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Williams and Comcare [2010] AATA 129 (19 February 2010)

Last Updated: 19 February 2010

Administrative Appeals Tribunal

DECISION AND REASONS FOR DECISION [2010] AATA 129

ADMINISTRATIVE APPEALS TRIBUNAL )

) No 2008/3034

GENERAL ADMINISTRATIVE DIVISION
)

Re
Cherie Williams

Applicant
And
Comcare

Respondent

DECISION

Tribunal
Professor RM Creyke
Dr M Miller AO

Date 19 February 2010

Place Canberra

Decision
The Tribunal sets aside the reviewable decision and makes a decision that Comcare is liable to compensate Ms Williams under section 14 of the Act. The Tribunal also orders that the costs of these proceedings incurred by Ms Williams be paid by the responsible authority subject to any submissions from the parties. The parties are given 14 days to apply.

.....................[sgd]...................
Professor RM Creyke, Senior Member

CATCHWORDS

COMPENSATION – whether Applicant suffered a disease contributed to in a material way by her employment – causation of occupational asthma – renovations in a sealed, highly secure ‘vault-like area’ over three weeks – Applicant has ‘highly brittle’ asthma – decision under review set aside

Safety, Rehabilitation and Compensation Act 1988 (Cth) ss 4, 5, 7, 14, 67(8)


Comcare v Sahu-Khan [2007] FCA 15; (2007) 156 FCR 536

Comcare v Canute [2005] FCAFC 262; (2005) 148 FCR 232


19 February 2010 REASONS FOR DECISION
Professor RM Creyke, Senior Member
Dr M Miller AO, Member

  1. Ms Williams had been employed full-time by the Department of Defence since February 1994, and in 2005 was working in the Defence Signals Directorate, Canberra. In 2005, she developed severe asthma for which she made a claim for compensation on 16 March 2007. Ms Williams retired on 18 April 2008.
  2. On 10 September 2007, Comcare denied liability, a decision upheld on reconsideration on 30 June 2008. On 7 July 2008, Ms Williams sought further review by the Tribunal. The matter was heard in both the Intensive Care Unit of Canberra Hospital and at the Canberra Registry of the Tribunal between 21 and 22 December 2009.
  3. It has been accepted that the date of injury was 8 March 2005.

LEGISLATION

  1. The relevant provisions of the Safety, Rehabilitation and Compensation Act 1988 (Cth) (the Act) as at March 2005 are:

4 Interpretation

(1) In this Act, unless the contrary intention appears:

ailment means any physical or mental ailment, disorder, defect or morbid condition (whether of sudden onset or gradual development).

disease means:

(a) any ailment suffered by an employee; or

(b) the aggravation of any such ailment;

being an ailment or an aggravation that was contributed to in a material degree by the employee’s employment by the Commonwealth ...

employee has the meaning given in section 5, and also applies to persons 65 years of age or older.

Impairment means the loss, the loss of the use, or the damage or malfunction, of any part of the body or of any bodily system or function or part of such system or function.

Injury means:

(a) a disease suffered by an employee; or

(b) an injury (other than a diseas) suffered by an employee, being a physical or mental injury arising out of, or in the course of, the employee’s employment; or

(c) an aggravation of a physical or mental injury (other than a disease) suffered by an employee (whether or not that injury arose out of, or in the course of, the employee’s employment), being an aggravation that arose out of, or in the course of, that employement;

but does not include any disease, injury or aggravation suffered by an employee as a result of reasonable disciplinary action taken against the employee or failure by the employee to obtain a promotion, transfer or benefit in connection with his or her employment.

5 Employees

(1) In this Act, unless the contrary intention appears:

... employee means:

(a) a person who is employed by the Commonwealth ...

7 Provisions relating to diseases

(1) Where:

(a) an employee has suffered, or is suffering, from a disease ...

(b) the disease is of a kind specified by the Minister by notice in writing as a disease related to employment of a kind specified in the notice; and

(c) the employee was, at any time before symptoms of the disease first became apparent, engaged by the Commonwealth ... in employment of that kind;

the employment in which the employee was so engaged shall, for the purposes of this Act, be taken to have contributed in a material degree to the contraction of the disease, unless the contrary is established.

(2) Where an employee contracts a disease, any employment in which he or she was engaged by the Commonwealth ... at any time before symptoms of the disease first became apparent shall, unless the contrary is established, be taken, for the purposes of this Act, to have contributed in a material degree to the contraction of the disease if the incidence of that disease among persons who have engaged in such employment is significantly greater than the incidence of the disease among persons who have engaged in other employment in the place where the employee is ordinarily employed. ...

(4) For the purposes of this Act, an employee shall be taken to have sustained an injury, being a disease, or an aggravation of a disease, on the day when:

(a) the employee first sought medical treatment for the disease ...

(6) An incapacity for work or impairment of an employee shall be taken, for the purposes of this Act, to have resulted from a disease ... if, but for that disease ...:

(a) the incapacity or impairment would not have occurred;

(b) the incapacity would have commenced, or the impairment would have occurred, at a significantly later time; or

(c) the extent of the incapacity or impairment would have been significantly less.

14 Compensation for injuries

(1)  Subject to this Part, Comcare is liable to pay compensation in accordance with this Act in respect of an injury suffered by an employee if the injury results in death, incapacity for work, or impairment.

(2)  Compensation is not payable in respect of an injury that is intentionally self-inflicted.

(3)  Compensation is not payable in respect of an injury that is caused by the serious and wilful misconduct of the employee but is not intentionally self-inflicted, unless the injury results in death, or serious and permanent impairment.

  1. For the purposes of section 7(1) relevant diseases were specified in the Schedule to the Safety, Rehabilitation and Compensation (Specified Diseases) Notice 2007(1) notified in the Gazette on 21 June 2007.[1] Item 1 in the Schedule listed the disease 'Occupational asthma caused by sensitising agents or irritants'. The specified employment which related to this disease was described as 'employment processes involving asthmagenic agents'.

ISSUES

  1. The following are the issues:

EVIDENCE

  1. In 2005, Ms Williams was working on the ground floor of the Defence building, premises known as ‘Russell Offices’, in Canberra. This floor contained a large compactus for personnel records along one wall. It was a high security area. The space was divided into a seven rooms, one of which was the Publications Cell. Ms Williams was a supervisor in the Publications Cell which was approximately 12m x 14m. The total space was classified as an A class vault and was roughly 47m x 23m. It was sealed off by two locked security doors which were the only entrances. There were no windows, the doors were closed all the time, and the area was ventilated solely by air conditioning ducts in the ceiling.
  2. Between 16 February 2005 and 1 March 2005, renovations were made in the space. The work involved demolition of several partition walls, their replacement with new walls in a different location, removal of existing benches and their relocation, the relocation of a whiteboard, and the removal of a sink. The walls were made of plasterboard or gyprock, with a steel metal frame. Rebuilding also involved building and installing cupboards. The first to be demolished was a wall of the Publications Cell. The second wall demolished was on the far side of the adjoining room to the Publications Cell. The work was undertaken over two days. The construction of a new wall took about 7-8 days.
  3. Following the demolition and erection of a new wall, the workmen used white acrylic paint to repaint areas affected by the work. The paint had strong fumes and repainting took two days. The total time involved in the renovations was 3 weeks. As the area was a secure area, the workmen could only do the work during business hours. Staff members had to be in the area at all times to ensure there was no breach of security, so they took it in turns to arrive at 7.00am to let the workmen in to the building; escort them within the secure areas during the day; and lock up after they had left in the evenings. The workmen needed to be in the line of sight of staff at all times. The need to see the workmen also meant no drop sheets were used to protect workers from the dust and fumes.

Mr R Stewart

  1. Mr Stewart was Ms Williams’s supervisor at Defence for 14 years. He gave evidence at the hearing and provided a statement dated 28 July 2008. His evidence was that Ms Williams worked as an APS4 Officer for approximately 14 years in the Russell Offices, Building 5. He said that prior to these events Ms Williams had been in good health. She did suffer pain in the neck, shoulder and arm (cervical brachialgia) from 1999 and was still being treated for this condition in 2004. However, she rarely took sick leave. After the renovations in 2005, her time off work increased due to illness.
  2. During the renovations, there was extensive dust in the area, and later on, strong paint fumes. The dust was visible in the air, and coated all the surfaces including desks, computers, chairs, the carpet, the compactus, the light fittings and the vinyl floor area. The excess dust was still present even after the work was completed. Although the workers cleaned up the visible area, this did not include speakers, and the top of the compactus which stretched some 32m along one wall. The staff were not issued with protective breathing apparatus and the workmen did not wear any masks either. At one stage, a staff member brought in a fan to see if the dust could be dispersed.
  3. Mr Stewart said Ms Williams’s workstation was no more than 5-10m away from the wall which was demolished. He recalled Ms Williams coughing more or less continuously shortly after the demolition work commenced, although he could not say precisely when she started. She also exhibited shortness of breath, and wheezing if she had to walk any distance. In the midst of a sentence she often needed to pause for breath after a bout of coughing. None of these symptoms was present prior to March 2005. After a prolonged bout of coughing, Mr Stewart would tell Ms Williams to see her doctor and he would send her home. Ms Williams retired in April 2008 on medical grounds. Mr Stewart noticed a significant decline in Ms Williams’s health from March 2005.
  4. Mr Stewart said Ms Williams was not the only person affected. Ms Macpherson and Ms Lloyd, who also worked in the area, were coughing. In Ms Macpherson’s case the coughing only lasted 2-3 months and then abated. Ms Lloyd did not cough as much as the other two and her symptoms disappeared reasonably quickly. Mr Mitchell also wheezed, but he was an asthmatic. Mr Mitchell complained to Mr Stewart because his symptoms increased at that time. For his own part, Mr Stewart said his nose was clogged up every day but this cleared when he left the building and he did not develop a cough. Mr Stewart said the room took about 2 days to paint, but the fumes remained for longer. He also smelt the burning metal from the grinders.
  5. In cross-examination, Mr Stewart said he had completed Ms Williams’s application for compensation. Questions 5 and 6 were in his handwriting. He could not recall when he completed the form but it may have been in March 2007. He acknowledged that Ms Williams was working reduced hours because of repetitive strain injury syndrome and was also being treated for anxiety and depression. He also remembered that she had fractured her wrist at work and was off work for about 2 months from early May 2005.

Ms K Lloyd

  1. Ms Lloyd said she is pedantic about dust. During the renovations, she remembers seeing dust on the computers; a film of dust on her computer’s monitor; dust on the floor; on the compactus; and on the shelving. In her written statement dated 29 April 2009, Ms Lloyd stated the dust emanating from the gyprock wall being demolished was ‘extreme’, and there was ‘extensive dust all over our work stations and it was difficult to breathe.’ The dust was everywhere throughout the period the construction work occurred. She said she was about 5m from the wall and Ms Williams was about 5.5m away. On reflection, however, she said she could not tell how far she was from the new wall and it could have been 10m.
  2. Ms Lloyd said she has had respiratory problems for a long time and carries a ventolin puffer with her all the time. She recalled experiencing shortness of breath, tightening in the chest and difficulty breathing at night around June 2005. She said she is allergic to dust mites and takes anti-histamine because she gets itchy, watery eyes and a tickle at the back of her throat when she is exposed to dust mites. She recalls thinking she needed to see her general practitioner at that time, but did not do so and relied on her ventolin puffer instead. She said that at the time the work was being done, Ms Macpherson, Mr Stewart and Ms Williams were all coughing.
  3. Ms Lloyd said she had known Ms Williams for over 20 years. Prior to the period in late February/early March 2005, Ms Lloyd stated Ms Williams’s respiratory health was excellent. At that time she recalled Ms Williams coughing almost continuously and she heard her wheeze, although she could not recall whether this followed coughing. She was also pale and did not look well. Ms Lloyd said she told Ms Williams to go to a doctor. She said from early March 2005 Ms Williams’s health declined significantly.
  4. Ms Lloyd said she left the Publications Cell in 2007. Subsequently, on one occasion in 2007 when she had coffee with Ms Williams, she recalled Ms Williams having to walk to Russell Offices, Building 1 where Ms Lloyd was located, and being hardly able to breathe following the 5 minute walk. She said Ms Williams was much worse in 2007 than in 2005.
  5. Ms Lloyd said in cross-examination that Ms Williams’s wheeze came on later than March. In June 2005, Ms Lloyd went to the doctor for her asthma, but she did not have full-blown asthma in March 2005.

Ms J Macpherson

  1. Ms Macpherson said she worked with Ms Williams in the publications section, but for a shorter period than Ms Williams. She recalls the renovations in February/March 2005 and that staff were not provided with any personal protection equipment. She said Ms Williams’s desk was about 8m from the gyprock wall which was demolished. She said that dust and debris were everywhere, that lumps of dust emerged, and no-one cleaned the top of the compactus. If you touched anything in the compactus area, it was likely to be dusty. She said that after the construction was over the dust was still heavy and circulating in the air, so the staff brought in a couple of fans to try and redirect the dust away from their desks. She said some days the dust was a fine mist, in other days a cloud. Desks were grey with dust and it permeated the compactus, settled on the walls, and on the floor. Any movement of roof tiles or lighting fixtures dislodged more dust which settled on the workstations. She said you could not escape it. She said she had developed a cough and used a puffer but only needed it for a couple of months in late February/early March 2005. She attended her general practitioner in May 2005.
  2. She also said she recalled the glue smell when the plasterboard wall was being put up and the smell of paint. Ms Williams was badly affected and was coughing and sneezing and wheezing and could hardly breathe. She brought an electric oxygen fibrillator to work, which Ms Macpherson encouraged her to use. Ms Macpherson described Ms Williams as very pale, short of breath, and whenever someone said a joke her breath became ‘staggered’. Ms Macpherson said they were concerned about her and thought at times she might need an ambulance. After the wall came down, Ms Williams’s health deteriorated. Prior to these events, her health had been good and she rarely took time off work.

MEDICAL EVIDENCE

  1. In the hearing, Dr Sanderson gave evidence on his own; whereas Professor McKenzie, Dr Johnson and Dr Nogrady gave concurrent evidence, with Dr Nogrady appearing in person and Professor McKenzie and Dr Johnson appearing via video-link.

Dr J Sanderson

  1. Dr Sanderson, Ms Williams’s general practitioner since 1998, said he had seen her on 102 occasions since 1999. His records indicated she had had no respiratory problems in the period 1999-2005. She had no history of asthma or of smoking. On 8 March 2005, she presented with a cough and he diagnosed bronchitis. Thereafter, he generally saw her after the sudden onset of acute episodes of asthma. He said he recalled her telling him that other co-workers were also having respiratory problems during the renovations at her workplace in early 2005.
  2. On 27 May 2005, he diagnosed her with a viral or streptococcal illness. The results of the blood tests ordered by Dr Dillon on 9 May 2005 were confusing. The tests were positive for only 2 out of 3 conditions for whooping cough or for a form of pneumonia. In Dr Sanderson's view, the results of the blood tests were inconclusive and should be ignored.
  3. Dr Sanderson requested further tests on 9 June 2005. On 17 June 2005, he referred Ms Williams to Dr Nogrady who diagnosed her with asthma on 5 July 2005. Dr Sanderson said he accepted the diagnosis of asthma following Ms Williams’s emergency visit to Canberra Hospital on 29-30 April 2005. With hindsight, he believed she had developed asthma earlier. In his written opinion, he said Ms Williams had adult onset asthma. However, the condition is unusual in someone with no prior history and normally onset in such cases is gradual rather than sudden. In Ms Williams’s case, she became profoundly unwell soon after her exposure to dust in the workplace.
  4. In his view, Ms Williams suffered an acute onset of severe respiratory illness precipitated by some trigger. In his opinion, the illness was consistent with exposure to dust or another pollutant in the workplace. He noted that by the time of her retirement in April 2008, she was extremely disabled by her symptoms and that the effects had worsened over time. In his written report dated 3 May 2008 he said:
In Chris Williams case there is a clear cut chain of events. She went from never ever experiencing a respiratory illness or asthma prior to the single episode of fumes and dust inhalation to the development of severe life-threatening asthma afterwards. From a medico-legal point of view there is no more obvious indication that she has reacted severely and permanently to the exposure of paint fumes and dust at her work place in March 2005.
  1. Although he confirmed that her ex-husband had smoked for many years and one of her sons continues to smoke, and he noted Dr Nogrady’s suggestion that a possible trigger could have been her son’s smoking, these factors had not changed his mind.

Associate Professor D McKenzie

  1. Associate Professor McKenzie is the Head of the Department of Respiratory Medicine at the Prince of Wales Hospital, Sydney, and the Chair of the Respiratory Clinical Division of the South Eastern Sydney and Illawarra Area Health Service. He examined Ms Williams on 20 September 2008 and provided a report dated 27 October 2008. He also provided a supplementary medical report of 11 February 2009 and a further report dated 24 August 2009.
  2. In his report of 27 October 2008, Associate Professor McKenzie said:

The onset of Ms Williams’ asthma appears to have been precipitated by a severe lower respiratory tract infection, which had clinical features consistent with whooping cough but serological results suggestive of Mycoplasma pneumonia. Both of these infections are well documented as common initiators of asthmatic inflammation in susceptible individuals. ... There is nothing in Ms Williams’ former occupation that is likely to have initiated an episode of asthma. ... It is my considered opinion that the work environment has played no role in the initiation or progression of her illness.

  1. In his report of 11 February 2009, having reviewed Dr Johnson’s report, he said there was nothing ‘that would lead me to alter my opinion in relation to the diagnosis of [Ms Williams] condition and the probable aggravating factors for it in my previous report.’ He went on:

In my opinion the illness described by Ms Williams and documented in the medical records that I have examined does not satisfy the diagnostic criteria for either irritant induced asthma or RADS. ... The basic difference between the two is that RADS may develop following a single exposure to an irritant with the exposure lasting for minutes to hours. Irritant induced asthma or airways disease covers a similar syndrome but when the exposures may have occurred on several or even many occasions.

  1. In his 11 February 2009 report, Associate Professor McKenzie identified 7 factors which are commonly included in the diagnostic criteria for RADS or irritant induced asthma. In his opinion, Ms Williams satisfied only three of those. One contra-indicator among the criteria was that ‘[o]ther pulmonary diseases are ruled out’. In his view, ‘a plausible alternative diagnosis of asthma induced by lower respiratory tract infection, namely Mycoplasma pneumoniae, has been documented.’ In other words, in his view, in Ms Williams’s case other pulmonary diseases could not be ruled out. He was of the view that her diagnosis was late onset asthma precipitated by a lower respiratory tract infection. That infection occurred before or during the period of the renovation.
  2. In his report of 24 August 2009, Associate Professor McKenzie said of RADS:

This is a condition which resembles asthma, which has been initiated by a single heavy exposure to an extremely irritating substance. This condition is relatively rare and would usually only occur in exceptional circumstances such as extreme exposure to highly irritating substances such as chlorine gas or the fumes emanating from heated concentrated sulphuric acid or hydrochloric acid. Irritant induced asthma is an asthmatic illness or syndrome which has been induced by repeated exposure, usually over months or years, to moderately irritating substances. ... Irritant induced asthma would not usually be diagnosed in someone who had a casual exposure to mildly irritating substances such as paint fumes or general carpentry dust. ...

Broadly speaking, occupational asthma can be divided clinically into people who had pre-existing asthma, which is aggravated or exacerbated by the occupational exposure and new onset asthma which has developed as a result of exposure to sensitising agents which are known to be asthmagenic.

  1. In his view, ‘none of the exposures that Ms Williams is likely to have encountered during those renovations was to an agent that is known to be a respiratory sensitiser’. He noted she was exposed to gyprock:

[gyprock was] probably the dominant dust particle in the work environment. This is not known to be asthmagenic. She was exposed to various types of wood dust including particle board and laminex. These agents can give off small quantities of formaldehyde during normal carpentry work ... [but] any exposure to formaldehyde would almost certainly have been less than the occupational standards.

  1. He concluded: ‘Ms Williams was not exposed to any known primary sensitisers of the airways or “asthmagenic agents”’.

Dr A Johnson

  1. Dr Johnson is a respiratory physician working in private practice and at Liverpool Hospital, Sydney. He appeared at the hearing but also provided four written reports dated: 16 September 2008, following his interview with Ms Williams; 22 December 2008, reviewing Associate Professor Mackenzie’s report of 27 October 2008 and Dr Sanderson's 3 May 2008 report; 18 March 2009, considering whether Ms Williams’ suffered a specified disease under section 7(1) of the Act; and 10 July 2009 following his review of the statements of Ms Williams’s co-workers and copies of documents referring to the composition of the materials used in the wall which was demolished.
  2. In his report of 16 September 2008, Dr Johnson noted that Ms Williams had been admitted to Canberra Hospital with respiratory problems 8 times since July 2005; that she had attended the emergency department at the Canberra Hospital due to shortness of breath in April, May, July and August of 2005; and that she had been regularly on prednisone and seretide since June 2005. The doctors at the Canberra Hospital diagnosed her as suffering from asthma in April 2005, a diagnosis confirmed by Dr Nogrady who first saw Ms Williams on 17 June and provided a report on 5 July 2005. Dr Johnson also noted that around the time of onset of the asthma Ms Williams had developed a mycoplasma pneumonia chest infection which resolved with antibiotic therapy. In his view ‘the commencement of the asthma would be consistent with irritant-induced asthma.’
  3. Dr Johnson's report of 22 December 2008 cited an article in the recent literature which noted that dust and fumes, for example, from paint, were among the most common exposures leading to reactive airways dysfunction syndrome.[2] He also noted that Ms Williams had stated that her symptoms commenced within the first week of the renovations. He concluded:

It is impossible to know at this stage whether the exposure at work induced [Ms Williams] asthma. There may have been other factors involved in inducing asthma such as respiratory tract infections. ... I think it is more probable than not that the exposure at work aggravated any asthma occurring at that time and that they were involved in inducing the asthma. .... I think given the clear temporal relationship and also the exposure to renovation dust and paint fumes the work exposures were probably involved in the causation of her asthma.

  1. In his report of 18 March 2009, Dr Johnson noted that in her employment, Ms Williams was exposed to paint fumes, a potentially asthmagenic agent, and he expressed the opinion that Ms Williams ‘probably suffers from occupational asthma caused by irritants’ which, in his view, was more probably than not ‘induced and aggravated by irritants present [in her] employment during renovation works during March 2005’. In his report of 10 July 2009, Dr Johnson said the wall which was demolished during the renovations contained urea formaldehyde, resin and wood dust and he noted the ‘[f]ormaldehyde and wood dust are ... known to be asthmagenic.’
  2. At the hearing, Dr Johnson maintained his view that Ms Williams has asthma, most likely irritant induced asthma, or occupational asthma, from her exposure to irritants in her workplace. In his view, having a cough can be the first evidence of irritant induced asthma, and the symptoms emerged quite soon afterwards. Those symptoms met many of the factors of irritant induced asthma identified by Brooks.[3] While he acknowledged that the degree of Ms Williams’s exposure may have been light and that there was no measurement of the quantity of dust nor of the intensity of the paint fumes during the renovations, he pointed out that in some of the cases referred to in the literature, there was also an absence of high exposure. In his view there was no plausible alternative explanation to explain Ms Williams's development of the condition.

Dr S Nogrady

  1. Dr S Nogrady, senior specialist at the Canberra Hospital and Clinical Senior Lecturer, University of Sydney, saw Ms Williams on several occasions. Dr Sanderson referred Ms Williams to Dr Nogrady on 17 June 2005. Fourteen of his reports on Ms Williams are included in the evidence provided to the Tribunal. In his report of 5 July 2005, he diagnosed ‘mild asthma ... compounded by a recent significant mycoplasma infection and also compounded by a high level of anxiety and confusion’. He noted she had no previous respiratory disease but presented with a history of 4 months of cough and increasing breathlessness, in the ‘last week or so.’
  2. A report by Dr R Wee on behalf of Dr Nogrady on 21 September 2005 noted that Ms Williams had been admitted to the Canberra Hospital for seven days in August 2005 with ‘an exacerbation of asthma secondary to an upper respiratory tract infection’ and also had two visits to the emergency department with an acute asthma attack on 27 August 2005 and 13 September 2005.
  3. In his reports of 6 March 2006, and 5 June 2006, Dr Nogrady refers to Ms Williams’s sudden and severe attacks of asthma despite compliance with her medication. In his search for causes of these acute episodes, Dr Nogrady said in his 14 August 2006 report that possible triggers were ‘minor upper respiratory infections and a runny nose ... and there is also a trigger related to the smoke in the house from her son.’ However, in his report of 16 July 2007, he concluded following his search for triggering factors ‘there don’t appear to be any obvious ones’.
  4. In his 6 January 2009 report Dr Nogrady pointed out:
Gyprock dust is not known to be toxic to the lungs, nor is it known to be either an inducer causing the onset of asthma as a disease nor as a trigger for symptoms. Non-specific irritant dusts can cause short term increases in asthma symptoms but these normally settle fairly quickly. Similarly there is no evidence for commonly used plastic flat wall paints in the same setting... [O]n the balance of probabilities I believe the development of asthma in [Ms Williams] is not related to the exposures so described. I do however qualify this by saying that Mrs Williams has an unusual form of highly brittle asthma and its onset has at least temporal co-incidence with the described exposures.
  1. However, Dr Nogrady then changed his opinion. In his report of 23 November 2009 he acknowledged that the recurrence of acute episodes of Ms Williams's asthma led him ‘to reconsider my original thoughts on the etiology of her asthma and its possible relationship to her work exposure.’ He said he now believed her asthma was ‘of the reactive airway dysfunction syndrome variant. The criteria Brooks et al identified for irritant-induced asthma,[4] as adapted by Dr Nogrady, are:
  1. Applying those factors to Ms Williams, he concluded that her condition related to the events in February/March 2005 because she had no asthma symptoms nor any respiratory illness prior to the development of the asthma; her symptoms came on within 12 hours of exposure to contaminants in her workplace; the symptoms had persisted; and while none of the dusts in her workplace in February/March 2005 were known to be asthma sensitisers, her major exposure to the mixture of building dusts fitted with the syndrome, particularly since an extension to non-specific dusts and building materials following the 9/11 attacks in New York city, had now been established.[5]

Other medical specialists

  1. Although Dr R Powell, of the Kingston Family Surgery, did not give a diagnosis her clinical notes of 1 April 2005 show Ms Williams was prescribed a seretide inhaler. Seretide by means of an inhaler is a recognised treatment for asthma as well as other respiratory problems.
  2. On 9 May 2005, Dr Dillon, in his clinical notes refers to ‘persisting phlemy cough and SOB [shortness of breach] over 2 months or more... finds puffers bit hard to manage.. Some dust at work.’ He requested pathology tests for possible 'mycoplasma/respiratory Chlamydia/Pertussis.’ The clinical record of 13 May 2005 noted blood tests results: [s]hows pertussis +/- Chl.pneumoniae’ and Ms Williams’s reason for visit as: ‘Pertussis RTI’. Dr Dillon prescribed an antibiotic.On 27 May 2005, Dr Dillon's clinical notes stated 'Attended A + E [emergency] – acutely short of breath. Responded to ventolin. Keep going with Seretide and ventolin.’ In his reason for the visit he noted: ‘Asthma – Infective exacerbation'. Dr Dillon, in a written submission of 25 March 2009, said in his opinion ‘the March 2005 work place incident played a significant role in precipitating [Ms Williams’s] asthma condition.’
  3. Dr B Burke, a respiratory and general physician, in his report of 23 March 2006, noted that her ‘symptoms certainly have a very asthmatic flavour with cough, wheeze and breathlessness, nocturnal predominance and response to inhaled bronchodilator and oral steroid’.’ He also noted Ms Williams’s suggestion that the only trigger she was aware of was cold air.
  4. Dr RJ Mullins, consultant physician, Clinical Immunology & Allergy, in his report on Ms Williams of 22 May 2006, noted the diagnosis of asthma made in 2006 but said there was evidence of significant anxiety and depression as well. He confirmed that she was not allergic. He also noted that ‘many of her episodes are more consistent with hyperventilation attacks and vocal chord dysfunction than they are of asthma’. He acknowledged that she had asthma, but said ‘anxiety is playing a significant role in at least some of her symptoms.’
  5. Dr AJ Nicholls, consultant thoracic physician, in his report of 3 April 2008, noted Ms Williams’s suggestions that her asthma could be triggered by viral infections, exposure to cold air, possibly eating potato chips and laughing. He concurred with the diagnosis of late onset asthma. However, in his opinion, it was coincidental that the onset of her symptoms occurred at the same time as the office renovations.

Ms Williams

  1. Ms Williams said she had no respiratory problems in the period 1999-2005. Renovations commenced in her workplace on 16 February 2005 involving demolition of a gyprock wall, installing office fittings, chipboard, plasterboard, and laminated bench tops and cupboards. When the renovations started in February 2005 she said there was a lot of noise and dust everywhere for the two to three week duration of the work. According to Ms Williams in her supplementary statement dated 8 April 2009, the first wall demolished was located about 5m from her work station. Subsequently, she said while repainting was in train, there were strong paint fumes for 1-2 days. Ms Williams also noted in her written statement that the basement below the R5 Building in which she worked and which she had to visit on occasions, contained mould, mildew and spores. This often found its way into the air conditioning system servicing the area in which she worked.
  2. She said once the renovations started, her eyes started watering and she developed a cough. On 8 March 2005, she went to see Dr Sanderson for her coughing and wheezing and was diagnosed with bronchitis. On 1 April 2005, she went to Dr Powell at the Kingston surgery because her cough persisted. The medication she prescribed did not alleviate the cough. On 15 June 2005 she attended Dr Dillon, also of the Kingston Family Surgery, and the blood tests he ordered indicated possible chest infection. Despite extensive treatment and medical examinations subsequently, her symptoms persisted. On 29-30 April 2005, 26 May 2005, 4-5 July 2005 and 2-8 August 2005, she attended the Emergency Department of the Canberra Hospital. At the first visit, the Hospital doctors diagnosed asthma. She conceded that no formal diagnosis of asthma was made by her treating doctors or specialists until Dr Nogrady's report of 5 July 2005, although Dr Dillon had referred to her reason for a consultation on 27 May 2005 as ‘Asthma – Infective exacerbation’. . Ms Williams said in her evidence that fellow workers at that time also suffered respiratory difficulties. Ms Lloyd, who was asthmatic but had not used a puffer for some time, had to resort to her puffer and Ms McPherson developed a persistent cough and breathlessness.
  3. Ms Williams confirmed that her ex-husband had smoked for a long period, and that one of her sons living with her also smokes. However, she was adamant that her son's smoking does not trigger her asthmatic attacks since he smokes in a distant part of the house. Ms Williams noted her continued difficulty with managing her condition, indicated by the fact that she has been admitted to hospital 31 times since the condition developed. She is on daily prednisone, a nebuliser seretide and ventolin.
  4. Ms Williams conceded in cross-examination that the undated incident report she had completed following the effects on her of the renovations was probably filled out later than March 2005. She noted that Dr Sanderson advised her to fill out a claim for workers’ compensation for ‘severe asthma’. That claim was dated 16 March 2007. Her evidence, however, was that she felt breathless ‘long before May 2005’.

OTHER EVIDENCE

  1. On 22 June 2009, the Defence Department produced documents concerning the materials used in the renovation and safety information relating to the various products. The relevant items in this matter are particle board, formaldehyde, wood dust, paint, sealants, and jointing compounds. In summary the safety information says:

CONSIDERATION

  1. Counsel for Ms Williams contended that the reviewable decision was against the weight of the evidence, there was a clear temporal connection between her asthma and her exposure to dust in the work place in or about March 2005, and that there were factual inaccuracies in respect of the proximity of her work place to the partition wall being demolished.
  2. Counsel for Comcare denied that her condition was contributed to by her employment, a view supported by the specialist evidence of Associate Professor McKenzie, the earlier reports of Dr Nogrady, and the absence of references to this possibility in the reports of Dr Nicholls, Dr Burke and Dr Mullins. An alternative explanation for the development of her asthma was that the bronchitis she was suffering at the time of the renovations caused her asthma.

Whether Ms Williams suffered an ‘injury’, namely a ‘disease’?

  1. ‘Injury’ is defined in section 4 of the Act as a ‘disease suffered by an employee’. There is no issue that Ms Williams was an employee of the Department of Defence, a Commonwealth department, in 2005. There is also no dispute that Ms Williams has asthma, an ‘ailment’ (section 4 of the Act), and hence a 'disease'.[12]
  2. How to characterise her asthma is, however, more controversial. Dr Sanderson, Dr Dillon, Associate Professor McKenzie, Dr Johnson, Dr Nogrady, and Dr Nicholls all agree that Ms Williams has adult onset asthma. Whether her asthma can be classified as an occupational disease for the purposes of section 7 of the Act, or is an ‘injury’, namely, a ‘disease’ which has been contributed to, to a material degree, by Ms Williams’s employment for the purposes of section 14 of the Act is a key question. The form of asthma which Ms Williams suffers and what caused it are inextricably linked to the answer to these questions.
  3. The Tribunal was provided with copious literature on occupational asthma.[13] The material refers to two forms of occupational asthma: irritant induced asthma, and a subset, reactive airways dysfunction syndrome (RADS). The latency period for the development of asthma varies between the two. As Associate Professor McKenzie noted (see paragraph 30 of these reasons):
The basic difference between the two is that RADS may develop following a single exposure to an irritant with the exposure lasting for minutes to hours. Irritant induced asthma or airways disease covers a similar syndrome but when the exposures may have occurred on several or even many occasions.
  1. While not using the same terminology, the Australian Safety and Compensation Council reflected a similar dichotomy when it noted of occupational respiratory diseases:
For inhalational accidents, the respiratory effect is seen almost immediately or within a few hours following exposure. ... For occupational asthma, the symptoms usually don’t start until some weeks to months after first exposure.[14]
  1. Clearly, it is easier to identify a cause or causes for the more immediately occurring RADS, than for irritant induced asthma or other forms of occupational asthma.
  2. At the same time, the Tribunal notes that it is possible that her condition could be classified as RADS, assuming that there may have been an initial misdiagnosis by her doctor when Ms Williams first presented on 8 March 2005. For example, Malo notes that in cases of RADS (which he described as 'acute irritant-induced asthma’):
... coughing is generally a predominant symptom. Thereafter, bronchial obstruction, if present, does not respond as well to bronchodilators. ... In addition, obliterative bronchiolitis has been described in victims of the Bhopal accident and, more recently, in soldiers exposed to mustard gas'.[15]
  1. The Australian Safety and Compensation Council also noted:
Occupational asthma is defined as asthma caused by exposure to agents encountered in the working environment in workers without pre-existing asthma. Airways responsiveness is obstruction in nature and results in wheeze, chest tightness, cough and shortness of breath.[16]
  1. These descriptions fit closely with the circumstances of Ms Williams. She was coughing and sneezing in the period from 16 February to 1 March 2005, and by early March 2005 was exhibiting shortness of breath and wheezing. The diagnosis by Dr Sanderson on 8 March 2005 of 'acute bronchitis' is present, and the fact that a bronchial infection, if it existed, did not respond well to seretide, a bronchodilator, when prescribed on 1 April 2005, also fits within the description. So although asthma was not diagnosed until the end of April 2005 when Ms Williams presented at the emergency department of the Canberra Hospital, she may have been suffering from asthma earlier.
  2. Her asthma was not caused by a single high intensity incident. Rather it was the cumulative effect over several weeks of a trigger or triggers which caused her asthma. Nonetheless, the two forms of asthma are closely connected and many of the factors identified in the literature on RADS may also be applied to irritant-induced asthma as well. For these reasons, the Tribunal has relied on the literature on both.
  3. The Tribunal notes the absence of evidence as to the level of dust or fumes during the renovations. In terms of Brooks’s criteria for RADS this raises doubts as to whether the exposure can be considered 'high level'. Nonetheless the research is not definitive on the criteria, distinguishing irritant-induced asthma from its subset, RADS. Even Brooks's research, which is frequently cited, noted that though ‘our definition of RADS is restrictive and requires the presence of a high level exposure, it is conceivable that a low level chronic exposure could cause a similar type process in some individuals.’[17] In the absence of evidence the Tribunal is not able to find that Ms Williams’s exposure was high level. However, she may be among those individuals for whom a 'low level chronic exposure' could cause RADS. Again, it is not possible given the evidence before the Tribunal to make that finding. On balance, the Tribunal finds that Ms Williams suffered from irritant-induced asthma rather than the subset, RADS, both being forms of occupational asthma. The Tribunal also finds that Ms Williams’s exposure, although not high level, was likely to occur since her desk was situated some 8-10m from the wall which was first demolished.

Whether Comcare is liable to compensate Ms Williams under section 7(1) of the Safety, Rehabilitation and Compensation Act 1988 (Cth) (Act)?

  1. Section 7 identifies certain occupational diseases which, if contracted in the circumstances outlined in the section, create a presumption that the disease has been contributed to by employment. The occupational diseases and the employment which attracts the provision are set out in the Schedule to Notice 1 of 2007 published in the Gazette, 21 June 2007. The relevant prescribed disease is 'Occupational asthma caused by sensitising agents or irritants'. The specified employment which related to this disease was described as 'employment processes involving asthmagenic agents'.
  2. Ms Williams suffered irritant induced asthma, a form of occupational asthma. Whether it was caused by sensitising agents or irritants has yet to be established. However, assuming that the dust and fumes from the renovation were responsible for causing Ms Williams's asthma, and that these are asthmagenic agents, it must also be established that:
[t]he incidence of that disease among persons who have engaged in such employment is significantly greater than the incidence of the disease among persons who have engaged in other employment in the place where the employee is ordinarily employed.[18]

The Tribunal has interpreted ‘such employment’ to be employment during the renovations in February/March 2005 in the Department of Defence ‘vault’ area. The evidence does not indicate that any of Ms Williams's workmates developed asthma from the events of February/March 2005. One other person, Mr Mitchell, was already an asthmatic. Ms Macpherson, Ms Lloyd and Mr Stewart were also coughing, but Mr Stewart said Ms Lloyd's coughing stopped reasonably quickly, Ms Macpherson's cough in disappeared after between 2-3 months, and in his own case, Mr Stewart’s nasal blockage cleared after he left the workplace. Nor was evidence provided that the workmen who were exposed to the conditions in the vault suffered from asthma. So there was no evidence at all that her workmates developed irritant induced asthma and that this was significantly greater than the incidence of the disease among other staff or workmen in that area. Since no evidence was provided as to other staff or forms of employment conducted in the ‘vault’ area, it was not possible to establish that the incidence was greater among staff or workmen not involved in or affected by the renovations within the ‘vault’ area, of Defence. In those circumstances, section 7 is not applicable to Ms Williams's case.

If Ms Williams suffered from a disease, whether that disease was contributed to, in a material degree, by her employment by the Department of Defence?

  1. A contribution to a 'material degree' as required by section 4 of the Act in 2005. What amounted to a ‘material contribution’ was considered in Comcare v Sahu-Khan[19] by Finn J who endorsed the decision of the Full Federal Court in Comcare v Canute[20] that the expression was ‘intended to require that the contribution be “more than a mere contributing factor”’.[21] This view is now accepted as the correct interpretation of that expression. As His Honour put it, the inclusion of the term ‘material’ imposed an ‘evaluative threshold below which a causal connection may be disregarded’.[22] Finn J concluded that the correct test for ‘in a material degree’ was probably best captured by the meaning in the Shorter Oxford English Dictionary as ‘4. In a material degree; substantially, considerably’[23] and that ‘in a material degree’ required an evaluation of all relevant contributing factors.[24]
  2. There is no question of aggravation of a pre-existing condition. The principal issue is what was the trigger for Ms Williams’s late onset asthma? Candidates are her ex-husband's smoking over many years and that one of her three sons still living at home smokes; a viral infection such as the possible bronchitis she was diagnosed as suffering on 8 March 2005; or the dust and fumes from the renovations in her workplace. Another potential trigger was the mould, mildew and spores circulated through the air conditioning system. Ms Williams also suggested that cold air, eating potato chips, and laughing might be possible causes of her attacks. Allergies can also cause asthma.
  3. Dr Nicholls, to whom the suggestions about cold air, eating potato chips and laughing were made by Ms Williams, did not endorse any of them in his report, and was not called to give evidence. Nor is there scientific support for at least two of those triggers - eating potato chips and laughing. Cold air is a recognised factor but there is insufficient evidence to indicate this is a causal trigger in Ms Williams's case. Although mould, mildew and spores can be triggers for asthma, given that these potential triggers would have been in the air conditioning long before Ms Williams developed asthma, and there was no indication that others in the workplace who had respiratory conditions were suffering any effects from these agents, these potential triggers too can be discounted. Allergies can also be discounted since, as Dr Mullins report indicates, no evidence was provided that allergies were implicated in Ms Williams's condition.
  4. Associate Professor McKenzie was of the view that the trigger for Ms Williams's asthma was more likely to have been a severe lower respiratory tract infection given what he noted as the 'casual exposure to mildly irritating substances' in her workplace, and the absence of evidence of exposure in her workplace to agents known to be respiratory sensitisers. His view was supported by the report of Dr Nicholls, who was not called to give evidence.
  5. Initially, Dr Nogrady also appeared to be of the view that her condition was more likely to be due to an upper respiratory tract infection, coupled with her significant level of anxiety and depression (the latter also being conditions noted by Dr Mullins). Dr Nogrady, too, in his 6 January 2009 report noted that gyprock dust and paint fumes were not usually regarded as triggers for asthma. However, Dr Nogrady resiled from that view and in his 23 November 2009 report, faced with the continuation of Ms Williams’s acute asthma attacks and the difficulty of managing her symptoms, said he then believed she suffered from asthma of the RADS variant.
  6. The later view of Dr Nogrady was strongly supported by Dr Johnson and by her treating medical practitioners, Dr Sanderson and Dr Dillon. Nor were Dr Nogrady, Dr Sanderson, and Dr Johnson dissuaded from their views on cross-examination. Dr Burke did not give his opinion as to the cause of Ms Williams's asthma. Dr Mullins advised of multiple causes, and said anxiety was playing a significant role.
  7. The Tribunal finds that although Associate Professor McKenzie pointed out that Ms Williams only had 'casual exposure to mildly irritating substances', he may have given insufficient attention to the environment in which Ms Williams worked. The Tribunal heard that the 'vault-like’ area of Russell Offices in which Ms Williams worked had no windows, was sealed off by two locked doors, and air was provided solely through air conditioning ducts. The safety information about the materials being used and the dust produced during the renovations universally stated[25] that exposure in poorly ventilated areas or in areas without natural ventilation could cause irritation to upper respiratory functions and increased risks for those with asthma or for the development of asthma. In these circumstances, even casual contact with mildly irritating substances may have an enhanced effect.
  8. Others in Ms Williams's workplace developed respiratory symptoms during this time, and their symptoms only settled when the renovations were complete. So the dust and fumes did have an effect on her fellow workers. In Ms Williams's case, Dr Nogrady diagnosed her as having a 'highly brittle' form of asthma, which suggests a greater likelihood on her part to have a reaction to asthmagenic agents or other triggers.
  9. Wood dust was classified as 'hazardous' by the NOHSC. It is significant that the Australian Safety and Compensation Council noted too that 'the two most commonly reported causative agents for asthma in the SABRE notification scheme are wood dust and isocyanates (13.5% and 5.8% respectively).’[26]
  10. So, although the length and extent of Ms Williams's exposure may not have been high, and there was a possible alternative trigger in her upper respiratory condition at the time, given the doubts about the accuracy of the diagnosis of the respiratory infection, the safety information, the peculiar nature of the premises, Ms Williams's special sensitivity, the medical view about the significant of the temporal correlation with the renovations, and the fact that others in her workplace were affected, the Tribunal finds that Ms Williams’s exposure to dust and fumes at work in 2005 did have a material role in her development of asthma.

If there was a material contribution between Ms Williams’s claimed disease and her employment, whether the employment-related effects of that condition have now ceased?

  1. Ms Williams has provided evidence that the severity of her condition has abated to a degree. Nonetheless, at the time of the hearing in late 2009, Ms Williams had again suffered an acute attack of asthma and was in the Intensive Care Unit at the Canberra Hospital. It is evident that she continues to suffer the condition and that control of symptoms remains a problem. Research by Malo et al on a group with acute irritant-induced asthma has indicated that between 7.4 and 16.6 years after diagnosis: 'respiratory symptoms were common at the time of follow-up, wheezing being present in 80% of subjects' and 'one third of the subjects were on inhaled steroids'.[27] The research concluded that:
... the long-term outcome of subjects with 11A [acute irritant-induced asthma] is at least as poor as found in subjects with allergic OA [occupational asthma]. From the functional point of view, only six subjects (17%) included in the current study [of 68 subjects] had normal airway caliber and responsiveness at follow-up. This is to be compared with 28 cured subjects/103 subjects (27%) with allergic OA who were examined at a mean interval of 9 years after stopping exposure'.[28]
  1. In a related study by Tarlo containing a Consensus Statement by the American College of Chest Physicians, the prognosis for occupational asthma (OA) was described in these terms:
The long-term consequences of OA are variable and require prolonged follow-up. ... A systematic review of the outcome of sensitizer-induced OA reported a pooled estimate of symptomatic recovery of 32% varying from 0 to 100% within a median duration of follow-up of 31 months. The pooled prevalence of persisting nonspecific bronchial hyperresponsiveness was 73% and was significantly greater for those with OA from HMW [High Molecular Weight] agents compared with those with OA from LMW [Low Molecular Weight] agents. Outcomes were best in those patients with a shorter duration of exposure.[29]
  1. This is confirmed by research by Chan-Yeung which found:
The majority of patents with occupational asthma with latency do not recover, even after several years away from exposure. They have permanent impairment or disability. ... The increased bronchial responsiveness is associated with chronic airway inflammation. Once initiated, the inflammatory process in the airways may perpetuate itself.[30]
  1. The Tribunal finds that the research suggests that there are long-term effects of occupational asthma. In these circumstances, and given the history of Ms Williams's condition, the acute nature of her ongoing asthma attacks and the continuing difficulty of management of its symptoms, she would appear to fall within the high percentage of subjects surveyed in whom the effects continue for some time and possibly indefinitely. On that basis, Ms Williams’s asthma continues to be experienced and the effects can be directly attributed to the initiation in 2005 of the condition. The employment related effect of Ms Williams's disease has not ceased.

Whether Comcare is liable to pay compensation to Ms Williams under section 14 of the Act?

  1. It follows that the Tribunal sets aside the reviewable decision and makes a decision that Comcare is liable to compensate Ms Williams under section 14 of the Act. The Tribunal also orders that the costs of these proceedings incurred by Ms Williams be paid by the responsible authority subject to any submissions from the parties. [31] The parties are given 14 days to apply.

I certify that the 84 preceding paragraphs are a true copy of the reasons for the decision herein of Professor RM Creyke

Dr M Miller AO.


Signed: ............................[sgd]........................................

C. Kocak, Associate


Date/s of Hearing 21 December 2009 - 22 December 2009

Date of Decision 19 February 2010

Counsel for the Applicant David Richards

Solicitor for the Applicant Maurice Blackburn Lawyers

Counsel for the Respondent Ben Dubé

Solicitor for the Respondent Sparke Helmore


[1] J Ballard and P Sutherland Annotated Safety, Rehabilitation and Compensation Act 1988 (Federation Press, 2007) note at [7.02] that the schedule of diseases was first published in Gazette S 365 of 30 November 1988, revoked and replaced without substantive change, by the 2007 Notice.
[2] MS Shakeri, FD Dick and JG Ayres, ‘Which agents cause reactive airways dysfunction syndrome (RADS)? A systematic review’ (2008) 58 Journal of Occupational Medicine 205; SM Brooks, MA Weiss and IL Bernstein, ‘Reactive airways dysfunction syndrome (RADS): Persistent Asthma Syndrome After High Level Irritant Exposures’ (1985) 88 CHEST 376.
[3] Eg Shakeri et al, above n 2.
[4] SM Tarlo, Balmes, Balkissoon, Beach, Beckett, Bernstein, Blanc, Brooks, Cowl, Daroowalla, Harber, Lemiere, Liss, Pacheco, Reclich, Rowe and Heitzer, Diagnosis and Management of Work-Related Asthma: American College of Chest Physicians Consensus Statement (2008), 134 CHEST, Suppl 1S.
[5] GI Banauch, D Alleyne, R Sanchez, K Olender, HW Cohen, M Weiden, KJ Kelly and DJ Prezant, 'Persistent Hyperactivity and Reactive Airway Dysfunction in Firefighters at the World Trade Center' (2003) 168 American Journal of Respiratory and Critical Care Medicine 54.
[6] Chem Alert Report – Extended Summary Report
[7] Material Safety Data Sheet.
[8] Material Safety Data Sheet 301: Trade Essentials – Particleboard.
[9] Chem Alert Report – Extended Summary Report.
[10] Material Safety Data Sheet.
[11] Chem Alert Report – Extended Summary Report.
[12] Safety, Rehabilitation and Compensation Act 1988 (Cth) s 4.
[13] Australian Safety and Compensation Council, ‘Occupational Respiratory Diseases in Australia (2006); RJ Martin, M Kraft, HW Chu, EA Berns and GH Cassell, ‘A link between chronic asthma and chronic infection’ (2001) 107 Journal of Allergy Clinical Immunology 595; PMaestrelli, P Boschetto, LM Fabbri and CE Mapp, ‘Mechanisms of occupational asthma’ (2009) 123 Journal of Allergy Clinical Immunology 531; N Nisar, R Guleria, S Kumar, TC Chawla and NR Biswas, ‘Mycoplasma pneumoniae and its role in asthma' (2007) 83 Postgraduate Medical Journal 100; Moira Chan-Yeung and Malo, 'Occupational Asthma' (1995) 333 New England Journal of Medicine 107; CE Mapp ,P Boschetto, P Maestrelli and LM Fabbri, ‘Occupational Asthma’ (2005) 172 American Journal of Respiratory and Critical Care Medicine 280; WM Alberts and GA do Pico, ‘Reactive Airways Dysfunction Syndrome’ (1996) 109 CHEST (the official journal of the American College of Chest Physicians) 1618; Brooks et al, ‘RADS’, above n2; Australian Government Department of Health and Ageing, ‘Asthma and Air Pollution: A guide for health professionals’ (2004); J Fahy and PM O’Byrne, ‘"Reactive Airways Disease: A Lazy Term of Uncertain Meaning that should be Abandoned’ (2001) 163 American Journal of Respiratory and Critical Care Medicine 822; MS Shakeri et al, above n 2; Banauch et al, above n4; SM Marlo, Balmes, Balkissoon, Beach, Beckett, Bernstein, Blanc, Brooks, Cowl, Daroowalla, Harber, Lemiere, Liss, Pacheco, Redlich, Rowe and Heitzer, 'Diagnosis and Management of Work-Related Asthma' (2008 Supplement) 134 CHEST 1S; J Malo, J L’Archeveque, L Castellanos, K Lavoi, H Ghezzo and K Maghni, 'Long-Term Outcomes of Acute Irritant-induced Asthma' (2009) 179 American Journal Respiratory Critical Care Medicine 923.
[14] Australian Safety and Compensation Council, ‘Occupational Respiratory Diseases in Australia (2006) 3.
[15] J Malo, J L’Archeveque, L Castellanos, K Lavoi, H Ghezzo and K Maghni, 'Long-Term Outcomes of Acute Irritant-induced Asthma' (2009) 179 American Journal Respiratory Critical Care Medicine 923, 923.
[16] Above n 14, 7.
[17] SM Brooks et al, above n 13, 382.
[18] Safety, Rehabilitation and Compensation Act 1988 (Cth) s 7(2).
[19] (2007) 156 FCR 536.
[20] [2005] FCAFC 262; (2005) 148 FCR 232, paras 11 – 12.
[21] Ibid, para 12.
[22] Ibid.
[23] Ibid, para 15.
[24] Ibid, para 16.
[25] There was an exception for jointing compounds but the impact of this substance is likely to have been minor.
[26] Australian Safety and Compensation Council, 'Occupational Respiratory Diseases in Australia' (2006), v.
[27] J Malo et al, above n 15, 924.
[28] Ibid, 925.
[29] Susan M Marlo, above n 13, 27S – 28S.
[30] M Chan-Yeung and Malo, above n 13; see also Brooks et al, ‘Reactive airways dysfunction syndrome (RADS): Persistent Asthma Syndrome After High Level Irritant Exposures’, 382.
[31] Safety, Rehabilitation and Compensation Act 1988 (Cth) s 67(8).

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