.

167. Transcript p 4839.

168 . Exhibit 1472, pp 1

I X- 22 0

APPENDIX I CHAPTER IX

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