MORONSKI and COMCARE
[2010] AATA 277
•20 April 2010
Administrative Appeals Tribunal
DECISION AND REASONS FOR DECISION [2010] AATA 277
ADMINISTRATIVE APPEALS TRIBUNAL )
) No 2008/5599
) 2008/5600
GENERAL ADMINISTRATIVE DIVISION ) Re SARA PATRICIA MORONSKI Applicant
And
COMCARE
Respondent
DECISION
Tribunal Mr S. Webb, Member
Dr M. Miller AO, MemberDate20 April 2010
PlaceCanberra
Decision The decisions under review are affirmed. ..................[sgd].....................
Mr S. Webb, Presiding Member
CATCHWORDS
COMPENSATION - claim for work-related death - ischaemic heart disease - accepted depression injury - psychosocial changes following retirement on invalidity grounds - multiple risk factors for coronary artery disease - cause of death - evaluation of causal chain - meaning of 'results in' - ischaemic heart disease not materially contributed to by employment - death not work caused - decisions affirmed
Safety, Rehabilitation and Compensation Act 1988, ss 4, 14, 17, 67
Telstra Corporation Ltd v Hannaford (2006) 151 FCR 253
Ilsley v Wattyl Australia Pty Ltd (1997) 75 FCR 1
March v E & MH Stramare Pty Ltd (1991) 171 CLR 506
Briginshaw v Briginshaw (1938) 60 CLR 336
Jones v Dunkel (1959) 101 CLR 298
Bater v Bater [1950] 2 All ER 458
Seltsam Pty Ltd v McGuiness and Anor; James Hardie & Coy Pty Ltd v McGuiness and Anor (2000) 49 NSWLR 262
Amaca Pty Ltd v Ellis; South Australia v Ellis; Millennium Inorganic Chemicals Ltd v Ellis (2010) 84 ALJR 226
Comcare v Sahu-Khan (2007) 156 FCR 536
Chappel v Hart (1998) 195 CLR 232
REASONS FOR DECISION
20 April 2010 Mr S. Webb, Member
Dr M. Miller AO, Member1.
Patricia Moronski is the widow of Dr Marek Moronski. Many years ago
Dr Moronski successfully claimed compensation for work-related depression. He was medically retired as a result of that condition some years later. He did not work again. Dr Moronski died suddenly in April 2006. His death was attributed to ischaemic heart disease, although no post mortem investigations were undertaken. Subsequently, Mrs Moronski and her daughter claimed compensation for her husband’s death, asserting that Dr Moronski abused alcohol, he became socially isolated, physically inactive and morbidly obese as a result of his work-caused depression, and these factors contributed to the disease that caused his death. Comcare rejected the claim, deciding that his death and the disease that caused his death were not work-related. On reconsideration, both determinations were affirmed. Unhappy with this result, Mrs Moronski requested review of these decisions.
2. At the outset of the hearing we were informed that Mrs Moronski’s daughter did not press her claim as a dependant in relation to either application.
3. At this point it is necessary to note that the two reviewable decisions arise from Mrs Moronski’s claim for compensation for her husband’s death. Comcare dealt with her application in two separate determinations, one concerning ischaemic heart disease as a fresh injury under section 14 of the Safety, Rehabilitation and Compensation Act 1988 (the Act) and the other concerning death under section 17. Despite some initial confusion among those representing Mrs Moronski about the existence and nature of the two applications, we understand that both matters are pressed and are to be dealt with in these proceedings.
4. There is no dispute that:
(a)Dr Moronski was in Commonwealth employment from 1981 until he was retired on invalidity grounds in March 1990;
(b)he was retired as a result of a chronic severe depressive disorder that caused him to leave work on 1 March 1988 – he never returned;
(c)Dr Moronski died on 29 April 2006, he was 55 years old;
(d)Mrs Moronski was legally married to Dr Moronski and at the time of his death she was his dependant, within the meaning of that term at section 4 of the Act.
5. The issues for determination are:
(a)did Dr Moronski suffer a compensable psychological injury, and if so
(b)did the injury materially contribute to ischaemic heart disease, giving rise to a fresh injury, and
(c)did the injury or injuries result in his death?
did dr moronski suffer a compensable psychological injury?
6.
Comcare asserts that Dr Moronski’s “aggravation of a disease, namely biological depression with acute onset to a moderately severe degree”[1] in 1988 was accepted as an injury on the basis of medical knowledge at the time, but with the benefit of hindsight and in consideration of advances in psychiatry, the depression
Dr Moronski suffered was not related to anything in his former employment.
In Comcare’s submission, there is no bar to the Tribunal making a finding that is contrary to the original acceptance of liability for the depression injury, even though that acceptance determination has not been the subject of a reconsideration decision.[2] Comcare says that Dr Moronski’s depression was of an endogenous kind, being of constitutional origin, and it would have arisen in any event without any relationship to employment. Comcare’s position is that Dr Moronski’s depressive disorder predated and gave rise to the difficulties he experienced at work in December 1987. Comcare relies on the recent reports and oral evidence of
Dr John Saboisky,[3] and asserts that Dr Moronski’s depressive disorder was not an injury that occurred in compensable circumstances.
[1] T27 folio 87.
[2] Telstra Corporation Limited v Hannaford (2006) 151 FCR 253 at [57].
[3] Exhibit R1.
7. We do not agree.
8. The issue is to be considered under section 124 of the Act and sections 27 and 29 the Compensation (Australian Government Employees) Compensations Act 1971 (the 1971 Act). Essentially, an injury includes a disease, or the aggravation, acceleration or recurrence of the disease, to which the employment was a contributing factor.
9. Dr Moronski had no serious history of depression prior to 1987.[4] He commenced Commonwealth employment in January 1981 and undertook the duties of his employment without issue and without apparently suffering from depression until 1987.
[4] See 26 and 26a, for example.
10.
We are reasonably satisfied that Dr Moronski suffered a depressive disorder that commenced or emerged in 1987. On 29 January 1988 he complained to
Dr Stephen Jamieson, his treating general practitioner, of gradually increasing symptoms from November 1987.[5] Dr Jamieson reported that Dr Moronski complained of intense anxiety and depression and of “being trapped in an impossible situation”.[6] The Doctor diagnosed “severe depression” and identified three precipitating factors: “ongoing conflicts with a superior officer culminating in an extremely unpleasant scene in front of colleagues”; “the obligation of all Public Servants to stop smoking at their place of work. This had proved to be an extremely unpleasant experience”; and “very considerable workload”.[7] Dr Jamieson referred
Dr Moronski to Dr Peter D. Grivell for assessment and treatment.
[5] Dr Jamieson, T15 folio 35.
[6] T15 folio 35.
[7] T15 folio 35.
11.
On 14 April 1988 Dr Grivell, Dr Moronski’s treating psychiatrist, noted a two to three month history of symptoms and diagnosed “biological depression with acute onset and of moderately severe degree”. Dr Grivell reported that Dr Moronski’s “history indicated that two premorbid factors have played a significant part in precipitating the depressive illness. The first is that he had stopped smoking just before the onset of his first symptoms, and the second is that he had experienced conflict with his new superior at work at about the same time”. In Dr Grivell’s opinion
Dr Moronski’s “depressive illness would have significantly impaired his ability to perform his duties over the 2-3 months since it’s [sic] onset”.[8]
[8] T14 folio 33.
12.
On the evidence of Mr Allan Anforth, a previous supervisor and personal friend of Dr Moronski, it appears that from September 1987 Dr Moronski was “greatly disturbed by the then pending total smoking ban” and that he had twice previously attempted to give up his smoking habit, without success. On both occasions
Mr Anforth reported that Dr Moronski experienced symptoms of “restlessness, agressiveness [sic], depression, lowered work output”.[9] On 31 March 1988
Ms Michelle Dawson, a case officer under Dr Moronski’s supervision, stated that she was aware that Dr Moronski had been “trying to stop smoking… for some time, without success”; she could not say what pressure the new non-smoking policy caused Dr Moronski, but she was not aware of any increased work pressure.[10]
On 20 April 1988 Mr Robert Davidson, a colleague of Dr Moronski’s, stated that
Dr Moronski “had made several attempts over the preceding 12 months to ‘quit’ his smoking habit. These were in the main short-lived and fraught with fairly radical behaviour changes. The most notable of these changes were his agitated behaviour and a [sic] increasing of his irascibility”.[11]
[9] T8 folio 23.
[10] T9 folio 24.
[11] T20a folio 45.
13. On this evidence and the evidence of Dr Grivell we are reasonably satisfied that Dr Moronski’s depression first emerged in association with his efforts to stop smoking in 1987. These efforts occurred prior to September 1987, while Dr Moronski was on holiday and while he was at work. It is not clear whether the introduction of a non-smoking policy may have been foreshadowed at that time, but the new policy did not come into effect until 1 March 1988.
14.
We are not persuaded, however, that a causal nexus is established between the emergence of Dr Moronski’s smoking-related depressive symptoms in mid-1987 and his employment. The proposition that Dr Moronski’s depressive disorder was causally attributable to the impending policy change concerning smoking at work is not supported by the present evidence; any association between the depressive symptoms he experienced and his efforts to stop smoking is too tenuous and remote to be accepted as a material or operative cause of his depressive disorder in any meaningful sense. It may be accepted, generally, that a person with a smoking habit may experience mood or behavioural changes for a time when attempting to break that habit. But that does not explain the depressive symptoms Dr Moronski experienced from mid-1987. Furthermore, we note that the policy was one of broad application across the Commonwealth, thereby rendering any possible link to
Dr Moronski’s employment even more tenuous, but that is not in our view determinative.
15.
Even though there was no formal diagnosis of depression in 1987, we are satisfied that in all likelihood the symptoms to which Mr Anforth and Mr Davidson referred are consistent with early signs of the emerging depressive disorder that increasingly afflicted Dr Moronski and ultimately caused him to consult Dr Jamieson on 29 January 1988. We note that Dr Grivell reported that Dr Moronski attempted to give up smoking in “mid 1987 and that he subsequently developed tension symptoms”, but those symptoms subsided after several weeks when Dr Moronski resumed smoking.[12] It is not clear whether Dr Grivell had access to information provided by Mr Anforth and Mr Davidson concerning the range of behaviours
Dr Moronski exhibited when attempting to stop smoking in 1987. On the evidence of Dr Saboisky and Dr William Knox, it appears likely that those early symptoms point to emerging psychological disturbance, being early indicators of disease rather than simply symptoms of tension. This is consistent with Dr Moronski’s evidence. In the Notification of Injury he lodged on 28 March 1988, Dr Moronski summarised the onset of his depressive disorder in the following terms: “the condition was of gradual onset over the period mid 1987 – February 1988”.[13]
[12] T17 folio 38.
[13] T7 folio 21; see also T7 folio 18.
16. Thus, as it appears to us, the disorder first emerged in mid 1987 and it progressed to the extent that Dr Moronski was rendered unfit for work on 1 March 1988; he left under medical certificates of Dr Jamieson and Dr Grivell and was not able to return. Dr Moronski was hospitalised, voluntarily, on 2 July 1988 as a result of a sudden increase in symptoms of anxiety and panic apparently associated with an impending job interview on 4 July 1988.[14] Dr Grivell reported at the time that “the clinical picture is unchanged. He remains vulnerable to pressure or stress, particularly to demands on cognitive function, with sudden high levels of anxiety”.[15] As can be seen, Dr Moronski’s depressive disorder was consistently associated with any increase in stress or pressure, for example in relation to his efforts to stop smoking in mid 1987, his response to perceived stress and conflict at work in November and December 1987, and his response to an impending job interview in July 1988.
[14] T28 and T28b.
[15] T31 folio 97.
17. It does not follow, however, that the depressive disorder was caused by the stresses that accentuated its symptoms. Even though we are not able to determine the precise causes of the depressive disorder with any certainty, we are reasonably satisfied that it was of an endogenous character, that is, it arose from previously existing constitutional or genetic or personality factors, or disease processes that were not related to Dr Moronksi’s employment.
18. Dr Saboisky treated Dr Moronski for a time in 1989 and, at that time, reported that Dr Moronski’s depression was chronic and was, by perception at least, materially related to factors in his previous employment.[16] Dr Saboisky’s recent report and his oral evidence is that Dr Moronski suffered a biological depression that occurred in the setting of his workplace and resulted in the conflicts and other difficulties in employment that he perceived as causative.[17] Dr Saboisky’s reasons for this conclusion include the long duration of the depressive disorder after the removal of alleged causative stressors, the increased prominence of behavioural patterns, such as obsessive behaviours, that are not associated with reactive depression, and his opinion that endogenous depression typically emerges in vulnerable people in their mid thirties. We note that Dr Moronski was approximately 37 years old when his depression emerged.
[16] T41 folio 113.
[17] Exhibit R1, Report dated 16 March 2010 p2.
19. Dr Knox, a consultant psychiatrist, does not agree with Dr Saboisky’s assessment; in Dr Knox’s opinion, even though “More severe depressions do however have a tendency to be more genetically influenced”, Dr Moronski’s difficulties in the workplace pre-dated his depressive illness and “the workplace events were of such material contribution to Dr Moronski’s Depressive Disorder that without them he would not have become ill”.[18] Dr Knox identified three important factors in “a constellation” of factors that contributed to the onset of Dr Moronski’s depressive disorder: stopping smoking, conflict with Mr R. Eadie and losing his work identity on ceasing employment. Dr Knox informed us that Dr Moronski “may well have become depressed as a result of other factors”, “including genetic factors”, but the major factors he identified affected the degree of the disorder and the timing of its onset.
[18] Exhibit A1, pp3 and 4.
20.
We agree with Dr Knox that the severity of the depression Dr Moronski suffered did not occur “out of the blue”, but the contemporaneous evidence does not suggest that Dr Moronski’s difficulties with Mr Eadie preceded the onset of his depressive disorder. Mr Eadie had no contact with Dr Moronski prior to becoming his supervisor, in place of Mr Anforth, in September 1987. We have found that
Dr Moronski’s depressive disorder first emerged before that time. Dr Grivell reported onset of symptoms in association with Dr Moronski stopping smoking.[19] On the unchallenged evidence of Mr Anforth, Dr Moronski suffered bouts of depression and other psychological symptoms when attempting to stop smoking at work and on holiday, prior to any contact with Mr Eadie in 1987.[20] Mr Davidson’s unchallenged evidence supports this assessment.[21] The evidence of Mr Anforth and Mr Davidson is largely consistent with Dr Moronski’s own account.[22] For this reason we do not accept that Dr Moronski’s difficulties in the workplace preceded the emergence of his depressive disorder. We note that Dr Jamieson reported the onset of symptoms in or about November 1987,[23] but it is not clear whether the doctor had a full history concerning Dr Moronski’s previous symptoms in association with his earlier efforts to stop smoking.
[19] T14 folio 33.
[20] T8 folio 23
[21] T20a folio 45.
[22] See T22 folios 54 to 57 and folio 58 at [G], for example.
[23] T19 folio 42.
21. Dr Knox attributed a greater degree of causal importance to workplace factors than we are prepared to accept. The simple reason for this arises from Dr Knox’s own evidence: he did not have the benefit of examining Dr Moronski and making a clinical assessment of psychodynamic and personality factors, and he was provided with only sparse information concerning relevant aspects of the case – he was not provided any clinical notes, for example, and he had access to only scant information concerning relevant aspects of Dr Moronski’s history. Dr Saboisky and Dr Grivell both treated Dr Moronski and were in a position to form clinical judgements at the time, and Dr Saboisky has the benefit of developments in psychiatry over the intervening years to inform his present assessment. For this reason the evidence of Dr Saboisky and Dr Grivell carries greater weight than that of Dr Knox on this issue.
22.
That is not the end of the matter, however. We must determine whether work factors contributed to aggravate Dr Moronski’s depressive disorder. The particular factors Mrs Moronski asserts were causative include work stress and conflict with
Mr Eadie.
work stress
23. Dr Moronski asserted that he was subject to undue work stress and increased pressure of work and workload under Mr Eadie’s supervision from September 1987.[24] His assertions are not supported by other evidence, however.
[24] T22 and T24.
24.
In Mr Eadie’s opinion Dr Moronski’s work load was comparable to other Assistant Directors at the ASO Class 7 level, and he was not subject to undue pressure of work, even though he and other Assistant Directors had some difficult cases and deadlines. Ms Dawson was not aware of any increase in work pressure concerning Dr Moronski.[25] In February 1988 one experienced case officer in
Dr Moronski’s sub-section obtained a promotion to another section. On Mr Eadie’s evidence it is conceivable that this change may have precipitated a change in
Dr Moronski’s workload, although that is very far from clear. Mr Eadie observed in his report dated 5 April 1988 that Dr Moronski may have felt less comfortable with the supervision and guidance aspects of his work than handling his own case work, but there was “no reason to think that his standard of performance was unsatisfactory”, “Mr Moronski performed his management tasks competently, up to and including the period immediately before his sick leave began”.[26] Nevertheless, “before his departure on sick leave there were signs that he was becoming distinctly unhappy about aspects of his work which required him to meet deadlines or to deal directly with very senior officers”.[27] Mr Eadie continued, “Mr Moronski’s case work has been carried out to a high standard. In the month or two before his departure on sick leave the quality of the work he produced may have deteriorated slightly (though not to a significant extent) and there was some reduction in output”.[28] In a supplementary statement on 10 June 1988, however, Mr Eadie said that he “had less contact with Mr Moronski than with the other Assistant Directors, at any rate in the last 2 or 3 months before his departure, because his output of case work had slowed down appreciably”.[29]
[25] T9 folio 24.
[26] T10 folios 26 and 27.
[27] T10 folio 27.
[28] T10 folio 26.
[29] T25b folio 72.
25.
On this evidence we are not persuaded that Dr Moronski’s workload or work pressure changed in the latter part of 1987 into 1988. It is clear, nevertheless, that
Dr Moronski experienced increasing difficulty with his work in the months immediately before he left work on sick leave on 1 March 1988. As it appears to us, these changes in Dr Moronski’s capability and his altered perceptions in relation to his workload and the increased work pressure he complained about were, in all likelihood, the product of his depressive disorder or the product of his perceived difficulties with Mr Eadie, rather than a contributory cause of that disorder. We so find. The preponderance of the medical evidence supports this conclusion; in the words of Dr Grivell “his depressive illness would have significantly impaired his ability to perform his duties from the time of onset”.[30]
[30] T17 folio 39.
difficulties with mr eadie
26. Mr Davidson says that Dr Moronski became more agitated and restless in the period leading up to Christmas in 1987 – “he was much more volatile and heated in any discussion on normal work matters. He was intolerant of the changes being introduced by the new Director of our section [Mr Eadie] and the often summary rebukes meted out to him by that Director exacerbated this intolerance”.[31] Mr Davidson described in a supplementary statement an incident concerning an altercation between Dr Moronski and Mr Eadie in the following terms:[32]
I was present when Mr Eadie found it necessary to remonstrate with Mr Moronski over his pursuit of a particular issue in a case under reconsideration by the Commissioner for Superannuation. The nature of Mr Eadie’s language and his choice of words were both colourful and heated. Mr Eadie, in so many words, cast doubt on Mr Moronski’s ability to understand plain English and follow through instructions with any initiative.
I am in no doubt that Mr Eadie did not intend to offend Mr Moronski’s ethnic origins rather, in the heated tirade he subjected Mr Moronski to, he lost sight of such sensitivities. Nonetheless I believe that the effect of this episode was of critical importance to Mr Moronski as he constantly harped back to it as support for his contention that he could do little right in Eadie’s eyes and had less hope of doing so given the prejudice which this instance had demonstrated.
[31] T20a folio 45.
[32] T20a folio 46.
27.
It is not perhaps surprising that Mr Eadie and the then Commissioner for Superannuation, Mr G.N. Vanthoff, did not accept or agree with the version of events presented by Dr Moronski.[33] From this distance it is not possible to determine which version of events is correct. We have difficulty accepting Mr Eadie’s evidence that
Dr Moronski was performing to a high standard right up to the point of his departure on sick leave; this, in our opinion, is highly unlikely and Mr Eadie’s statements to that effect present his relationship with Dr Moronski in a rosy light that does not sit easily or well with the evidence of Mr Davidson and Dr Grivell, for example. We note that there are inconsistencies in Mr Eadie’s evidence concerning Dr Moronski’s performance at work during this period: Mr Eadie, too, reported that Dr Moronski’s work outputs reduced in the months before his departure on sick leave. We find aspects of Mr Davidson’s evidence compelling and have little difficulty finding that
Dr Moronski formed an adverse perception about events that actually occurred involving Mr Eadie. It is tolerably clear, too, that those perceptions preyed upon his mind and contributed to aggravate the symptoms of his depressive disorder in December 1987. We accept the evidence of Dr Saboisky and Dr Grivell in this regard.
[33] See the Commissioner’s statement at T21 (folio 48, for example); Mr Eadie’s statements at T10 and T25b; and Dr Moronski’s statements at T22 and T24.
28. For these reasons we find that the aggravation of Dr Moronski’s depressive disorder constitutes an injury under the 1971 Act (“the psychological injury”).
did the psychological injury materially contribute to ischaemic heart disease or death?
29. In Mrs Moronski’s submission her husband’s ischaemic heart disease and his death were the result of the psychological injury he suffered at work. She raises a number of grounds: the disease or the death was the result of depression, or pharmacological treatment for depression, or psychosocial changes in his lifestyle and behaviour, or medical conditions relating to such changes.
30. Mrs Moronski asserts that her husband underwent serious psychosocial changes after and as a result of his psychological injury and his retirement from employment on medical grounds. She says he adopted a nocturnal lifestyle and became increasingly socially isolated; he consumed increasing amounts of alcohol and his diet deteriorated; he became physically inactive and obese; he exhibited mildly obsessional behaviours; and there were significant problems in their marriage – Mrs Moronski informed us that she and her husband did not communicate for long periods even though they lived in the same house. In Mrs Moronski’s submission these changes were features of Dr Moronski’s depression, which, she says, continued unabated and without relief for the rest of his life as it was not responsive to treatment. In Mrs Moronski’s submission, these behaviours and lifestyle changes were the direct effects of his compensable depression and they materially caused or contributed to his ischaemic heart disease and his death.
31. Mrs Moronski asserts that her husband suffered a number of related medical problems, including hypertension, hyperlipidaemia, morbid obesity and artheroschlerosis. In her submission these conditions, too, were the result of his psychological injury and were operative factors in his death.
32. Mrs Moronski relies on the epidemiological evidence of Dr David Colquhoun that her husband’s depression, inactivity, social isolation, alcohol abuse, obesity and raised cholesterol are all risk factors for and causes of ischaemic heart disease and sudden death relating to that disease.
33. For these reasons, in Mrs Moronski’s submission, her husband’s ischaemic heart disease is an injury for the purposes of the Act and, his death is directly or indirectly the result of injury. For these reasons, as his dependant, she asserts that she is entitled to compensation.
34. We do not agree.
35. Under section 14 of the Act Comcare is liable to pay compensation if an ‘injury’ suffered by an employee results in death, incapacity for work or impairment. Section 17 applies where an injury results in death. ‘Injury’ is given meaning at section 4 of the Act and includes a disease or the aggravation of a disease that was materially contributed to by the employment.[34] As can be seen the causal tests to be applied under sections 14 and 17 are the same. The phrase ‘results in’ refers to a concept of causation that is well understood in the law; it refers to an operative cause that is not confined to the immediate proximate cause and imports a test of causal connection that requires a commonsense evaluation of the causal chain.[35]
[34] Subsection 4(1), Safety, Rehabilitation and Compensation Act 1988.
[35] Ilsley v Wattyl Australia Pty Ltd (1997) 75 FCR 1 at 6; March v E & MH Stramare Pty Ltd (1991) 171 CLR 506.
36. The causal test is one of probability and it requires findings on the balance of probabilities, applying the reasonable satisfaction civil standard; mere possibility is not sufficient, even if the possibility is real rather than fanciful. Reasonable satisfaction should not result from indefinite evidence or indirect inferences.[36] The balance of probabilities test does not authorise us to choose between guesses, on the ground that one guess seems more likely than another.[37] Nevertheless, as Lord Denning observed “in civil cases, the case may be proved by a preponderance of probability, but there may be degrees of probability within that standard”.[38] As Spigelman CJ said in Seltsam Pty Ltd v McGuiness “an inference as to the probabilities may be drawn from a number of pieces of particular evidence, each piece of which does not itself rise above the level of possibility”.[39] If an inference is to be drawn from epidemiological studies, it is first necessary to relate the results of such studies to the particular case.[40]
[36] Briginshaw v Briginshaw (1938) 60 CLR 336 at 362-363.
[37] Jones v Dunkel (1959) 101 CLR 298 at 305.
[38] Bater v Bater [1950] 2 All ER 458 at 459.
[39] Seltsam Pty Ltd v McGuiness and Anor; James Hardie & Coy Pty Ltd v McGuiness and Anor (2000) 49 NSWLR 262 at 278.
[40] Amaca Pty Ltd v Ellis; South Australia v Ellis; Millennium Inorganic Chemicals Ltd v Ellis (2010) 84 ALJR 226 at [62].
37. As can be seen, in relation to a ‘disease’ the causal test is limited by degree to some extent: the contribution by employment must be of a material degree.[41] The phrase ‘in a material degree’ has been taken to mean a substantial or considerable degree that is greater than minimal; one must assess all of the contributing factors when determining the degree to which employment has contributed to a disease and deciding whether that degree is above the evaluative threshold.[42] Thus, when determining whether ischaemic heart disease is an injury under the Act, it is necessary to establish that the employment contribution to the disease was of a material degree.
[41] Section 5B, Safety, Rehabilitation and Compensation Act 1988.
[42] Comcare v Sahu-Khan (2007) 156 FCR 536 at [13]-[16].
38. Furthermore, it can be accepted, and it is well established law, that the particular formulation ‘results in’ does not impose a sole cause test.
39. Applying these tests, there are a number of difficulties with this case. The precise cause of Dr Moronski’s death is not known. There are substantial gaps in the evidence concerning Dr Moronski’s lifestyle, behaviour and medical conditions over the 16 years prior to his death following his medical retirement from employment. There are difficulties with the epidemiological evidence as a basis for drawing an inference as to the causation of Dr Moronski’s ischaemic heart disease and his death.
40. In sum, there are two reasons why we conclude that Dr Moronski’s psychological injury did not materially contribute to the ischaemic heart disease or result in his death. The first is that the nature of the injury was in the form of an aggravation; we are satisfied that the aggravation was transient with only a temporary effect. The second is that, even if we are wrong on this first ground, there is insufficient probative evidence to establish a causal chain between Dr Moronski’s injury and his ischaemic heart disease or his death.
temporary aggravation
41. It is probable that Dr Moronski’s psychological condition deteriorated and his depressive disorder continued to progress in the period following his departure from work on 1 March 1988. He was hospitalised in June of that year. Mrs Moronski attributes this progression to causal factors in his previous employment, but that is not indicated by the present evidence.
42.
Dr Knox gave evidence that when Dr Moronski ceased work he suffered a major rupture, “an avalanche” that caused him “to slip into a very unhealthy physical and psychological state that snow-balled”. Dr Knox thought that the loss of his employment identity and status was the most important factor in the subsequent deterioration of Dr Moronski’s psychological state and the progress of his depressive disorder. On the advice of the Commonwealth Medical Officer (CMO), in March 1990
Dr Moronski was retired from employment on invalidity grounds as a result of “endogenous depression”.[43] The CMO reported:
Since I last saw Mr Moronski in December 1988 his condition appears to have deteriorated. His affect was depressed and there were obvious signs of psychomotor retardation. He was not very communicative but mentioned hypersomnia, stating that he remained in a “dazed condition”, half asleep, for 2 to 3 hours during the day. He has now, he says, given up all hope of ever being able to work again. He is presently on Tolvon 60 mg/day. In spite of various medications over a period of almost 2 years Mr Moronski is still not fit for work. I attach Dr Grivell’s report and agree with him that he should be retired on grounds of invalidity.
[43] T42a folio149.
As it appears to us these reported symptoms are greater and different than the symptoms about which Dr Moronski complained in the period from November 1987 to 1 March 1988 when he left work. We note that on 20 September 1989
Dr Saboisky reported that Dr Moronski complained of “poor concentration and memory, lack of motivation, difficulty sleeping together with feelings of anxiety, depression and incompetence”. On this evidence of the CMO and Dr Saboisky the deterioration in Dr Moronski’s condition can clearly be seen. We note, too, that
Dr Saboisky reported a new factor, additional to “having to give up cigarette smoking” and “a significant problem with his immediate superior”, that may have been significant in the deterioration of Dr Moronski’s depressive disorder: “difficulties with his marriage primarily because his wife did not believe that he is as disabled as he claims to be”.[44] Mrs Moronski’s evidence is that these difficulties emerged in 1988 after he left work; by 1989 she and her husband “began to live substantially independent lives” and from 1990 they would not communicate for days or weeks at a time. [45]
[44] T41 folio 112.
[45] T50b folio 171.
43. As it appears to us, Dr Moronski’s depressive disorder progressed in a course that is consistent with the endogenous nature of the condition rather than as a result of the aggravating factors in employment to which we have referred above. Furthermore, it appears likely that the marriage difficulties Dr Moronski experienced after leaving work in March 1988 may have contributed to and been exacerbated by his on-going depressive disorder. Even though Dr Moronski continued to attribute his disorder to work factors, it is does not follow that those factors were material in the production of symptoms over the course of months and many years following his departure from work. As it appears to us, Dr Moronski’s previous employment became a focus of his attention in the context of disease.
44. On the evidence of Dr Saboisky concerning reactive depression, we accept that in most cases the affected person would “move on” and the symptoms of depression would diminish and resolve within a relatively short period of months following the removal of the precipitating stressors, whereas an endogenous depression, or a chronic depressive disorder, may never resolve. We have found that Dr Moronski experienced early symptoms of the depressive disorder in 1987 prior to any alleged stressors in his employment. These symptoms were recognised by Mr Anforth and Mr Davidson and included increased restlessness, depression, aggression, agitation and irascibility, and reduced work output. It can readily be accepted that the disorder was refractive and did not resolve within a period of months; rather than resolving or diminishing with the removal of work stressors in March 1988, his condition deteriorated thereafter and became chronic. As it appears to us the manner in which Dr Moronski’s disorder emerged and progressed is not consistent with a reactive disorder. The only reactive aspect of the disorder occurred in December 1987 in the form of an increase in symptoms of the disorder that was already present at that time.
45. Disentangling cause and effect presents a significant difficulty at this point. On the one hand symptoms of the disorder were apparent in the workplace, from time to time, and adversely affected Dr Moronski’s performance, his behaviour and his ability to cope with work stresses over a period of several months from mid-1987 to February 1988. On the other hand it appears likely enough that actual or perceived difficulties between Dr Moronski and Mr Eadie aggravated symptoms of the disorder in December 1987: the difficulties became the focus of Dr Moronski’s attention and apparently caused him to become increasingly agitated, irascible and depressed.
46.
Thus, considering the manner in which Dr Moronski’s depression emerged and progressed, especially after he left work in March 1988, and the long duration of that disorder thereafter, we are reasonably satisfied that the aggravation of the disorder by factors in Dr Moronski’s former employment in December 1987 was in all likelihood of a transient nature, with a temporary effect. We cannot determine with any certainty when the aggravation effects resolved or ceased to play any material part in the progress of Dr Moronski’s disorder. It is tolerably clear, however, that in all likelihood those aggravation effects would have ceased within a period of months following March 1988 or, if not, they would have diminished as material factors in
Dr Moronski’s depressive disorder as the disorder continued to progress and his psychological health further deteriorated. Even if we are wrong about this, for reasons that will appear, it does not assist Mrs Moronski’s case.
insufficient evidence
47. Essentially, the greatest difficulty for Mrs Moronski is the absence of evidence to support each link in the causal chain that must be established to our reasonable satisfaction if her case is to succeed. There are a number of things to say about this. As we understand Mrs Moronski’s case the links in the chain follow two courses, as follows: first, the psychological injury was a materially contributed to changes that occurred in Dr Moronski’s behaviour and lifestyle over subsequent months and years, and those changes were material factors in the ischaemic heart disease he later suffered that resulted in his death; second, the psychological injury itself resulted in ischaemic heart disease or Dr Moronski’s death.
48. At this point it is relevant to note that no diagnosis of ischaemic heart disease was made while Dr Moronski was alive and no post mortem investigation or autopsy was conducted after his death. Thus, even though the Coroner certified the cause of death was ischaemic heart disease,[46] the particular pathological event that actually caused Dr Moronski’s death is simply not known. Nevertheless, we will proceed on the basis of the Coroner’s finding.
[46] T45a and T50d.
49. With regard to the first link in the causal chain contended for by Mrs Moronski, there is very scant evidence concerning the alleged changes in Dr Moronski’s behaviour and lifestyle after his departure from work on sick leave in March 1988. We note the medical certificates at T89 and Mrs Moronski’s unsigned statement at T58a. Mrs Moronski gave evidence that her husband drank heavily after leaving employment, in 1991 for example,[47] but there is little probative evidence concerning when this commenced, or the amount of alcohol he consumed, or the period over which this is said to have occurred. That is perhaps not surprising as Mrs Moronski’s evidence is that she “found it very hard to work out how much Marek was consuming because he tried to keep the volume of it hidden from me”.[48] Dr Michael Cameron gave similar evidence concerning the period from 1998 to 2006: “I suspect I may not have been fully aware of the amount of alcohol he was consuming”.[49] Furthermore, Mrs Moronski stated that:
Gradually after his loss of employment in 1988 he emotionally and physically withdrew from the marriage.
From 1989 Marek and I began to live substantially independent lives. From 1990 onwards there would be at times no communication for days, sometimes extending to weeks, between us.[50]
[47] T58a folio 203.
[48] T58a folio 202.
[49] T50b folio 171.
[50] T58a folio 20..
In her oral evidence Mrs Moronski explained that at the time of Dr Moronski’s death she and her husband had not communicated for roughly three years. In those circumstances Mrs Moronski’s difficulty quantifying the degree and timing of her husband’s alleged lifestyle changes can be more clearly understood.
50.
The evidence of Mr Anforth does not assist in this regard. We accept that
Dr Moronski and Mr Anforth were friends over many years, but we have no evidence about the frequency and extent of contact between them over the many years from 1988 to 2006. After Dr Moronski’s death Mr Anforth stated that he and Dr Moronski “often had drinks at the Club or at my place” and “On many occasions I witnessed him buying bottles of wine to take home from the club after we had been drinking for hours”. It appears that Mr Anforth understood that Dr Moronski “would drink wine almost every night as a way of dealing with his depression”.[51] Simply put, the extent and timing of any change in Dr Moronski’s consumption of alcohol is not established – Mrs Moronski said that there was no alcohol in the house prior to the index events that are said to have caused his illness, but she also gave evidence that he drank socially with his Polish friends; Mr Anforth’s evidence concerning his experiences drinking with Dr Moronski are not clearly located in time, and appear to relate to experiences before and after the events presently in issue. The nature and extent of Dr Moronski’s consumption of alcohol over time is simply not established on the present evidence.
[51] T50c at folios 173 and 174.
51. It can be accepted that Dr Moronski adopted nocturnal habits after leaving work in 1988. It appears that he became focussed on computers and spent many hours at night on the internet. Precisely what Dr Moronski was doing on the internet and who he communicated with using that medium is not clear, although it can be accepted that he researched topics in which he found an interest or relevance to his own case, concerning medical disorders for example. On Mrs Moronski’s evidence, however, we are reasonably satisfied that this change in lifestyle was attributable to difficulties in his marriage at the time and not to any effect of the aggravation injury he suffered at work in December 1987.
52.
It appears that Dr Moronski exhibited obsessive behaviours over ensuing years, concerning water, health and computers, for example. On the evidence of
Dr Saboisky and Dr Knox these behavioural changes were likely to be a product of Dr Moronski’s underlying personality or possibly the chronic depressive disorder that afflicted. On that basis these changes are not attributable to the aggravation injury he suffered in 1987.
53. Similarly with Dr Moronski’s alleged eating habits, inactivity and obesity: there is no probative evidence about when these changes occurred, or how they progressed in degree and over time. It can be accepted that Dr Moronski adopted a nocturnal lifestyle at some point after leaving work in March 1988, probably in or about 1989. It appears likely that this was related to difficulties in his marriage with Mrs Moronski at the time.[52] On Mrs Moronski’s evidence Dr Moronski developed certain obsessive behaviours after ceasing work, these included particular diets, treating and storing water, hypochondriasis and computer-related activities. On that evidence it is likely that Dr Moronski’s dietary habits were related to his nocturnal lifestyle and his obsessive behaviours; neither of these factors, however, are attributable to the effects of the work aggravation – the psychological injury.
[52] T58a folio 201.
54.
Also, Dr Moronski’s alleged social isolation is not supported by probative evidence of any detail. On Mrs Mononski’s evidence her husband was “not the life of the party” and was somewhat withdrawn by nature throughout their marriage.
Mrs Moronski stated that her husband “had a tendency to be withdrawn but was able to maintain friendships” prior to 1987,[53] but his friends dropped away in the period from 1988 to 1992.[54] Mrs Moronski gave oral evidence that her husband became socially isolated after ceasing work and adopted a nocturnal lifestyle; Dr Knox referred to this as “hibernation”. The evidence, however, paints a slightly different picture. Dr Moronski maintained a close friendship with Mr Anforth and at least one other person,[55] over many years until his death. Mr Anforth refers to interacting with Dr Moronski on many occasions at a club. There is evidence that Dr Moronski attended German language classes in order to improve his social network. Furthermore, even if we were to accept that Dr Moronski did become socially isolated, it appears to us that this may well have been the result of him adopting a nocturnal lifestyle, and that change was attributable to difficulties in his marriage in 1988 and 1989 rather than to the effects of his psychological injury.
[53] T58a folio 200.
[54] T58a folio 201.
[55] T58a folio 201.
55. We are urged to accept that all these changes occurred as a result, at least in material part, of a work injury. We cannot make any such finding on the present evidence, however. As it appears to us, even if we accept that Dr Moronski’s lifestyle and behaviour changed after he left work, his social withdrawal, difficulties in his marriage, his nocturnal and sedentary habits, his obsessive behaviours concerning water, diets and health, and his consumption of alcohol and unhealthy food are not attributable to the aggravation injury he suffered in employment.
56.
Thus, we are satisfied that the first proposed causal chain linking
Dr Moronski’s work-related injury and his subsequent development of ischaemic heart disease is not established on the balance of probabilities: the assertion fails at the first link in the causal chain concerning lifestyle changes. We are reasonably satisfied therefore that Dr Moronski’s injury did not materially contribute to cause changes in his lifestyle and behaviour that are said to have caused his ischaemic heart disease or his death.
57. It is not necessary, therefore, to say anything about the second alleged link in that causal chain – whether changes in Dr Moronski’s lifestyle after 1988 were material causes of his ischaemic heart disease or his death. But this was the focus of much attention and evidence during the hearing, especially in relation to the second proposed causal chain – that depression and specifically the psychological injury resulted in Dr Moronski’s ischaemic heart disease or his death. For that reason, we will address this point.
risk factors and epidemiological evidence
58. Mrs Moronski asserts that the behaviour and lifestyle changes to which we have referred already and the depressive disorder itself are significant risk factors associated with ischaemic heart disease and related sudden death. It can readily be accepted that depression, social isolation, inactivity, high cholesterol, and even to some extent alcohol consumption and certain antidepressant medications may be associated with an increased risk of ischaemic heart disease and death. We heard evidence from Dr Colquhoun and Dr Eugene G. Galea; both doctors are cardiologists with expertise in cardiac epidemiology. Despite appearances, there is substantial concurrence in their evidence, even though Dr Colquhuon went further than Dr Galea in equating significant known risk factors for coronary heart disease with causes of that disease. Dr Colquhuon may be right that high cholesterol, for example, is not simply a factor that increases the risk of heart disease, but it is also a cause of heart disease. But that is beside the particular point that we must decide in Dr Moronski’s case.
59.
The task is one of determining whether the psychological injury resulted in
Dr Moronski’s heart disease or his death.
60. There is no direct evidence on this point for the simple reason that ischaemic heart disease was not diagnosed while Dr Moronski was alive and no post mortem investigation was carried out to ascertain the precise pathology that caused his death. Thus, the actual precise causes of the heart disease and the pathological cause of death have not been unequivocally established. This gives rise to two difficulties, for present purposes. The first is that death from ischaemic heart disease may result from a number of different pathological events in different locations, including the erosion or rupture of arterial plaque with associated clotting and blockage of an arterial vessel or coronary structure, or an accumulation of plaque causing an arterial blockage. Without knowledge of the precise nature and location of the event that caused death it is not possible to determine with any certainty whether one or more possible causes are implicated; for example, if the event that caused death was an arterial blockage arising from the deposition of cholesterol, or if the terminal event involved the rupture of a coronary vessel or clotting associated with the rupture of arterial plaque, one may be able to say that associated risk factors were implicated. We are not able to draw any such conclusions on the present evidence.
61.
The second difficulty is that the precise circumstances of Dr Moronski’s death are far from clear. The basis of the Coroner’s finding concerning ischaemic heart disease as the cause of death is not clear on the present evidence; the report of
Dr Sanjiv Jain on which the Coroner relied is not in evidence. Nevertheless, one can assume that a clinical judgement was made in consideration of the circumstances of what is said to be a sudden death, and that was sufficient to satisfy the Coroner.
Mrs Moronsk informed us that her daughter discovered Dr Moronski slumped over the toilet in a bathroom; he was dead and his body was cold. We note that
Mrs Moronski was not able to give any indication of her husband’s symptoms in the period immediately before his death, because, by her own account, she and her husband had not communicated for approximately three years prior to that event. Furthermore, there is no evidence that any doctor diagnosed a life-threatening illness in the weeks or months preceding his death and there are no clinical notes in evidence. We are not able to discern any clinical symptoms that Dr Moronski may have experienced in the minutes, hours and days immediately before the event that caused his death that may implicate a particular risk factor.
62. We note the evidence of Dr Cameron set out in a report dated 14 October 2007.[56] Dr Cameron reported that he treated Dr Moronski from 1998 to 2006 and stated:
I have no reservation at all in agreeing with the comments in your request letter referring to his “increasingly socially withdrawn life”. The specific elements of that lifestyle which you mention namely heavy consumption of alcohol, a total lack of exercise, poor diet, a nocturnal life on the Internet coupled with sleeping all day, high degree of pessimism about the value of life and apparent hypochondria in my opinion very accurate.
I can recall the general content of many consultations I had with Mr Moronski which revolved around exactly these matters and his lack of progress over the period of time that I saw him in addressing these issues.
[56] T50b folio 171.
Dr Cameron was “very comfortable to say that I believe his lifestyle would have been a very significant factor in the onset of this problem [ischaemic heart disease]” and apparently advised Dr Moronski about “lifestyle changes” in relation to risks associated with heart disease.[57] We note that Dr Cameron’s comments concerning the results of pathology tests and Dr Moronski’s family history of heart disease were based on information provided to him by Mrs Moronski’s lawyers after Dr Moronski’s death rather than on his clinical notes. Dr Cameron was not called to give evidence so this curious turn of events remains unexplained. No clinical notes of any treating doctor were adduced in evidence. Nevertheless, Dr Cameron’s evidence does not take the matter further; he does not distinguish the relative importance or significance of the risk factors to which he refers as lifestyle changes.
[57] T50b folio 172.
63. We were taken to epidemiological studies and the evidence of Dr Colquhuon and Dr Galea as a basis for drawing an inference as to the cause of the heart disease Dr Moronski suffered.
64. We note what the High Court said in Amaca Pty Ltd & Ors v Ellis on this point:[58]
To draw an inference about causation from what was established by the epidemiological studies, it would be necessary to decide whether the particular case under consideration should be treated as conforming to the pattern described by the epidemiological studies. Absent evidence which suggests that the individual may stand apart from the ordinary, there may be sufficient reason to assume conformity, but whether or not that is so, it is important to recognise that the first step that must be taken, if an inference is to be drawn from epidemiological studies, is to relate the studies of populations to the particular case at hand. That step is not inevitable.
[58] Amaca Pty Ltd v Ellis; South Australia v Ellis; Millennium Inorganic Chemicals Ltd v Ellis (2010) 84 ALJR 226 at [62].
65.
The epidemiological studies to which we were taken,[59] and the evidence of
Dr Colquhuon and Dr Galea concerning those studies,[60] suggest that depression, social isolation and lack of social support are risk factors for coronary heart disease of equal magnitude to conventional risk factors such as smoking, high blood pressure, raised blood cholesterol and physical inactivity.[61] Dr Colquhuon went so far as to say that these risk factors are causes of coronary heart disease. While the actual mechanisms responsible for the association between depression and coronary heart disease are not known,[62] it appears that “the association between depressive symptoms and cardiovascular events was largely explained by health behaviors, especially physical inactivity”.[63]
[59] Exhibits R2 and R4.
[60] Exhibits A2, A3 and R5.
[61] National Heart Foundation Updated ‘Stress’ and Coronary heart Disease Position Statement, Heart, Lung and Circulation 2003, 12:208, Exhibit R5, Attachment; R2 p2379.
[62] R2 p2380.
[63] R2 p2387
66.
It can readily be accepted that Dr Moronski had a number of significant risk factors for heart disease. He was a smoker of long standing; he attempted to stop smoking at various times in 1987 and 1988, although it remains unclear whether he eventually succeeded and, if so, when. On the evidence of Dr Cameron he suffered from hypertension, hyperlipidaemia and hyperuricaemia, although precisely when and over what period these conditions arose or persisted is far from clear. Dr Galea reported that in 2000 and 2001 Dr Moronski “had a mixed type of dyslipidaemia with raised triglycerides as well as a raised LDL cholesterol”; the doctor also reported the likelihood of gouty arthropathy and a tendency to Type 2 diabetes mellitus.[64] It appears that Dr Moronski may have been physically inactive for many years, but there is scant probative evidence on this point. Mrs Moronski asserts that he became less physically active after 1988. On the present evidence it is very far from clear whether he was physically active, or to what extent, prior to 1988; we note that he had a sedentary job for many years previously. The evidence is plain enough that
Dr Moronski was morbidly obese when he died; he was 55 years old. When
Dr Moronski became obese is not established on the present evidence, however. He was not obese on examination on 14 June 1988 (BMI of 21) but he was obese on examination on 18 November 2005 (BMI 35).[65] He suffered from endogenous depression that commenced in 1987. He had a family history of heart disease: his father died of a heart attack at the age of 57. His consumption of alcohol may have been a factor, but that is less clear.
[64] Exhibit R5 p3.
[65] Exhibit R5 p1 and p3.
67. Thus it can be seen that Dr Moronski was exposed to a number of significant risk factors for coronary heart disease. There is no evidence, however, that the relative importance of these risk factors, separately or in combination, was ever assessed insofar as Dr Moronski was concerned. On the evidence of Dr Galea and Dr Colquhuon, the longer the exposure to significant risk factors, the greater the actual risk, and the greater the risk, the greater the probability of heart disease or death. The evidence of these doctors, however, does not establish a clear hierarchy of risk strength relative to actual risk across the various risk factors in Dr Moronski’s case.
68. Nevertheless, Dr Colquhuon’s evidence is that the three most important risk factors identified in the 2004 INTERHEART study were raised lipids, smoking and psychosocial factors.[66] The National Heart Foundation 2003 position paper reveals that depression, social isolation and lack of social support are of similar magnitude to “conventional risk factors such as smoking, high blood pressure, raised blood cholesterol and physical inactivity”.[67] This paper reported “no strong or consistent evidence for a causal association between chronic life events, work related stressors (job control, demands and strain), Type A behaviour patterns, hostility, anxiety disorders or panic disorders and CHD [coronary heart disease]”. We note the evidence concerning the Framingham Risk Equation and the assessment of absolute cardiovascular disease risk.[68] We have not attempted to assess Dr Moronski’s risk using these devices.
[66] Exhibit A2, p2.
[67] Exhibit R5, Attachment.
[68] Exhibit R4.
69. With regard to the epidemiological evidence, we must assess “the relative dangers of all causes”.[69] The present evidence, however, does not assist us to differentiate the relative importance of the risk factors in Dr Moronski’s case; we are not able to determine whether one risk factor or another was the probable cause of ischaemic heart disease or death. All that the evidence allows is that Dr Moronski was exposed to many risk factors over varying periods of time, any one of which or any combination of which may have been material in the onset or progress of his heart disease and, ultimately, in his death. Thus, on the present evidence, it cannot be said that Dr Moronski’s case conforms to the pattern described by the epidemiological studies to the extent that an inference can be drawn about the probable cause of his ischaemic heart disease or his death. All that can be said is that the epidemiological evidence establishes that his family history of heart disease, or his long history of smoking, or his obesity, or his depression or any of the other risk factors to which he was exposed may have been a cause. But that is not sufficient to establish a probable cause.
[69] Amaca Pty Ltd v Ellis; South Australia v Ellis; Millennium Inorganic Chemicals Ltd v Ellis (2010) 84 ALJR 226 at [56]-[57].
70.
It was put to us that this case is simply one of common sense: Dr Moronski became depressed in compensable circumstances, his lifestyle changed for the worse as a result, those lifestyle changes increased the risk of him dying from ischaemic heart disease, and that unfortunate end occurred some years later.
On that basis, if it is not possible to determine whether one risk factor or another was a significant factor in Dr Moronski’s heart disease or his death, it does not matter so long as the range of possibly significant risk factors are causally associated with his psychological injury in employment: it is not necessary to determine with precision which factor or factors caused the disease or death so long as the likely candidates can be causally attributed, in relevant degree, to the psychological injury in employment. Even if that is correct, it does not assist Mrs Moronski’s case: all of the significant risk factors cannot be causally attributed to injury or employment, a family history of heart disease for example.
71. Thus, setting philosophical or scientific theories of causation to one side and addressing the question of causation raised by sections 14 and 17 of the Act in a commonsense way,[70] the evidence, including epidemiological studies and the expert evidence based on such studies, is not sufficient to justify an inference as to the probabilities in the manner contended for by Mrs Moronski. As it appears to us, to draw such an inference in this case would be a step too far.
[70] March v E & MH Stramare Pty Ltd (1991) 171 CLR 506 at 509 per Mason CJ (with whom Toohey and Gaudron JJ agreed); Chappel v Hart (1998) 195 CLR 232 at 237-238, 242-243, 254-256.
72. Evidence of risk does not equate to evidence of cause in the particular circumstances unless it is establish that the actual risk had eventuated or materialised: it must be established as more probable than not that the actual risk had eventuated. Simply asserting that a risk factor may have been a cause is not sufficient. Thus, even if we were to accept the possibility that Dr Moronski was exposed to an increased risk of ischaemic heart disease or death as a result of his injury in employment, and that is not established, the increased risk alone is not a sound basis on which to draw an inference that the risk materially contributed to cause or accelerate or aggravate his heart disease or resulted in the coronary event that caused his death. Increased risk is not sufficient to establish a causal nexus between employment and injury or between injury and death; risk of harm remains in the realm of possibility unless and until the actual risk is realised.[71] To that end it is necessary to establish that “The ‘possibility’ or ‘risk’ that X might cause Y had in fact eventuated, not in the sense that X happened and Y had also happened, but that it was undisputed that Y had happened because of X”;[72] “it is more probable than not that X was a cause of Y”.[73] No such finding can be made in the present case.
[71] Chappel v Hart (1998) 195 CLR 232 at 245 per McHugh J.
[72] Seltsam Pty Ltd v McGuiness and Anor; James Hardie & Coy Pty Ltd v McGuiness and Anor (2000) 49 NSWLR 262 at 280.
[73] Amaca Pty Ltd v Ellis; South Australia v Ellis; Millennium Inorganic Chemicals Ltd v Ellis (2010) 84 ALJR 226.
73.
All that can be said on the present evidence is that it is possible that
Dr Moronski’s death may have been contributed to in some degree by depression and certain lifestyle factors or behavioural patterns, and that the depression and lifestyle factors and behavioural patterns, separately or in combination, may have been contributed to by circumstances in his employment. Dr Moronski was exposed to a number of risks of significance some of which were clearly not related to his previous employment, and, as we have said, it is not possible on the present evidence to differentiate the relative importance of the risk factors to which he was exposed in causal terms. To go further would be to enter into speculation about changes in Dr Moronski’s lifestyle and his behaviour, and about the causes of his heart disease and his death.
74. Thus, in sum, the proposition that Dr Moronski’s ischaemic heart disease and his death resulted from a work-related injury is not made out to the reasonable satisfaction standard. For that reason we find no liability against Comcare to compensate Mrs Moronski for her husband’s ischaemic heart disease or his death.
75. The decisions under review are affirmed.
I certify that the 75 preceding paragraphs are a true copy of the reasons for the decision herein of Mr S. Webb, Member and Dr M. Miller AO, Member.
Signed: ...................[sgd]......................................................
J. Lakin, AssociateDate of Hearing 18 & 19 March 2010
Date of Decision 20 April 2010
Counsel for the Applicant Mr R. Livingston
Solicitor for the Applicant Hansteins LawyersCounsel for the Respondent Ms L. Walker
Solicitor for the Respondent Dibbs Barker Solicitors
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