Howarth and Military Rehabilitation and Compensation Commission

[2011] AATA 163

Administrative Appeals Tribunal

DECISION AND REASONS FOR DECISION [2011] AATA 163

ADMINISTRATIVE APPEALS TRIBUNAL      )

)          No 2010/1709

GENERAL ADMINISTRATIVE DIVISION		)
Re		Mr Anthony Howarth

Applicant

And Military Rehabilitation & Compensation Commission

Respondent

DECISION

Tribunal M D Allen, Senior Member  &  Dr M E C Thorpe, Member

Date              11 March 2011

PlaceSydney

Decision The decision under review is AFFIRMED.

..................[sgd].....................

M D Allen, Presiding Member  

CATCHWORDS

COMPENSATION:    Applicant former member of Australian Regular Army.  Claimed that cerebral haemorrhage caused by service induced smoking.  Not satisfied on balance of probabilities that smoking caused or materially contributed to Applicant’s cerebral haemorrhage.

LEGISLATION

Safety, Rehabilitation and Compensation Act 1988, section 4, 14.

CASES

Kennedy Cleaning Services Pty Ltd v Petkoska (2000) 200 CLR 286

Australian Postal Corporation v Burch (1998) 26 AAR 312

Australian Postal Corporation v Burch (1998) 28 AAR 30.

REASONS FOR DECISION

11 March 2011

M D Allen, Senior Member

Dr M E C Thorpe, Member

1.      By this application the Applicant sought review of a “reviewable decision” that affirmed a prior determination rejecting his claim for compensation for the diagnosed conditions of right cerebral haemorrhage (commonly referred to as a stroke) and left hemianopia.

2.      In a nutshell the Applicant’s case was that as a member of the Australian Regular Army (“ARA”) in the years 1956 to 1962 he developed a smoking habit and that this smoking habit led to his suffering a right sided cerebral haemorrhage and left hemianopia on or about 15 July 1997.

3.      The medical evidence adduced makes it clear that the left hemianopia was caused by the cerebral haemorrhage.

4.      The Respondent conceded that whilst a member of the ARA the Applicant did develop a smoking habit and that this habit was a result of his military service, and that the Applicant was so habituated to cigarette smoking during service that he continued to smoke after military service.

5.       The uncontradicted evidence is that the Applicant ceased to smoke in mid to late 1986.

6.      Given the decision of the High Court in Kennedy Cleaning Services v Petkoska (2000) 200 CLR 286 affirming Zickar v MGH Plastic Industries Pty Ltd (1996) 187 CLR 310 it is clear that the cerebral haemorrhage constituted an “injury” simpliciter as the term injury was defined in section 4 of the Safety Rehabilitation and Compensation Act 1986 (“SRC”) as it stood at the date of the Applicant’s injury.  See also Australian Postal Corporation v Burch (1998) 26 AAR 312 at 318-9. (Affirmed on appeal Australian Postal Corporation v Burch (1998) 28 AAR 30.)

7.      The issue is therefore whether the Applicant’s smoking habit, which ceased in mid to late 1986, caused or materially contributed to his “stroke”.

8.      Two opposing medical opinions were put before the Tribunal.  Dr Robin Fitzsimons, Neurologist for the Applicant opined that the Applicant’s smoking made a material contribution to his cerebral haemorrhage.

9.      In her report of 14 July 2010 Dr Fitzsimons states:

“On the information available therefore, heavy cigarette smoking in the past would seem to be the only substantive identifiable vascular risk factor.  This may have caused some weakening of the blood vessel walls within the brain, resulting more than a decade later in cerebral haemorrhage.  It should be noted that risk of vascular events is generally helpful to decrease gradually following the cessation of cigarette intake.  However, it may not revert to a risk identical to that of the general population”.

10.     In a later report dated 3 November 2010, replying to the opinion by Dr Mellick, Neurologist for the Respondent, Dr Fitzsimons referred to papers which implicate smoking as a risk factor for “stroke”.  Dr Fitzsimons opinion was however qualified as she stated:

“The question of how Mr Howarth would fit into these various statistical analyses is also not straightforward, as he was an exceptionally heavy smoker for 30 years, but he did discontinue smoking some 10 years before suffering a lobar cerebral haemorrhage.” 

And she ultimately opined:

“On current information I consider that both ongoing alcohol consumption and past very heavy tobacco consumption are likely to have contributed to damage of his cerebral vasculature and predisposed to a vascular event such as he experienced.  I acknowledge that the length of time which elapsed between cessation of smoking and the event would have decreased the impact of his smoking as a factor and as a relative contribution in any multi-factorial situation (as this is likely to be with ‘unknown’ factors also at play).  It may well be that the ongoing alcohol consumption was more relevant”.

11.     Dr Mellick was quite firm in his opinion that smoking played no part in the Applicant’s cerebral haemorrhage.

12.     In his report of 12 July 2010, Dr Mellick stated:

“Mr Howarth smoked from 1956 until 1986, ceasing about 11 years prior to the time of the stroke.  I understand that when he had the stroke there was no history of hypertension, nor was he aware of any other risk factor.

A Meta-analysis was published in the British Medical Journal 1989 covering 32 separate studies and cigarette smoking was not found to be a ‘cause’ of cerebral haemorrhage.

A more recent study published by The American Heart Association and The American Stroke Association (27.03.03) involved a prospective cohort study among 22,000 US male physicians.  There was a 17.8 year follow-up and 108 intracerebral haemorrhages were recorded.  It was found that ‘never smokers’ and ‘past smokers’ had equal rates of intracranial haemorrhage.”

13.     A later report by Dr Mellick, dated 15 September 2010, addressed Dr Fitzsimons opinion.  At page two of that report, Dr Mellick stated:

“I am also, with respect, unable to agree with the hypothesis that the exposure to cigarettes 11 years previously ‘may have caused some weakening of the blood vessel walls within the brain resulting more than a decade later in cerebral haemorrhage’.  There is no evidence that the exposure to cigarettes 11 years previously produced ‘some weakening of the blood vessel walls within the brain’. 

There are a number of recognised causes of haemorrhage in the younger age group, such as an arteriovenous malformation of small size.  Such pathology may be destroyed by the haemorrhage itself and is not therefore identified subsequent to its occurrence.

A failure to identify another cause, accordingly, is not a persuasive argument to establish that cigarette smoking 11 years previously has been a substantial cause of the haemorrhage.”

14.     Cross examined, Dr Mellick again referred to papers on the causes of stroke and was quite unequivocal that current data does not establish that smoking is a cause of cerebral haemorrhage.  The only concession he made to Dr Fitzsimons opinion was to state that “evidence-based medicine leaves the matter uncertain”.

15.     In assessing the competing opinions we note that Dr Fitzsimons opinion is qualified and she takes into account the cessation of smoking and the Applicant’s alcohol consumption which is itself a cause of cerebral haemorrhage.

16.     Two papers referred to by Dr Mellick were tendered as exhibits.  In the first of these papers entitled “Meta-analysis of relation between cigarette smoking and stroke” by Shinton and Beevers, the authors state:

“This study did not, however, confirm smoking as a cause of cerebral haemorrhage.”

17.     The second paper referred to by Dr Mellick is entitled “Smoking and the Risk of Hemorrhagic Stroke in men” by Kurth et al.  In that paper the authors state:

“Compared with never smokers past smokers had no increase in the risk of total hemorrhagic stroke”.

18.     In the extract of the Kurth paper the authors state as their results that:

“Never smokers and past smokers had equal rates of intracranial hemorrhage and subarachnoid hemorrhage.”

19.     Of the extract of papers annexed to Dr Fitzsimons report, one simply states, “smoking and alcohol consumption favoured hemorrhagic stroke” without referring to either non or past smokers, whereas the other paper states that smoking doubled the risk for primary intracranial hemorrhage.

20.     As Dr Fitzsimons herself states in her report of 14 July 2010 smoking “would seem to be the only substantive identifiable vascular risk factor”.  As pointed out in submissions for the Respondent, a risk factor is not a cause.

21.     We are satisfied that the Applicant’s cerebral haemorrhage and consequent left hemianopia constituted an injury simpliciter for the purposes of the SRC Act.  There was no “disease” shown to be present (unlike an ischaemic cerebrovascular accident). Much less could it be shown that any disease arose out of, or was caused by, the Applicant’s employment.

22.     The hypothesis propounded by Dr Fitzsimons that smoking was a contributory factor in the Applicant’s stroke remains just that, a mere hypothesis.  Even accepting that smoking is a risk factor in cerebral haemorrhage, a risk factor is not a cause.  All that can be said in the case of this Applicant is that smoking may have been a risk factor but we are not satisfied on the balance of probabilities that his smoking that ceased some 11 years prior to the injury was a cause of, or materially contributed to, his cerebral haemorrhage.

23.     The decision under review is AFFIRMED.

I certify that the 23 preceding paragraphs are a true copy of the reasons for the decision herein of Senior Member M D Allen and Dr M E C Thorpe.

Signed:         ...........[sgd].......................
  K. Lynch, Associate

Dates of Hearing   28 February 2011
Date of Decision   11 March 2011
Counsel for the Applicant           Mr Mark Vincent
Solicitor for the Applicant            Legal Aid Commission
Counsel for the Respondent       Mr Brendan Kelly
Solicitor for the Respondent       Dibbs Barker