McLoughlin and Military Rehabilitation and Compensation Commission

[2006] AATA 825

Administrative

Appeals

Tribunal

 

DECISION AND REASONS FOR DECISION [2006] AATA 825

ADMINISTRATIVE APPEALS TRIBUNAL      )

)          No Q2003/19

VETERANS' APPEALS  DIVISION		)
Re		MAURICE McLOUGHLIN

Applicant

And MILITARY REHABILITATION AND COMPENSATION COMMISSION

Respondent

DECISION

Tribunal Mr RG Kenny, Member
Dr M Denovan, Member

Date28 September 2006  

PlaceBrisbane

Decision

The Tribunal:

· sets aside the decision under review and substitutes its decision that the respondent is liable to pay compensation to Mr McLoughlin for asbestosis under section 14 of the Safety Rehabilitation and Compensation Act 1988;

·     remits the matter to the respondent with the direction that it calculate Mr McLoughlin’s entitlements in accordance with its decision; and

·     orders that the respondent pay the applicant’s costs of these proceedings in accordance with the general practice direction.

..........[Sgd]..........

RG Kenny

Presiding Member

CATCHWORDS

WORKERS’ COMPENSATION – benefits and entitlements – asbestosis – condition attributable to employment with the Royal Australian Air Force – respondent liable under section 14 of the Safety, Rehabilitation and Compensation Act – calculation of compensation remitted to respondent – costs awarded in accordance with general practice direction.

Safety, Rehabilitation and Compensation Act 1988 ss 4, 14

Treloar and Australian Telecommunications Commission (1990) 26 FCR 316

REASONS FOR DECISION

28 September 2006   Mr RG Kenny, Member
Dr M Denovan, Member        

1.      Mr McLoughlin was born on 3 March 1946.  He joined the Royal Australian Air Force (RAAF) in March 1965. After recruit training, he served as a plant operator in the Northern Territory RAAF base at Tindal for 12 months and then he spent the remainder of his service at RAAF base Amberley, until his discharge in 1971.  In the mid 1990s, he experienced difficulty breathing and has been diagnosed with fibrosing alveolitis, a condition that now results in him being extremely incapacitated due to shortness of breath. The diagnosis was confirmed by lung biopsy performed in 1998.

2. Whilst there are many possible causes of fibrosing alveolitis, Mr McLoughlin believes that he has a form known as asbestosis, and that this developed as a consequence of occupational dust exposure which occurred during his work in the RAAF. On 29 April 2002, he lodged a claim for compensation in accordance with section 14 of the Safety, Rehabilitation and Compensation Act 1971 (the Act).  In a decision dated 2 October 2002, the Military Rehabilitation and Compensation Commission (the respondent) determined that the correct diagnosis of Mr McLoughlin’s condition is idiopathic fibrosing alveolitis.  It also determined that this was not associated with his service.  That decision was affirmed by the respondent on 22 November 2002 and Mr McLoughlin now seeks review of that decision by the Administrative Appeals Tribunal (the Tribunal).

Issues

3. Section 14 of the Act provides that the respondent is liable to pay compensation in respect of an injury suffered by an employee if the injury results in incapacity for work or impairment. In subsection 4(1) of the Act, the term “injury” is defined to include a disease and, in turn, that term is defined to include any ailment or aggravation of any such ailment contributed to in a material degree by the person’s employment. The Tribunal is to determine from what lung condition Mr McLoughlin suffers and whether or not that condition resulted from his employment with the RAAF.

4.      Mr McLoughlin also suffers from emphysema. That condition appears to be attributable to his long history of smoking tobacco and it is not contended that it is associated with his service in the RAAF.

The Condition from which Mr McLoughlin Suffers

5.      Respiratory physician Dr Charles Mitchell completed reports on 25 November 2003, 16 January 2005 and 12 May 2006.  He believes that Mr McLoughlin has idiopathic interstitial fibrosis, meaning that the cause of the condition is unknown, not established or is otherwise intrinsic i.e. caused by an auto-immune process.  Respiratory physicians, Dr Maurice Heiner and Dr Roger Allen also provided reports.  Dr Heiner’s were dated 16 June 2004, 12 August 2004, 11 October 2004 and 3 April 2005.  Dr Allen’s was dated 20 January 2006.  Radiologist, Dr Richard Slaughter, also provided reports, dated 5 February 2004 and 3 August 2006.  These three specialists disagreed with Dr Mitchell. They believe Mr McLoughlin has interstitial fibrosis caused by exposure to occupational dusts, including asbestos, and that the condition is asbestosis. 

6.      While medical science has not yet developed an investigative procedure that can, in all circumstances, accurately define the cause of intersitital fibrosis, all three respiratory physicians that gave evidence to the Tribunal agreed that, in order to determine whether interstitial fibrosis is idiopathic or is caused by occupational dust exposure, the relevant considerations are:

·the history of exposure to dust;

·the clinical history of the condition, in particular the time between the onset of the condition and possible exposure to asbestos, and the clinical progress of  the condition after onset; and

·the presence of plural plaques.

History of exposure to environmental dusts

7.      When Mr McLoughlin consulted respiratory physicians Dr James McKeon in 1998, Dr Allen in September 2002, and Dr Mitchell in June 2003, he reported exposure to concrete dust and silicone dust.  However, he was of the opinion he had little if any exposure to asbestos.  All three physicians opined at the time that Mr McLoughlin was suffering from idiopathic fibrosing alveolitis.  At that time, Dr Allen opined that there was no evidence in the literature that concrete dust causes fibrotic lung disease.

8.      In his evidence, Mr McLoughlin said that it was not until he was contacted by a delegate of the respondent that he was aware that he had been exposed to asbestos during his service.  He then turned his mind to consider the totality of his exposure to asbestos during his service.  He subsequently prepared two affidavits in which he itemised his occupational exposure to asbestos and other dusts.  Mr McLoughlin described his involvement in erecting huts and toilets made of asbestos cement sheeting which was cut with power saws.  He also did electrical work which involved drilling holes through and cutting up asbestos cement, for about six months. He then was involved in digging trenches and putting in drains and piping, some of which were made of asbestos cement.  The smaller piping was cut with angle-grinders and he also used asbestos lagging to seal the pipes together.  On RAAF bases, Mr McLoughlin lived in huts made of material which included asbestos.    He also worked on “super six” asbestos roofing and was required to unstack “super six” and other asbestos cement sheeting from trucks.  At Amberley, he assisted in the demolition of huts and building of huts with fibrocement sheeting and he did further work with pipes including stormwater drainage.  At that base, he also worked with concrete aggregate and was exposed to large amounts of dust from blue metal and quartz.  Mr McLoughlin said that, at the end of a day’s work at both Tindal and Amberley when he was involved in dealing with asbestos, he could recall being covered by dust from those asbestos products.

9.      Peter James Wilkinson gave evidence which supported that of Mr McLoughlin concerning dust exposure.  Mr Wilkinson does not know Mr McLoughlin personally, and did not serve with him.  However, he also served at Tindal and Amberley.  Mr Wilkinson told the Tribunal that he had read Mr McLoughlin’s affidavits, and recalled that he had personally witnessed all the tasks that Mr McLoughlin claimed to have performed during his RAAF service and he had experienced the dusty conditions, associated with asbestos products, involved with that work.

10.     Dr Mitchell told the Tribunal that an accurate and reliable history was critically important when diagnosing asbestosis.  He said that there must be at least moderate exposure to asbestos over a reasonable period of time.  According to Dr Mitchell, the disease is usually confined to those who have worked in the mines or have put on installation or pipe “lagging” on ships.  Dr Mitchell questioned the reliability of the history provided by Mr McLoughlin in his affidavits given that, when he saw Mr McLoughlin in 2003, he had very little recollection of the details of asbestos exposure.  Dr Mitchell said that it was highly unlikely, if not impossible, that Mr McLoughlin had sufficient asbestos exposure to develop asbestosis.  He said that he was mostly dealing with “bound up” asbestos in cement products, such as roofing materials, and that there was only a small probability of it entering the lungs.  Dr Mitchell said it was unlikely that the living conditions Mr McLoughlin found himself in would have resulted in any significant asbestos exposure.  However, he conceded that the cutting of asbestos products with tools such as power saws and grinders would generate considerable asbestos dust.

11.     Dr Allen was not concerned that Mr McLoughlin initially gave a history of no exposure to asbestos at the initial consultation.  He said that it was, in fact, common for patients to give no such history and that the problem was often due to the history-taker not asking the correct questions.  Dr Allen opined that Mr McLoughlin’s condition was due to a mixture of dusts, asbestos playing a significant part.  He considered that Mr McLoughlin had sufficient exposure to asbestos to cause asbestosis.  Dr Allen said that angle-grinding of asbestos products causes intense exposure and that this is close to the operator’s face.  In 2002, Dr Allen was not aware that Mr McLoughlin had performed that sort of work.  He now understood it to be the case that Mr McLoughlin did so for approximately a year.  Dr Allen referred to a change in the current thinking within the medical community in relation to cement dust.  Whilst it was previously thought that this dust did not cause fibrosing alveolitis, according to the most recent edition of Cropman and Douglas, a respiratory medical text, there is a possible causal association.

12.     Dr Heiner first saw the applicant in January 2004.  He agreed that an accurate history was an important factor in the diagnosis of asbestos.  He said that the material in Mr McLoughlin’s affidavits was consistent with the history that he had provided during his consultations. Dr Heiner opined that Mr McLoughlin had sufficient exposure to asbestos whilst cutting pipes to cause asbestosis.

Clinical history of the condition

13.     Dr Mitchell opined that the clinical picture presented by Mr McLoughlin was far more consistent with idiopathic fibrosing alveolitis than asbestosis.  He noted that finger clubbing had been reported in 1997 and said that phenomenon is usually far worse in idiopathic fibrosing alveolitis.  Dr Mitchell said that the long time interval of approximately 30 years between Mr McLoughlin’s exposure to asbestos and the development of his first symptoms suggested that there was no causal association.  Asbestosis, according to Dr Mitchel is an insidiously progressive condition, sometimes revealing no changes for 20 years.  Dr Mitchell opined that the sudden onset of shortness of breath experienced by the applicant in 1998, and his significant deterioration in lung function tests since that time is consistent with a diagnosis of idiopathic fibrosing alveolitis. While Dr Mitchell acknowledged that idiopathic fibrosing alveolitis is usually a more aggressive disease than Mr McLoughlin has experienced, he said there is a wide spectrum of clinical pictures and Mr McLoughlin’s case was entirely consistent with the diagnosis.

14.     Dr Allen said that finger clubbing is not a significant marker for idiopathic fibrosing alveolitis.  He acknowledged that it was less likely to be present in asbestosis than in idiopathic fibrosing alveolitis.  The significance of finger clubbing, according to Dr Allen, was that its presence in 1997 indicated that Mr McLoughlin has had fibrotic disease of the lung for many years.  As idiopathic fibrosing alveolitis is an aggressive disease, and has a similar prognosis to lung cancer, Dr Allen opined that it was highly unlikely that Mr McLoughlin would still be alive today, nearly ten years later, if he had the condition. He considered that the fact that Mr McLoughlin continued smoking and suffers from emphysema would have made his prognosis even worse had he had idiopathic fibrosing alveolitis.  According to Dr Allen, there had been only a small decline in his lung function since the condition was diagnosed in 1998 until 2006.  He considered that this was far more consistent with a diagnosis of asbestosis than idiopathic fibrosing alveolitis.  Dr Heiner agreed that the clinical progress of idiopathic fibrosing alveolitis was much more rapid than demonstrated in Mr McLoughlin.  He said that, if Mr McLoughlin had idiopathic fibrosing alveolitis, given that he had severe clubbing in 1997, he would have died within two years.

15.     In relation to the time interval between exposure to asbestos and development of symptoms of interstitial fibrosis, Dr Allen said that there was tremendous variability between patients.  Dr Heiner agreed.  He said that whilst the mean latency period is 20 years, the shortest latency period that he was aware of was 5 months, and the longest was 50 years. 

16.     In his report dated 19 February 1998, Dr McKeon diagnosed idiopathic fibrosing alveolitis and said that he advised Mr McLoughlin that the condition is usually progressive, with an average survival of only five years.  Dr McKeon opined that the prognosis was even worse in those who smoked cigarettes.

The presence of plural plaques

17.     Mr McLoughlin has had a number of CT scans of his lungs since 1998.  With the exception of that performed on 2 August 2006, none of these investigations were reported as exposing pleural plaques.  In his radiological report dated 3 August 2006, Dr R Slaughter stated that he could identify a small posterior pleural plaque.  In that report, Dr Slaughter opined that, on review of early CT scans, the plaque was probably present on the previous studies and that it would be consistent with a plaque from asbestos exposure.

18.     Dr Mitchell suggested that the absence of pleural plaques until recently meant that the area of thickening identified in the August 2006 CT scan was of little significance.  He suggested it could be due to another cause, such as an infection. Dr Mitchell said that, if Mr McLoughlin had had significant asbestos exposure, he would have expected significantly more pleural plaques.  Dr Mitchell acknowledged that not everyone with asbestos develops pleural plaques.

19.     Dr Slaughter stated that what was actually identified in the scans was an area of pleural thickening.  He said that such thickening was not specific for a plaque and could also be explained due to infection or other abnormality.  He told the Tribunal that the position of the plaque was in a common position for asbestosis.  He said that had it been due to infection it would be more likely be found in a different position (the lung base). Because the thickening was more discrete and more local, this made the likely cause to be an asbestos plaque.  Dr Slaughter said that a plaque was a marker of exposure to asbestos, and that there was no correlation between the number of plaques and the amount of exposure to asbestos. He acknowledged, however, that the presence of more plaques would make him more confident that there had been asbestos exposure.

20.     Dr Allen said that there was no difference between the significance of one plaque and multiple plaques.  He said that the only significance of the plaque identified was that it validates the history given by the applicant.  However, he considered that the absence of plaques would not exclude a diagnosis of asbestosis.

21.     Dr Heiner told the Tribunal that 11% of patients with asbestosis have no plaques.  While he acknowledged that there were other possible causes of pleural thickening, he considered that, in this case, the finding was likely to be an asbestos plaque.

Conclusion in relation to diagnosis

22.     In matters of diagnosis, immediate decisiveness is not always a luxury afforded to the medical profession.  Mr McLoughlin first presented with a history, clinical picture and investigative results more consistent with a diagnosis of idiopathic fibrosing alveolitis.  Dr Mitchell favours that diagnosis because, inter alia, Mr McLoughlin initially gave no history of exposure to asbestos. 

23.     The Tribunal found Mr McLoughlin to be a credible witness and accepts his account that, after being alerted to the fact that there had been exposure to asbestos and what products might contain that substance, he was able to provide a history of the nature and length of exposure that he had during his RAAF service.  Dr Allen and Dr Heiner are confident that Mr McLoughlin has had sufficient exposure to asbestos to develop asbestosis.

24.     Significantly, Dr Allen, Dr McKeon and Dr Heiner, and even Dr Mitchell, all expressed the opinion that idiopathic fibrosing alveolitis is usually a rapidly progressive disease, with very short life expectancy and with a prognosis that would likely to be significantly worsened by Mr McLoughlin’s smoking.  Given the medical evidence, the fact that Mr McLoughlin is still alive in 2006 makes that diagnosis most unlikely.

25.     The opinion of Dr Allen, Dr Heiner and Dr Slaughter is that the presence of a likely pleural plaque in the most recent CT scan, whilst not definitive, strongly supports the diagnosis of asbestosis.  Dr Mitchell agreed that the absence of a pleural plaque does not eliminate the possibility of the diagnosis.

26.     On all of the medical evidence before it, the Tribunal finds, on the balance of probabilities, that Mr McLoughlin has asbestosis.

Relationship to Employment

27.     Reference has been made above to the nature of the employment-related exposure that Mr McLoughlin had to various dusts including asbestos.  The Tribunal is satisfied that that exposure made a material contribution to his lung condition:  see Treloar and Australian Telecommunications Commission (1990) 26 FCR 316 at 323. Accordingly, the Tribunal is satisfied that the requirements of section 14 of the Act are met and that the respondent is liable to pay compensation to Mr McLoughlin in respect of the incapacity for work or impairment that he has from his asbestosis.

Decision

28. The Tribunal sets aside the decision under review and substitutes its decision that the respondent is liable to pay compensation to Mr McLoughlin for asbestosis under section 14 of the Act and remits the matter to the respondent with the direction that it calculate Mr McLoughlin’s entitlements in accordance with its decision and orders that the respondent pay the applicant’s costs of these proceedings in accordance with the general practice direction.

I certify that the 28 preceding paragraphs are a true copy of the reasons for the decision herein of Mr RG Kenny, Member
Dr M Denovan, Member

Signed:         Michelle Brazier
  Legal Research Officer

Date/s of Hearing  14 and 15 August 2006
Date of Decision  28 September 2006
For the Applicant  Dr G Cross, of Counsel
  Turner Freeman, Lawyers
For the Respondent                  Mr C Clark, of Counsel
  Dibbs, Abbott Stillman, Lawyers