Briggs v RTL Mining and Earthworks

IN THE MAGISTRATES’ COURT OF VICTORIA
AT LATROBE VALLEY
WORKCOVER DIVISION

Case No. J11213661

DAVID BRIGGS	Plaintiff
v
RTL MINING & EARTHWORKS PTY LTD	Defendant

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MAGISTRATE:	S GARNETT
WHERE HELD:	LATROBE VALLEY
DATE OF HEARING:	19-21 MARCH & 22 MAY 2019
DATE OF DECISION:	1 AUGUST 2019
CASE MAY BE CITED AS:	BRIGGS V RTL MINING & EARTHWORKS
MEDIUM NEUTRAL CITATION:	[2019] VMC004

Submissions filed on behalf of the Plaintiff: 8 July 2019
Submissions filed on behalf of the Defendant: 23 July 2019

CATCHWORDS – Plaintiff employed as an Excavator Operator during Hazelwood Mine Fire between 3 March 2014 and 27 May 2014 – Exposure to smoke, fumes, dust and air toxins including; carbon monoxide, sulphur dioxide, nitrogen dioxide and particulate matter – Pre-employment spirometry detected no lung impairment – Development of ‘flu-like’ symptoms in November 2014 – Expert medical opinion in conflict regarding diagnosis and causation - Diagnosis of interstitial lung disease and amyopathic dermatomyositis/autoimmune condition: ‘overlap myositis’ associated with PM/Scl antibody leading to interstitial lung disease - connective tissue disease – Issue of causation: arising out of or in course of employment or due to ‘nature of employment’ – Temporal connection - Application to court to refer medical questions to a Medical Panel refused. Claim for weekly payments of compensation, medical treatment expenses and a determination of ‘injury’ for purposes of a S 98C Impairment Benefit entitlement – Accident Compensation Act 1985 - Workplace Injury Rehabilitation and Compensation Act 2013.

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APPEARANCES:	Counsel	Solicitors
For the Plaintiff	Mr Horner	Maurice Blackburn
For the Defendant	Mr Scully	Minter Ellison

HIS HONOUR:

Mr Briggs is aged 59 years and was employed as an Excavator Operator with the defendant from 3 March 2014 until 27 May 2014. His work involved excavating ‘hot spots’ at the Hazelwood Open Cut Mine fire which started on 14 February 2014 because of embers entering the Mine from bushfires near the Mine. The fire in the Mine burnt for a period of 45 days.

In November 2014, Mr Briggs developed ‘flu like’ symptoms including a dry cough, sore throat and shortness of breath.

Mr Briggs lodged a WorkCover claim form dated 27 January 2015 claiming weekly payments and medical treatment expenses because of an injury to his ‘lungs’. The claim was rejected by Allianz on 13 March 2015. Mr Briggs issued these proceedings on 10 May 2018 and in his Statement of Claim alleges that he sustained the following injuries which arose out of or in the course of his employment or due to the nature of his employment as a consequence of his exposure to ash, coal dust and smoke;

- injury to lungs

- diffuse pulmonary fibrosis

- secondary pulmonary hypertension

- interstitial lung disease

- amyopathic dermatomyositis

- anxiety and depression

The defendant in its Notice of Defence dated 16 August 2018 denies liability on the grounds that Mr Briggs has not sustained an injury which arose out of or in the course of his employment, that his employment was not a significant contributing factor to his claimed injury and that his incapacity for work, if any, does not result from and is not materially contributed to by an injury arising out of or in the course of his employment.

Mr Briggs also lodged a s 98C Impairment Benefits Claim Form dated 25 July 2017 for injuries described as; ‘lung-interstitial lung disease and amyopathic dermatomyositis’. This claim was rejected by Allianz on 1 November 2017.

At the commencement of the hearing on 19 March, the defendant renewed a previous application made by it on 7 February 2019 for the court to refer medical questions to a Medical Panel for an opinion pursuant to s 274(1)(b) of the Act. Based on the information given to the court on that date, the court ruled that the resolution of factual issues was more appropriately determined by the court and the defendant’s application was refused. On 13 March 2019, the plaintiff filed a Notice to Admit which the defendant said was not contentious save and except for two of the alleged chemicals Mr Briggs was alleged to have been exposed to during the period of his employment with the defendant. Accordingly, the defendant made a further application to the court for it to refer medical questions to a Medical Panel on the grounds that the parties had agreed on all but three factual issues being; the chemical exposure to the two named substances; PAHs and Benzo(a)pyrene; the precise period of employment (which differed by one week); and, whether the cabin of the excavator used by Mr Briggs was pressurised, noting that the defendant admitted dust entered the cabin whilst he was operating the excavator.

The defendant contended that aside from these factual issues, the essential issue in the proceeding was one of causation with there being a significant divergence in medical opinion. Mr Briggs opposed the defendant’s application to the court to refer medical questions to a Medical Panel on the basis that;

- factual issues remained unresolved and were more appropriately determined by the court; and

- if medical questions were referred to a Medical Panel there would be an inordinate delay of approximately 4 to 6 months before a Medical Panel would provide an opinion which would be unacceptable having regards to Mr Briggs deteriorating health.

After considering the submissions, the court concluded that the resolution of all issues in dispute would be more appropriately resolved by the court in addition to the the courts view that a ‘permissible’ medical question cannot address the issue as to whether the ‘nature’ of Mr Briggs employment caused his alleged injuries.[1]
[1] See Stewart v GUD & MMI Judge Rendit 4 May 1999.

Mr Briggs gave evidence concerning his past employment activities, the nature of the work he performed for the defendant and his pre and post-employment medical condition. The defendant made admissions in relation to the Notice to Admit as follows:

i. The plaintiff was employed by RTL Mining & Earthworks Pty Ltd from 3 March 2014 until 27 May 2014 to work at the Hazelwood Power Station in relation to the Mine fire.

ii. In the course of the plaintiffs work with RTL Mining & Earthworks Pty Ltd during the Hazelwood Mine fire the plaintiff was exposed to smoke, fumes, dust and air toxins.

iii. The plaintiff operated an excavator to assist in the excavation of the burning coal during the fire during the plaintiffs work with RTL Mining & Earthworks Pty Ltd during the Hazelwood Mine fire.

iv. The plaintiff did other duties outside of the excavator with RTL Mining & Earthworks Pty Ltd during the Hazelwood Mine fire including but not limited to labouring work, rolling up hoses, setting up sprinklers, setting up pipes.

v. During the plaintiffs work with RTL Mining & Earthworks Pty Ltd during the Hazelwood Mine fire, the plaintiff was working outside the excavator approximately 25% of the time.

vi. The plaintiff was exposed to the following substances that were contained within the smoke/dust/fumes emanating from the mine fire: carbon monoxide, sulphur dioxide (SO2), Acrolein, nitrogen dioxide (NO2), particulate matter (PM2.5 and PM10), benzene, toluene, xylenes and formaldehyde.

vii. The plaintiff was not provided respiratory protection while working at the Hazelwood site.

viii. At the end of a shift during the plaintiffs work with RTL Mining & Earthworks Pty Ltd during the Hazelwood Mine fire, dust would be visible inside the cabin of the plaintiff’s excavator.

ix. The plaintiff’s excavator cabin, during his work with RTL Mining & Earthworks Pty Ltd during the Hazelwood Mine fire, was air-conditioned, but was not pressurise sealed and as a result dust, particles, gases, smoke and fumes entered the cabin of his excavator.

x. At the end of a shift during the plaintiffs work with RTL Mining & Earthworks Pty Ltd during the Hazelwood Mine fire, the plaintiff would have visible dust on his face and clothes.

xi. During the Hazelwood Mine fire while working with RTL Mining & Earthworks Pty Ltd the dust, smoke and fumes sometimes caused visibility to be diminished, sometimes down to zero.

Mr Briggs gave evidence that for many years he has been employed in the earthworks industry operating equipment in Australia and overseas which has included; the Thompson Dam Project; Yallourn Power Station; Western Ring Road; the Desalination Plant and the new Hong Kong Airport. He told the court that he has never suffered from a serious illness or smoked. He said that immediately prior to commencing employment with the defendant he was working for three years assisting in the construction of a new coal mine in Queensland for which he was required to undergo a regular and complete medical examination including lung function testing which did not indicate any lung problems or deficiencies.

Mr Briggs told the court that he returned to Victoria in November 2013 and was then requested by senior management of the defendant to work for them at the fire at the Hazelwood Mine as from 3 March 2014. He told the court that he was requested to undergo a pre-employment medical examination which included a drug and alcohol and lung function test, the results of which he was told by the nurse were “excellent”. He gave evidence that his role involved excavating ‘hot spots’ in the coal as the fire had dropped below ground level and was burning the coal underneath. He said that the depth of the burning coal varied between 4 to 5 metres and 12 to 15 metres with the length of the ‘hot spots’ varying between 20 metres and 100 metres. He said it could take as long as 2 to 3 nights for him to excavate the larger areas. Mr Briggs told the court that initially he worked 7 days x 12 hour shifts from 6:30 PM to 6:30 AM as it was easier to identify the ‘hot spots’ at night.

Mr Briggs gave evidence that the work groups would consist of an excavator operator and five labourers and they would be directed by a supervisor as to which areas within the mine they would be required to target. He said there were 5 to 6 different types of excavators in use ranging from 25 to 35 tonnes. He also said the cabins were not pressurised but did contain air-conditioning units. He told the court that the cabins would be covered in fine grey dust, including on the control panel and floor and his clothing. He said that he wore high visible orange work clothes which would be “black” by the end of each shift. Mr Briggs said that he was not provided with respiratory masks or other breathing equipment. He told the court that he would regularly clean the cabin during breaks and at the end of his shift for use by the next operator. He said that during a normal shift he was required at times to help the labourers move floodlighting or water hoses which would result in him working up to 4 hours of a 12-hour shift outside the cabin. He also said that on other occasions he would operate the excavator for the full 12-hour shift.

Mr Briggs gave evidence that by its very nature the digging up of burning coal created more dust and smoke in the areas in which he was working. He said the dust would rise several hundred metres with some of it being blown away, but it would cover all the ground and surrounding areas. He told the court that regular monitoring and recording of carbon monoxide levels were conducted. He said that all workers were tested at the start and end of each shift by the CFA/MFB and that during the shift if the area readings were too high they would be directed to move to a higher level in the mine. He estimated this direction would occur 2 to 3 times a week. He also told the court that individual workers were also provided with personal monitors to measure the carbon monoxide levels during night shift and that every 30 minutes or so, each workgroup would be in radio contact to monitor their readings.

Mr Briggs gave evidence that after the first six weeks he was transferred to dayshift working 9 to 10 hours each day of the week. A two-minute video taken by Mr Briggs on his mobile phone for the benefit of his partner of the working conditions in April 2014 was shown to the court. He told the court that during his employment period he would consistently have a blocked nose (from the dust) and a parched mouth and would have to drink a lot of water to stay hydrated. He said that he did not experience any shortness of breath or other symptoms during this period.

Mr Briggs told the court that when he ceased work at the mine at the end of May 2014, he continued working for the defendant at Loy Yang for a period and then on the highway duplication at Rosedale.

Mr Briggs told the court that he began to suffer from “flu like symptoms” in September 2014 (the medical records indicate these symptoms commenced in November 2014) which included; feeling tired, experiencing aching shoulders, arms and legs and shortness of breath on exertion. He told the court he attended a doctor at the Moe Medical Group (5 December 2014) who diagnosed that he had the flu and prescribed antibiotics and referred him for a chest x-ray (performed 7 December 2014). Mr Briggs said that by December his breathing was “poor”, and he was told he had a chest infection and was prescribed a Ventolin inhaler and prednisolone.

Mr Briggs gave evidence that because his symptoms were deteriorating he ceased work on 15 January 2015 and on the recommendation of his partner, he attended Dr Foo in Sydney who arranged for him to undergo blood tests, a chest x-ray and CT scan. He said he was then referred to Dr Katsolotos at St Georges Hospital where a lung biopsy was performed, and he was then referred to Dr Moses, Dr Boers, Rheumatologist and then Dr Levin, Respiratory Physician at the Alfred Hospital. Mr Briggs told the court that consideration was given to him undergoing a lung transplant but due to a deterioration to his joints and bones, that option no longer exists. He told the court that he now requires the use of oxygen cylinders and a concentrator when at home to perform normal daily activities. He said that he continues to experience pain in his hips, elbows, shoulders, lower legs and hands when it is cold, and experiences sleep disturbance.

The time sheet records tendered by the defendant indicate that Mr Briggs worked night shift from 3 March until 5 April and then day shift from 7 April to 27 May 2014. Thereafter, he commenced work at Loy Yang.

Mr Briggs tendered reports from Mr Kottek, Occupational and Environmental Health Consultant dated 21 December 2017 and 13 March 2019. Mr Kottek obtained a work history and details of Mr Briggs employment duties with the defendant and referred to the probable chemical, substance, toxins and airborne hazards that he was likely to have been exposed to whilst performing his duties at the Mine fire by reference to the information given to him by Mr Briggs and that contained in the Mine Inquiry Report. The details recorded by him are not in dispute between the parties. Mr Kottek concluded that although the extent of Mr Briggs exposure to respiratory irritants is unclear, that based on his description of his working conditions and in the absence of measurements it is plausible that his exposure to ash, coal dust, smoke from the burning coal, carbon monoxide, organic compounds, chemical derived firefighting foam, ozone, nitrogen dioxide, sulphur dioxide, benzene, toluene, formaldehyde and fine respirable particles from the smoke. He stated that acrolein, nitrogen dioxide, ozone and sulphur dioxide exceeded recognised exposure standards, at least from time to time. He reported that all these compounds are respiratory irritants, and the exposure standard for acrolein is based on a variety of respiratory effects observed in animal studies, including focal emphysema. Mr Kottek noted that appropriate respiratory protection would have greatly reduced his exposure to particulate matter, gases and vapours when working at the Mine fire.

Medical Evidence

In order to understand the medical terminology used it is appropriate at the outset to provide a definition of the medical conditions referred to as provided by Professor Needham in a report from her dated 12 March 2019 which was tendered by the defendant.

Interstitial Lung Disease (ILD): comprise a group of die diffuse parenchymal infiltrative lung disorders classified according to aetiology, clinical, radiological and histopathological features. Some are of unknown cause (idiopathic), some have identifiable causes such as environmental exposures, (e.g. asbestos), genetic, and some are associated with auto immune diseases including connective tissue diseases (CTD) characterised by immune-mediated lung injury.

CTD-ILD: is interstitial lung disease (ILD) associated with a systemic autoimmune connective tissue disease. Common associated connective tissue disorders include scleroderma, rheumatoid arthritis and the idiopathic inflammatory myopathies.

Myositis: is a broad term describing muscle inflammation due to any cause. Different forms of immune-mediated myositis are referred to as inflammatory idiopathic myopathies, (IMM), which are a group of autoimmune diseases predominately affecting skeletal muscles, usually with raised muscle enzymes (creatine kinase – CK), with or without skin and extra muscular organ involvement. The current classification defines five categories of autoimmune myositis; polymyositis, dermatomyositis (inflammation of skin and muscle), necrotising autoimmune myopathy, overlap myositis (myositis overlapping with features of systemic connective tissue disease e.g. systemic sclerosis, Sjogren’s disease etc.) and inclusion body myositis.

Dermatomyositis: a subset of immune-mediated myositis with inflammation in both muscle, skin and blood vessels. There are different types including juvenile, malignancy-associated and amyopathic dermatomyositis.

Amyopathic Dermatomyositis (CADM): is a subset of dermatomyositis which is defined by the presence of cutaneous features of dermatomyositis without clinical muscle weakness or laboratory evidence of muscle damage. It is associated with the anti-melanoma differentiation-associated gene 5 (anti MDA5 antibody) which is characterised by the acute and rapidly development of ILD.

Overlap Myositis: muscle inflammation occurring in the context of extra muscular symptoms associated with CTD, associated with myositis-associated antibodies (especially anti-PM/Scl, SSA and anti-U1-RNP antibodies).

Autoantibodies: are antibodies directed against self-antigens. The importance of auto antibodies is that they often characterise patients with distinct clinical features and often have prognostic relevance in different connective tissue diseases.

Anti-PM/Scl antibodies: are antibodies against a nucleolar exosome. They are found in around 33/5 of myositis/systemic sclerosis overlap cases and in about 12% of IIM’s.

Systemic sclerosis: is a multi—system disease characterised by widespread fibrosis in the skin, vasculature and internal organs.

Anti-synthetase antibodies: are auto antibodies directed against the aminoacyl-tRNA synthetase enzymes involved in protein synthesis and include anti-Jo-1, anti-EJ/OJ, anti-PL7, PL 12, KS, Zo. They are associated with the clinical syndrome of an inflammatory myopathy, interstitial lung disease (ILD), “mechanics hands”, inflammatory non-erosive polyarthritis and fever.

The medical records from the Moe Medical Centre were tendered and reveal that Mr Briggs attended on 5 December 2014 complaining of a dry cough, sore throat and shortness of breath on exertion for the previous three weeks and complaints of left groin pain radiating to his left thigh. Dr Quamar recorded that on examination, Mr Briggs had no respiratory distress although he had a red throat and enlarged tonsils. Dr Quamar arranged for a chest x-ray to be performed and prescribed a Ventolin inhaler. On 12 December 2014, he recorded that Mr Briggs continued to experience shortness of breath on exertion and prescribed prednisolone medication. On 22 December 2014, Dr Belgaonkar diagnosed that Mr Briggs had a chest infection and prescribed amoxycillin. By 29 December 2014, following a spirometry test, it was recommended that Mr Briggs be referred to a respiratory physician. On 22 January 2015, Dr Xu reported that because there was a delay of some 3-4 months to see a respiratory physician in Melbourne, Mr Briggs attended Dr Foo in Sydney who organised a high definition chest x-ray showing pulmonary fibrosis.

The Discharge Referral Notes from St George Hospital Sydney were tendered. The Notes indicate that Mr Briggs was admitted on 10 February 2015 and discharged on 3 March 2015 after initially presenting with pulmonary fibrosis. The Notes record that Mr Briggs presented with a six-month history of progressive exertional dyspnoea with symptoms consisting of malaise and generalised myalgias without cough or chest pain. Mr Briggs also reported the onset of intermittent numbness and discomfort in his fingers bilaterally and an observation of associated colour change consistent with Raynaud’s phenomenon. The records indicate that a CT scan of his chest was performed which revealed an area of pulmonary fibrosis in both lung bases with the pattern of fibrosis not appearing to clearly identify with any interstitial lung disease from a radiological point of view. An observation was recorded of some dry skin over the dorsal aspect of the metacarpopharyngeal joints. The Notes also record that Mr Briggs had a series of investigations to screen for secondary causes of pulmonary fibrosis such as underlying connective tissue disease and he had a highly positive ANA titre and positive ENA antibodies (Ro-52 and PM-Scl antibodies positive) in addition to a mildly elevated rheumatoid factor and mildly raised inflammatory markers. The records indicate that given these results and Mr Briggs presentation, there was a high suspicion of underlying connective tissue disease. It is noted that Mr Briggs had a thoracoscopic biopsy performed and the histopathology confirmed non-specific interstitial pneumonia as the cause of his fibrosis. Mr Briggs was then referred to the rheumatology unit and an initial diagnosis of dermatomyositis was made having regard to the antibody results and the skin features observed. The records indicate that from a respiratory point of view, Mr Briggs improved as at the time of discharge he was able to ambulate around the ward on room air with no significant level of desaturation or dyspnoea. It is noted that the doctors concluded his condition was not work-related as pulmonary fibrosis secondary to dermatomyositis is not related to exposure to substances but is of an autoimmune nature.

Dr Levin, Respiratory and Sleep Medicine Physician gave evidence and medical reports prepared by him and dated 7 September 2015 and 5 December 2018 were tendered. Dr Levin gave evidence that he has practised as a Respiratory and Sleep Physician for a period of 4 years and is employed at the Alfred Hospital Allergy, Immunology and Respiratory Department. Dr Levin told the court that he is Mr Briggs treating respiratory physician and reported that Mr Briggs has been diagnosed with interstitial lung disease and associated amyopathic dermatomyositis. He opined that the condition, based on clinical, radiology and serological findings is an autoimmune condition. Dr Levin noted that the histopathology from the lung biopsy demonstrated fibrotic and cellular changes consistent with non-specific interstitial pneumonia (NSIP) which is believed to be the most common histopathological finding in patients with dermatomyositis associated interstitial lung disease. He also noted that the biopsy specimens demonstrated conspicuous eosinophils and significant organising ammonia, which is “unusual” in this condition.

Dr Levin opined that airway and interstitial eosinophils in a lung specimen can suggest an allergic type response to inhaled irritants. He stated that the aetiology of most autoimmune conditions is unclear, however there is presumed to be a genetic predisposition.

In relation to causation, Dr Levin opined that there is a ‘temporal relationship ’based on Mr Briggs exposure history and the development of his fibrotic lung condition after considering the normal spirometry prior to him commencing work with the defendant.

In his report dated 5 December 2018, which was based on his last consultation with Mr Briggs on 24 July 2018, he noted that his symptoms and physiological condition persist and have progressed. He maintained his previous opinion that there is a relationship between employment and irritant exposure and stated that it is reasonable to assume that Mr Briggs work contributed to his illness.

When giving evidence, Dr Levin told the court that he first saw Mr Briggs on 22 April 2015, some 10 months after he had ceased work at the Hazelwood Mine. When questioned as to why he stated that it was “unusual” that the lung biopsy specimens also demonstrated conspicuous eosinophils and significant organising pneumonia, he said that he had discussed the results in an interstitial lung disease multi-disciplinary meeting which included at least two respiratory physicians with an interest in interstitial lung disease, a thoracic radiologist and a histopathologist who reviewed the slides. He told the court that the ‘team’ concluded that what was not typical was the degree of organising pneumonia and the presence of significant eosinophils. He told the court that Mr Briggs has been diagnosed with two conditions because the findings are not completely consistent with there being only one diagnosis. He said there are two possibilities, firstly, the auto immune condition affecting the lungs-amyopathic dermatomyositis, and, secondly, the other which is related to an inhalation injury. Dr Levin said that when there are findings that are not completely consistent with a diagnosis they look for an alternative diagnosis or consider multiple diagnoses. He also said that non-specific interstitial pneumonia is more consistent with the auto immune condition affecting the lungs, the dermatomyositis, and potentially the eosinophils that were present are related to a separate pathology which is related to an inhalation injury and some type of immune or allergic response to that. He stated that although there was not a lot of evidence to go on concerning the amount of exposure, the clinical picture of Mr Briggs developing his lung disease after exposure was enough in his mind for him to opine that there was a temporal relationship and it may have been a cause.

In cross examination, he agreed that an autoimmune condition encompasses several conditions, the precise cause of which is unknown and that it is presumed to be a genetic condition of which infection may be a trigger but, in most cases, there is not a clear cause. He told the court that there are two schools of thought in the medical profession in respect to an auto immune condition, those being; firstly, it is not influenced by external factors at all; and, secondly, given several factors, it may be triggered by exposures. Dr Levin told the court that he was not aware of any literature or studies in relation to Mr Briggs condition that attributes it to work or occupationally induced conditions. He agreed that the current diagnosis is one of amyopathic dermatomyositis (his auto immune condition) and connective tissue disease-interstitial lung disease. Dr Levin agreed that in some cases an infection could trigger an autoimmune condition and a subsequent fibrotic process in the lungs. He also agreed that there could have been several different illnesses that could have been a trigger for his condition, with his employment being a “potential trigger”.

Professor Hall, Rheumatologist, gave evidence and a medical report prepared by him and dated 23 August 2018 was tendered. Prof Hall told the court that he has practised as a Rheumatologist for 35 years. He reported that he only examined Mr Briggs on one occasion, being 10 August 2016 on referral from Dr Boers and after taking a history of his work duties at the Hazelwood Mine noted that Mr Briggs was told that a pre-employment lung function test was “excellent”. Prof Hall also noted that a lung biopsy confirmed pulmonary fibrosis and testing showed Mr Briggs had positive antisynthetase anti-bodies with PM/Scl. Prof Hall reported that Mr Briggs had no symptoms to suggest underlying muscle disease and specifically he had no weakness and no rash to suggest dermatomyositis. He postulated that Mr Briggs might have amyopathic myositis. Ultimately, Prof Hall diagnosed that Mr Briggs has myositis associated with an underlying auto immune condition.

Prof Hall reported that it is more likely than not that his work at the Hazelwood Mine fire was a factor significantly contributing to his condition. He noted that there are several studies which have identified dust exposure as a risk factor precipitating interstitial lung disease in the setting of auto immune diseases. In his opinion, Mr Briggs work at the Hazelwood Mine fire put him at increased risk of developing the condition.

When giving evidence, he said Mr Briggs condition falls within three specialities; if it is dominantly a lung problem-respiratory; if it is dominantly a muscle problem or an overall connective tissue disease-rheumatology; and sometimes immunology. Prof Hall told the court that the auto immune disease is idiopathic (a term he defined as a “condition where we have no idea what causes them”) but research indicates that there are some potential triggers which vary, including; stress, exposures, infection and drugs, depending on the nature of the auto immune condition. He said the condition is rare with perhaps 8 to 10 cases per million of the population each year. Prof Hall referred to a study in Spain which indicated a significant association between environmental exposure (“dusts and other things”) where they saw a significant association with people who had the kind of antibody profile that is seen with certain forms of muscle disease called antisynthetase anti-bodies which is the same sort of anti-body that Mr Briggs has and an auto immune condition which he believed was applicable in this case because of Mr Briggs antibodies.

Prof Hall told the court that the medical profession has identified an antibody called PM/Scl which is an antibody seen in people who have an overlap between poly myositis and scleroderma, often associated with interstitial lung disease. He said that the Spanish study saw a strong association between prior environmental exposure to dusts and particulate matter and the development of the condition. Prof Hall agreed with the proposition that Mr Briggs environmental exposure could have triggered his condition. In relation to causation, Prof Hall noted that Mr Briggs had a normal lung function prior to commencing work with the defendant and believed he was exposed to particulate matter including dusts. He told the court that several people who survived the impact of the Twin Towers collapse in New York developed auto immune disease after being exposed to dust and other particulate matters.[2]
[2] Prof Hall referred to a Study by Tirmano Durada.

In cross examination, Prof Hall agreed that his opinion is based to a significant extent on the history provided by Mr Briggs. He also agreed that he understood that Mr Briggs was employed by the defendant at the Mine fire for a period of four months and that he first developed symptoms in September 2014. Prof Hall agreed that connective tissue disease-interstitial lung disease with secondary amyopathic dermatomyositis is generally accepted to be idiopathic-of unknown cause. Prof Hall said his support of Mr Briggs on the issue of causation is based on the work environment placing Mr Briggs at increased risk based on his clinical picture, his auto antibody profile and his occupational exposure. In reference to the study conducted in Spain, Prof Hall said that it found there was a strong connection with exposure to dusts, gases and fumes with anti-synthetase syndromes. He told the court that these syndromes are the clinical condition associated with the type of antibody found in Mr Briggs-(PM/Scl). He told the court that it was a controlled study on patients seen at a clinic (179 in total) based on recollection and survey involving 60 patients with 32 of them being reviewed and compared to several patients who also had muscle inflammation but who did not manifest the antibodies. He said the patients were seen over a 23-year period with the study conducted at a point in time. Prof Hall said that 60 of the 179 patients had ASA antibodies and only one had amyopathic dermatomyositis. In his cross examination, he agreed that none of the patients in the study had the same antibody as Mr Briggs and noted that the median time of dust exposure for those patients was 20.2 years. Prof Hall also agreed that Mr Briggs condition could have occurred spontaneously as he said in most cases it does.

Associate Professor Sasse’, Respiratory Specialist and Sleep Physician, gave evidence and a report prepared by him and dated 6 April 2017 was tendered. He told the court that he has practised as a Respiratory Physician for a period of 27 years. He reported that Mr Briggs presented on one occasion in 2017 in respect to non-specific interstitial pneumonitis. He noted that a pre-employment lung function test showed excellent lung function with FVC 124% of predicted at 5.65 litres. He also noted that a lung biopsy on his left lower lobe in 2015 was reported by Dr Tran, pathologist, as favouring non-specific interstitial pneumonitis.

Associate Prof Sasse’ reported that Mr Briggs was commenced on immunosuppressant therapy with prednisolone and varying doses since, together with another immunosuppressant, mycophenolate. He reported that there was no prior relevant exposures, smoking habit or allergies. He opined that Mr Briggs suffers from non-specific interstitial pneumonitis secondary to smoke exposure at the Mine fire.

When giving evidence, he told the court that non-specific interstitial pneumonitis is not completely understood but occurs where the normal tissue of the lung is replaced by fibrous material which is referred to as “organising”. Associate Professor Sasse’ gave evidence that the effect of this ‘replacement’ was that it impedes the function of the lungs causing breathlessness, limited exertional capacity and can result in premature death if it continues. He told the court that the appropriate treatment is in the form of anti-inflammatories and immunosuppression. He said that the key factor in his support for a causal connection between employment and his condition was timing in that Mr Briggs had good lung function prior to his employment with the defendant and six months later his condition developed with the only change being his work environment. Associate Prof Sasse’ agreed that Mr Briggs autoimmune condition is very rare and affects the skin but on rare occasions it may affect the lungs. He told the court that its aetiology is mysterious and unknown. He also told the court that Mr Briggs having two disorders at the same time makes it difficult in relation to causation and he did not discount the possibility that his primary lung condition triggered his auto immune disorder.

In cross examination, he agreed that non-specific interstitial pneumonitis has multiple causes including: insults, as in this case, Mine smoke, drug reaction, an autoimmune condition such as amyotrophic dermatomyositis and unknown causes. He told the court that in his opinion, “timing is the key” because if a patient has a substantial toxic exposure to anything and then within a period of some months develops an acute lung disease it is a ‘pretty reliable feature” but he did not discount the possibility that it was spontaneous, due to an infection or virus or “something we don’t know about yet in medical science”.

Professor Pain, Consultant Thoracic Physician gave evidence and medicolegal reports that he prepared for Allianz and the defendant’s lawyers dated 16 July 2015 and 20 December 2018 were tendered. He told the court that he has practised as a Thoracic Physician for a period of 53 years. In his initial report, Prof Pain noted that he first saw Mr Briggs on 16 July 2015 and after obtaining a work history and details of his current symptoms reported that the spirometry performed at his request demonstrated considerable lung restriction with no change following inhaled bronchodilator. He noted that other investigations showed the presence of interstitial pneumonitis on lung biopsy and that blood tests showed a chronic inflammatory condition.

Prof Pain diagnosed that Mr Briggs has diffuse pulmonary fibrosis probably complicated by some secondary pulmonary hypertension. He noted that as is usual in cases of pulmonary fibrosis, a definite causal factor is often not obvious. He opined that Mr Briggs has an autoimmune condition in which pulmonary fibrosis is one manifestation. He said that supporting his opinion is the muscular pain suggesting an arteritis or dermatomyositis. He considered that idiopathic pulmonary fibrosis is possible and consistent with the biopsy findings, but the absence of finger clubbing is slightly against this diagnosis.

Prof Pain noted that Mr Briggs was exposed to combustion products from burning coal over several months which meant he would have inhaled carbon monoxide, oxides of nitrogen and sulphur dioxide. He stated that whilst each of these are toxic and can produce respiratory conditions, he does not consider that they have been accepted as inducing pulmonary fibrosis. In his initial report, Prof Pain did not find any convincing evidence that employment was causative of Mr Briggs pulmonary fibrosis.

Prof Pain re-examined Mr Briggs on behalf of the defendant’s lawyers on 20 December 2018. A spirometry was again performed at his request the results of which he stated showed the presence of mild lung restriction with some small airway obstruction. Prof Pain noted that a thoracic CT scan performed on 29 June 2018 showed predominantly lower zone fibrosis with gross honey combing and traction bronchiectasis. He diagnosed that Mr Briggs has connective tissue disorder with interstitial lung disease which is an autoimmune disorder of unknown aetiology but is thought to have a genetic basis. He said that the positive serology makes it more likely that amyopathic dermatomyositis is the appropriate term. Prof Pain reported that connective tissue disorder-interstitial lung disease is not recognised as an occupationally related condition and that he is not familiar with exposure to bronchial irritants as being a recognised trigger for its development. However, based on Mr Briggs normal spirometry lung function results in 2010 and prior to commencing employment with the defendant in March 2014 and that by January 2015 he had developed symptoms of what became progressive lung inflammation and fibrosis, in addition to Dr Hoy finding some evidence in the literature linking the onset of autoimmune diseases to chronic bronchial irritation, he was persuaded that Mr Briggs rare condition was initiated by his employment activities with the defendant.

Prof Pain opined that employment with the defendant was a significant contributing factor in initiating the auto immune condition producing pulmonary fibrosis and possibly polyarthritis. He noted that this is a complex case involving a rare condition. He stated that it is possible Mr Briggs would have developed a connective tissue disorder with interstitial lung disease at some time in the future irrespective of his employment activities but accepts that his exposure between March and June 2014 probably caused the onset of the condition.

In cross examination, Prof Pain agreed that pulmonary fibrosis is but one of numerous manifestations of an autoimmune condition. He said that other symptoms can include; joint pain, headaches and fever. He also agreed that initially he did not consider Mr Briggs work duties were causative because of temporal issues and was not satisfied absent other specialists’ opinions or studies supporting the connection. After considering the opinion of Dr Hoy and the 2014 study referred to by him he said that he reconsidered that the work environment was a possible hypothesis. In relation to that study, Prof Pain told the court that he had read the study paper and understood that it was a controlled study involving 32 patients with antisynthetase syndrome who were compared with 32 patients with muscular disease without antisynthetase antibodies. Prof Pain told the court that synthetase are structures which lead to the building of tissue by bonding molecules. He said that antisynthetase antibodies breakdown that bonding and lead to the destruction of various tissues setting up an inflammatory response. He said that it is associated with what is called a multisystem disorder which can involve various organs, including the lungs, which sets off an inflammatory and fibrotic process. He also told the court that there are a number of different antisynthetase antibodies but he is not an expert in that field and could not give the court any expert evidence in relation to this area noting that Mr Briggs has a positive reading for the PM/Scl antibody although he noted that the study indicated that the incidence of having irritant exposure was much higher in the group of patients with the antisynthetase antibodies than those without but which did not include the specific antisynthetase antibody that Mr Briggs has. Whilst not knowing that the patients in the study had a 20-year median exposure and that it cannot be relied on to be determinative on the issue of causation, Prof Pain told the court that he thought the study is highly suggestive that there is a plausible hypothesis as to aetiology in this case. He agreed that occupational exposure is a rare cause and one that he has not seen, with other possible causes being; a genetic predisposition, infection or it being spontaneous. Prof Pain agreed that the precise cause is unknown and agreed with the proposition put to him that temporal connection alone cannot be the main determinant. Prof Pain told the court that this is the first case in which he has suggested that there is a plausible hypothesis for occupational exposure.

Dr Hoy, Respiratory and Sleep Disorders Physician gave evidence and medico-legal reports prepared by him and dated 24 May 2016 and 8 March 2018 were tendered. He told the court that he has practised as a Respiratory Physician for 11 years. After obtaining Mr Briggs employment and medical history he noted that the constituents of the exposure generated by the Mine fire is not certain, but was likely to have included; particulate matter, carbon monoxide, sulphur dioxide, hydrocarbons and other chemicals. Dr Hoy also noted that a pre-employment spirometry indicated normal lung function demonstrating that Mr Briggs clearly developed interstitial lung disease after that time.

Dr Hoy opined that due to the temporal association of the development of his symptoms after a significant inhalation injury it is more likely than not that the exposure at work was a contributing factor towards the development of his interstitial lung disease. He also opined that in the setting of his positive auto immune serology (ANA positive, anti PM/Scl) that it is possible the exposure triggered the onset of his connective tissue disease which included interstitial lung disease. He reported, whilst noting that amyopathic dermatomyositis is a rare condition, that there are some published reports of chemical exposures triggering connective tissue diseases with lung involvement. He stated that environmental factors have been noted to contribute to the onset of autoimmune diseases, especially smoking and occupational exposure to silica in rheumatoid arthritis and systemic lupus erythematosus. He also stated that other diseases such as scleroderma may be triggered by the inhalation of chemical solvents, herbicides and silica. Dr Hoy reported that due to the paucity of medical literature in this area and Mr Briggs specific exposure, it is very difficult to confidently attribute causation.

In his subsequent report, Dr Hoy noted a deterioration in Mr Briggs symptoms and restrictions on his activities of daily living. He referred to a CT chest scan report dated 22 January 2018, which indicated a predominantly lower lobe interstitial lung disease with traction bronchiectasis consistent with pulmonary fibrosis. Dr Hoy opined that Mr Briggs lung condition is most consistent with interstitial lung disease associated with amyopathic dermatomyositis. He maintained his opinion that it is more likely than not that Mr Briggs work was a contributing factor towards the development of his condition. He reported that Mr Briggs described a high level of respiratory exposure generated from the burning coal during his work over a 12-week period. Dr Hoy referred to the Hazelwood Mine Fire Inquiry Report which noted key pollutants emitted during the fire included; ash, carbon monoxide, particulate matter, nitrogen dioxide, sulphur dioxide, polycyclic aromatic hydrocarbons, volatile organic compounds, dioxins, furans and heavy metals. He stated, that as noted in the Mine Fire Inquiry Report, exposure to these agents have been associated with adverse respiratory effects. He also referred to the report of the Occupational Hygienist, Mr Kottek, who noted exposure to a variety of chemical vapours and high levels of respirable dust.

Dr Hoy noted that Mr Briggs pre-employment spirometry indicated normal lung function. He stated that his interstitial lung disease has therefore clearly developed after that time and that due to the temporal association of the development of the symptoms after significant exposure to respiratory irritants and other chemicals it is more likely than not that his exposure at work was a contributing factor towards the development of his interstitial lung disease. He noted, as did Dr Levin, that it is also possible that there are two separate underlying lung conditions one of which is autoimmune and the other related to an inhalation injury. He reported that amyopathic dermatomyositis is a rare condition and therefore studies regarding the cause of this condition are very limited. He stated that there are some published reports of occupational and environmental exposures triggering connective tissue and auto immune diseases with lung involvement. Dr Hoy referred to a study by Labirua-Iturburu and Colleagues[3] who identified a high proportion of patients with a connective tissue disease associated with interstitial lung disease to have had exposure to dusts, gases or fumes. He noted that environmental factors have been noted to contribute to the onset of autoimmune diseases, especially smoking and occupational exposure to silica in rheumatoid arthritis and systemic lupus erythematosus and that other connective tissue diseases such as scleroderma have also been reported to be associated with exposure to occupational factors including crystalline silica, white spirit, aromatic solvents, chlorinated solvents, trichlorethylene, ketones and welding fumes.[4]
[3] Labirua-Iturburu A, Selva-O’Callaghan A, Zock JP, Orriols R, Martinez-Gomez X, Vilardell-Tarres M : Occupational exposure in patients with the antisynthetase syndrome. Clinical rheumatology. 2014;33(2):221-5. The objective of the study was to analyse the exposure to inhaled environmental or occupational agents in a cohort of patients with antisynthetase syndrome (ASS) and to examine clinical and immunological associations.
[4] Marie l, Gehanno JF, Bubenheim M, Duval-Modeste AB, Joly P, Dominique S, et al. Prospective Study to evaluate the association between systemic sclerosis and occupational exposure and review of the literature. Autoimmunity reviews. 2014;13(2):151-6.

Dr Hoy concluded that Mr Briggs work did increase the risk of him developing his current condition. He considered him to be incapacitated for work because of the level of symptoms and although noting that radiologically his condition has not changed significantly between December 2016 and January 2018, symptomatically he has declined significantly and due to his long-term treatment with immunosuppressive medications, specifically prednisolone and mycophenolate, he is at risk of developing complications including the recently diagnosed osteoporosis, infections and complications related to his condition such as pulmonary hypertension. He expects Mr Briggs condition and symptoms will continue to deteriorate.

During his evidence, Dr Hoy told the court that Mr Briggs interstitial lung disease is associated with his connective tissue disease, namely amyopathic dermatomyositis. In relation to the issue of causation and his opinion that it is more likely than not that Mr Briggs employment is a contributing factor he said that it is known that amyopathic dermatomyositis associated with interstitial lung disease is a rare condition and that auto immune or connective tissue disease is associated with interstitial lung disease and has been reported to be associated with occupational exposure. He said it is appropriate to extrapolate on our knowledge from connective tissue diseases and their influence on interstitial lung disease. Dr Hoy told the court that based on Mr Briggs occupational history where he worked for a period of 12 weeks in an environment where there was a high level of exposure to respiratory irritants and chemicals, the temporal connection between that exposure and the onset of his symptoms “would certainly be in keeping” with the exposure contributing, most likely, towards the development of the disease process. He said he also considered the pre-employment normal lung function test which indicated that his lung function was normal at that time and that he did not have any symptoms to suggest significant lung disease prior to his employment with the defendant.

Whilst reluctant to give an opinion concerning antisynthetase syndrome as it is outside his expertise and “best left to a rheumatologist”, he told the court that broadly speaking it is an auto immune condition with connective tissue disease with there being a range of conditions that fall under antisynthetase syndromes. He said that there are a broad range of antisynthetase antibodies that have been implicated with connective tissue disorders that do have interstitial lung disease as well.

Dr Hoy was referred to a report prepared on behalf of the defendant by Prof Needham, who suggested that the study referred to by him has limited, if any, application in this case because Mr Briggs antisynthetase antibody is anti-PM/Scl and is not referenced in the study. Dr Hoy agreed that Mr Briggs specific antibody profile was not referenced in the study, but from memory, it did include at least one person with amyopathic dermatomyositis. He told the court that it is such a rare disease that there are no specific studies which look at his subtype of connective tissue disease. Dr Hoy said it is therefore necessary to look more broadly at the literature and similar types of diseases to make a statement as to whether Mr Briggs occupational exposure was relevant or not. Dr Hoy gave evidence that it is not only the duration of the exposure which Mr Briggs was subjected to but the intensity of it. He noted that exposure to silica is associated with autoimmune disease and that although Mr Briggs was not exposed to silica it does indicate that occupational exposures can trigger autoimmune diseases with associated interstitial lung disease. Dr Hoy told the court that the wide range of chemical agents involved in coal burning have been reported to be potentially harmful to the respiratory system. He noted that particulate matter are fine particles and if respirable they can be potentially hazardous if able to get through the upper airway down to the lower respiratory system and small air sacs.

Dr Hoy gave evidence that the best method of monitoring exposure to particulate matter is by personal monitoring where the worker wears a monitor throughout the course of their working day which samples their breathing zone to provide the most accurate assessment of what the worker it is exposed to. He said that static monitoring that is done in the vicinity is not as accurate as personal monitoring.

During cross examination, Dr Hoy told the court that he is a respiratory physician with experience in occupational lung diseases and associated interstitial lung disease but not an expert in the field of connective tissue disease as that is in the field of rheumatology. He estimated that he would see approximately 5 to 10 patients a year who have connective tissue disease-interstitial lung disease. He also said that rheumatoid arthritis is the most common connective tissue disease that is associated with interstitial lung disease. He said that he has seen no other cases of amyopathic dermatomyositis as it is an extremely rare disease. He told the court that he believed Mr Briggs antibody PM/Scl means polymyositis scleroderma which is a rare condition. He agreed that it is very difficult to be confident on the issue of causation because Mr Briggs has a rare disease and his exposure was rare as well. He said that the temporal connection was a factor to consider but not the sole factor.

Dr Hoy agreed with a statement made by Prof Needham that “temporal association of environmental exposures with illness onset does not imply causality, but rather exposures with temporal relationships to disease onset constitute a first step only in determining which factors may trigger the onset of illness and warrant further investigation”. Dr Hoy also agreed that he would defer to the opinion of a rheumatologist in relation to the specific rheumatological diagnosis but not the interstitial lung disease that has manifested. He disagreed that Mr Briggs interstitial lung disease is a manifestation of his underlying condition and said that it is a disease which is associated with his auto immune disease or connective tissue disease. Dr Hoy agreed with the proposition that the triggering of Mr Briggs amyopathic dermatomyositis then gave rise to his symptoms of interstitial lung disease. He said the root of the exposure to trigger a connective tissue disease can be via the lung.

Dr Hoy agreed with the proposition that the Study referred to in his report is not specifically relevant to Mr Briggs condition and despite his literature research he could not find any study that specifically looked at his condition and the specific exposure he experienced. He also agreed that there was no patient in the Study who had the same antibody as Mr Briggs – PM/Scl, only one patient who had amyopathic dermatomyositis and the Study did not focus on short-term exposure. Dr Hoy told the court that his reference to the Study is an extrapolation from what minimal literature there is because there have been no specific studies done of this specific type of exposure, its intensity or duration. Despite these concessions, Dr Hoy told the court that he did not agree with Prof Needham’s conclusion that the Study has no applicability because it furthers the understanding that there is an interaction between environmental exposures and the development of these types of diseases.

Dr Hoy, whilst noting that occupational exposure may trigger the onset of the condition in the context of an autoimmune disease, stated there may be a genetic predisposition for it which would increase the probability of developing the disease based on an exposure, or it could be triggered spontaneously or by way of infection. Dr Hoy told the court that a lot of his research has been in the field of silica related disease and it has been clearly demonstrated in workers exposed to high levels of silica dust that there is a clear association with auto immune disease. He referred to a study of workers in Israel exposed to silica dust from artificial stone, such as Caesar Stone with 30% of those assessed for possible lung transplantation also had features of auto immune disease. He said this demonstrates that occupational exposures to agents like silica dust can cause autoimmune disease. Dr Hoy stated that there has been insufficient research to demonstrate whether an initial insult to the lung may trigger an auto immune condition or whether the autoimmune condition is triggered via a lung irritation.

Dr Boers, Consulting Rheumatologist and General Physician gave evidence and a report prepared by him and dated 4 February 2019 was tendered as were his medical records. The records contain a medical report from Dr Boers to Dr Foo (Sydney) dated 9 December 2015. In that report, Dr Boers stated that he had a lengthy discussion with Mr Briggs about the diagnostic uncertainties not satisfying the diagnostic criteria for scleroderma or dermatomyositis. He noted that Mr Briggs had some facial skin changes which were suggestive but there is no obvious myositis. He told Dr Foo that ongoing treatment was to be directed along the lines of pulmonary fibrosis which he thought was related to underlying auto immune/connective tissue disease, but it was guesswork as to whether it is along the lines of dermatomyositis without myositis or scleroderma without sclerodactyly. On the question of causation, Dr Boers stated that he was not aware of any data about occupational exposure in terms of toxic gas exposure causing the auto immune illnesses or pulmonary fibrosis and suggested consultation with an occupational physician and further consultation with his lung specialist would be prudent. In a letter to Dr Hoy dated 6 April 2016, Dr Boers sought the opinion of Dr Hoy as to whether Mr Briggs occupational history contributed to his interstitial lung disease. He noted that Mr Briggs was not fitting into any nice category of dermatomyositis interstitial lung disease as he was ANA positive with a nucleolar pattern. He reported that Mr Briggs had a vague rash across his face but has never had a CK rise and his myositis specific antibodies apart from showing a non-specific anti-PM/Scl. Dr Boers noted that he told Mr Briggs and his lawyers that there was really no evidence to suggest that his employment contributed to his condition but would appreciate Dr Hoy’s opinion. The records indicate that Dr Boers then referred Mr Briggs to Professor Hall at the suggestion of Dr Hoy and informed Prof Hall by way of letter dated 4 July 2016, that Dr Hoy felt there may be some contribution to his occupational exposure, but causation was difficult to delineate. He further stated that he believed although there is a strong temporal relationship he was not aware of any strong data to suggest any significant causation absent of malignancy.

In his report dated 4 February 2019, Dr Boers noted that Mr Briggs experiences shortness of breath during personal activities of daily living, that he is limited in walking to 200 metres and is using oxygen up to 3 hours per day. He noted that the CT scan dated 29 June 2018 showed stable appearances with pulmonary fibrosis predominantly in the basal distribution with associated bronchiectasis with additional upper lobe subpleural fibrosis, signifying extensive changes. Dr Boers also reported that Mr Briggs has diffuse joint pains and a general sense of aching, his creatinine kinase (muscle inflammation marker) is not raised and the MRI of his muscles dated 7 August 2018 has not shown evidence of underlying myositis. He noted that Mr Briggs has severe joint aches and that his life expectancy is shortened because of his underlying pulmonary fibrosis.

When giving evidence, Dr Boers told the court that he has been a practising rheumatologist for a period of 15 years. Dr Boers confirmed that in his opinion, Mr Briggs has an auto immune lung condition which he thinks is amyopathic dermatomyositis. In relation to causation, Dr Boers said that initially he was concerned about apportioning any causality as he did not feel qualified to do so and that is why he referred Mr Briggs to Dr Hoy and Prof Hall for an opinion. He told the court that after monitoring Mr Briggs over time and obtaining the opinions of Dr Hoy and Prof Hall he also considered that Mr Briggs occupational exposure did contribute to his condition. After being referred to the studies mentioned by Dr Hoy and Prof Hall and being asked to comment on them, Dr Boers told the court that he thought it was hard to infer from the studies but thinks that they may provide a signal because it is an autoimmune induced lung disease overlapped with dermatomyositis scleroderma and there is literature to support environmental and dust exposure to those conditions. Dr Boers noted that there are not many cases of this type and after having treated more than 20,000 patients over 15 years he said that this was one of the most dramatic cases of rapidly progressive lung disease that he has seen. He told the court that has based his opinion on causation on his clinical experience rather than any studies referred to. Dr Boers told the court that he considers Mr Briggs unfit for any work.

In cross examination, Dr Boers confirmed that he first saw Mr Briggs in March 2015 on referral from St George Hospital in Sydney. He told the court that the hospital struggled with the diagnosis as did he. In relation to the issue of causation, Dr Boers said that he was not aware of any data about occupational exposure in terms of toxic gas exposure causing auto immune illnesses or pulmonary fibrosis and that initially he was hesitant to attribute cause to the Mine fire because, “I live in the area, I’ve worked in the area, I didn’t want to be the doctor who was blaming the Mine fire on it”. Dr Boers agreed that a precise diagnosis cannot be placed on Mr Briggs condition as he has an antibody (PM/Scl) which is associated with overlapping conditions. Dr Boers told the court that he believes there is a temporal relationship between Mr Briggs employment and the onset of his condition because he had a good lung function with no symptoms prior to March 2014 and then developed symptoms five months later, although he acknowledged that on its own, a temporal relationship is difficult to establish causation. He also agreed that he is not certain of the diagnosis but agreed with the proposition put to him that the PM/Scl antibody supports a potential diagnosis of amyopathic dermatomyositis. Dr Boers also agreed that Prof Hall had noted in his report that infections or stress factors as well as occupational exposures or bacterial disturbance may have some part to play in the onset of the condition. He agreed that the presentation of Mr Briggs in December 2014 with a red throat and enlarged tonsils is suggestive of an infection which potentially makes it a possible or a more possible cause of the onset of symptoms as does occupational exposure. Dr Boers agreed that his opinion concerning diagnosis and causation is based on his experience and the opinions of Dr Hoy and Prof Hall.

The defendant tendered a medico-legal report from Dr Burdon, Consultant Respiratory Physician, dated 27 March 2015, following his examination of Mr Briggs on 19 March 2015. In preparing his report, Dr Burdon was provided with two reports from Dr Katsoulotos, a report from Dr Foo, test results including radiology and blood test results and the Discharge summary from St George Hospital Sydney. When obtaining a history from Mr Briggs he was mistakenly told by Mr Briggs that he had enjoyed good health until the middle of 2014 when he developed a cough about 5 to 6 months after the Morwell fire. The balance of the history given is not contentious. Dr Burdon opined that Mr Briggs suffers from dermatomyositis related pulmonary fibrosis. He stated that interstitial pulmonary fibrosis is a recognised complication of dermatomyositis with the cause of dermatomyositis unknown. In his opinion, Mr Briggs condition is not associated with his occupation nor with his exposure at the Hazelwood Mine fire. Dr Burdon noted that Mr Briggs demonstrated raised muscle enzymes on blood examinations, and it was the view of the treating medical staff at St George Hospital that he suffered from dermatomyositis. He also noted that there are numerous causes of interstitial pulmonary fibrosis, some of which are related to industrial exposure, but in most cases no cause is found. He concluded that Mr Briggs pulmonary fibrosis is either idiopathic, meaning of unknown cause, or associated with the dermatomyositis. Dr Burdon reported that dermatomyositis is a condition which falls outside his expertise and stated that Mr Briggs reduction in functional capacity is entirely related to his pulmonary fibrosis which will require ongoing immunosuppressive therapy and possibly a lung transplant. Dr Burdon considered that Mr Briggs has no capacity for work at present nor will he in the foreseeable future. His opinion was not challenged by way of cross examination.

Professor Needham gave evidence and a ‘comprehensive report’ which included her Qualifications, Experience, References, Glossary of Terms used, Curriculum Vitae, Honours and Awards, Grants, a list of 58 Publications, Published Books and Chapters, Invited Lectures, Conferences Attended and a Timeline of medical events relating to Mr Briggs dated 12 March 2019 was tendered as were her Conference Notes dated 15 May 2019.

In preparing her report, Prof Needham had access to the relevant records of St George Hospital and Moe Medical Centre including x-ray and blood test results. Her report is split into several categories, being: A Summary of Connective Tissue Disease – Interstitial Lung Disease as it relates to amyopathic dermatomyositis and Overlap Myositis; Case Summary and Opinion based on the Medical records; Literature Review on Environmental triggers for patients with myositis/CTD; and My opinion regarding the question of whether the occupational exposure caused his CTL-ILD/amyopathic Dermatomyositis.

Prof Needham reported that the medical records indicate that Mr Briggs developed the sub-acute onset of shortness of breath on exertion, fatigue, myalgias, new onset Raynaud’s and pain in fingers and exercised intolerance over a period of weeks in late 2014 and progressing in early 2015, associated with elevated inflammatory markers (CRP/ESR), mildly elevated creatine kinase (CK), significantly positive auto antibodies (anti-nuclear antibodies ANA – nuclear and cytoplasmic and anti-PM/Scl). She noted that Mr Briggs underwent a lung biopsy confirming non-specific interstitial pneumonia (NSIP) and an electromyogram (EMG) which had the suggestion of tomb amyopathic units in his biceps muscle only, but no definite evidence for a myopathy. She also noted that he did not undergo any formal neurological examination.

Prof Needham diagnosed that Mr Briggs has an immune-mediated interstitial lung disease associated with a systemic connective tissue disease (CTD-ILD), specifically the anti-PM/Scl antibody based on:

- the history provided with a progression over weeks, systemic involvement beyond the lungs including painful muscles and sore fingers and new onset Raynaud’s;

- the examination findings of restrictive lung disease, swollen fingers, possible rash with facial erythema and cracked skin over his knuckles;

- investigation results demonstrating a significantly positive PM-SCL and ANA antibodies and lung biopsy results demonstrating non-specific interstitial pneumonia; and

- his response to immunosuppression with subjective and objective improvement of symptoms, function and respiratory function tests.

Prof Needham suspected that Mr Briggs may have had some mild muscle involvement in his anti-PM/Scl associated systemic connective tissue disease but noted that no formal neurological examination was documented nor were his muscles imaged when he was acutely unwell, and no biopsy was taken. She also noted that the nature of the skin involvement is unclear and that it was not a typical dermatomyositis rash as this was not reported in his records and the rheumatologist had looked for it. She further noted that no definite sclerodermatous changes were seen or recorded although Dr Lassene, Rheumatologist at the St George Hospital and Dr Boers did comment on some mild facial erythema and considered this skin involvement as part of his connective tissue disease. Prof Needham also noted that on presentation Dr Lassene had noted some cracked skin over Mr Briggs knuckles, but a skin biopsy was not undertaken to prove whether the skin was inflamed (such as in dermatomyositis) or thickened (as may be expected in systemic sclerosis). Prof Needham opined that the described skin involvement does not necessarily make this a form of dermatomyositis as additionally Mr Briggs does not have one of the typical DM-associated antibodies. Accordingly, she concluded that the diagnosis in retrospect is more accurately interstitial lung disease- connective tissue disease associated with the anti-PM/Scl antibody and overlap myositis.

In considering the literature review on environmental triggers for patients with myositis/connective tissue disease she noted that the aetiology of all these immune mediated myositis and connective tissue diseases is unclear and is poorly understood. She stated that there is increasing evidence for a gene-environment interaction-more specifically, that they are a complex genetic disorder initiated by immune activation due to a specific environmental trigger, causing specific tissue responses involving muscle, lung, skin, small vessel endothelium in genetically susceptible individuals. Prof Needham reported that the known genetic risk factors are largely associated with genes that regulate responses to environmental agents. She stated that environmental triggers are less well-defined in most cases and the evidence is extremely limited. She noted that an evaluation of the literature is also difficult due to changes in disease classification and nomenclature over time, lack of large prospective studies and the inherent difficulty in determining cause and effect. She stated that small case series and case reports suggest that different environmental triggers are reported to be involved in the development of certain myositis phenotypes and those suggested so far have included; infections, drugs, physical exertion, smoking and UV light.

Prof Needham noted that Mr Briggs was reported to have a red throat with enlarged tonsils and an emergency presentation on 8 December 2014 with dizziness and gastrointestinal symptoms. She stated that none of these symptoms or signs are atypical part of anti-PM/Scl overlap syndrome and she also noted that Mr Briggs returned positive pertussis serology. She suggested that this may indicate that there was an infection at the beginning of his symptoms.

Prof Needham reported that the study by Labirua-Iturburu & others referred to by Prof Hall and Dr Hoy is not relevant to the present case as Mr Briggs had none of the anti-synthetase antibodies involved in that study. She also noted that Mr Briggs would have formed part of the control group (which she said was not clearly described in the Paper) and the occupational exposures were defined by years of exposure and not a 12-week exposure as occurred with Mr Briggs. Prof Needham noted that when she conducted a literature review searching for environmental or occupational exposures in patients similar to Mr Briggs with interstitial lung disease- connective tissue disease and positive anti-PM/Scl antibodies she could find no systematic or prospective studies.

On the question of causation, Prof Needham opined that it is almost certainly multifactorial and extremely unlikely to be due to any one factor alone on the basis that she is confident that Mr Briggs is suffering an immune-mediated lung injury (Connective tissue disease-Interstitial lung disease) related to an underlying systemic autoimmune disease (systemic symptoms and positive ANA/anti-PM/Scl antibodies). In her opinion, it is likely that Mr Briggs has some genetic predisposing factors although none have been tested for or identified. She stated that the literature in autoimmunity is increasingly identifying genetic susceptibility factors as important determinants of how individuals respond to environmental antigens. She noted that not everyone exposed to environmental triggers will develop an autoimmune disease. However, she stated that given the literature review it is also likely that Mr Briggs disease was triggered by environmental factor(s). She noted that there is a temporal association to his exposure which means this is a possible aetiological factor.

Prof Needham noted that because there are many uncertainties regarding Mr Briggs exposure to chemicals and other substances is the reason why she favours it only as a possible trigger. She noted that;

- Mr Briggs exposure was for only 12 weeks and she could not find a similar case report of a short toxic exposure to similar environmental toxins causing the disease of PM-SCL associated connective tissue disease- interstitial lung disease;

- most studies she reviewed looked at environmental exposures from between 0-6 months prior to the onset of symptoms, with most identifiable infectious triggers being within three months noting that most occupational exposure histories are taken over years;

-Mr Briggs dose of exposure over the 12-week period is uncertain with the report of Mr Kottek noting that there was likely exposure to ash and coal dust but the “extent of respirable silica is unclear”. Prof Needham noted that Mr Briggs was exposed to smoke which included fine particulate matter as well as carbon monoxide, ozone, sulphur dioxide, nitrogen dioxide and air toxins but Mr Kottek did not have access to the CO results to allow insight into the extent of Mr Briggs exposure;

-there is no definite evidence in the literature suggesting a connection between the specific environmental toxins that it is suggested that Mr Briggs was exposed to or any case reports or case series with PM-Scl/CTD-ILD overlap syndrome, although this does not exclude it; and

-it is a rare disease (with only 4% of a large cohort of 949 idiopathic inflammatory myopathy patients at John Hopkins) and if it were due primarily to environmental exposure she would expect the disease to be far more common in other workers exposed to similar environmental toxins such as firefighters or miners.

Prof Needham opined that whilst Mr Briggs occupational exposure remains a possible, albeit unproven trigger, she considers it at least equally as likely that an infectious agent was a possible trigger because;

- the early findings of Dr Quamar on 5 December 2014 that Mr Briggs had a red throat and enlarged tonsils which is highly suggestive of pharyngitis;

- Mr Briggs symptoms when he presented to the emergency department on 8 December 2014 complaining of dizziness and gastrointestinal symptoms which are not typical of his overlap syndrome and which resolved quite quickly; and

- a positive pertussis serology - although not specific, was suggestive.

Prof Needham stated that a key component of the case is the fact that Mr Briggs is suffering an auto immune-mediated lung injury in which the aetiopathogenesis is not well understood or proven. She stated that this is distinct from a direct lung injury and idiopathic pulmonary fibrosis which in many cases are proven to be due to occupational exposures such as asbestos or silica. She also made comment of the fact that there are many unknowns is in Mr Briggs case relating to additional possible environmental triggers being; his prior occupational exposures; his hobbies and home life and exposures to organic solvents and fertilisers and most importantly, it is not known what environmental triggers are important in the development of connective tissue disease- interstitial lung disease associated with PM-SCL antibodies. Prof Needham concluded that although Mr Briggs exposures at the Mine fire was ‘possibly’ a factor in triggering his connective tissue disease- interstitial lung disease associated with PM-Scl antibodies given the temporal profile, it was not the only cause. She noted that temporal association does not prove causation but certainly raises possibilities. In addition, she considers an infectious agent at least equally likely to have contributed to the onset of Mr Briggs disease and it is possible it was an even combination of factors.

In her Conference Notes dated 15 May 2019, Prof Needham states that she currently manages approximately 250 myositis patients, five of which have the same antibody as Mr Briggs (anti-PMScl antibody). She confirmed the opinion she gave in her report dated 12 March 2019 that she is not certain that Mr Briggs has amyopathic dermatomyositis as there has been insufficient testing to allow the diagnosis to be confirmed. In particular, she noted that there are no skin or muscle biopsies that have been completed that would confirm the diagnosis. She notes that although other specialists may classify his condition as amyopathic dermatomyositis she believes the more accurate diagnosis or classification is of overlap myositis associated with the PMScl antibody. Prof Needham refers to the research group in which she is involved (the Myositis Discovery Program) and states that they have built an Australasian Myositis Registry, the purpose of which is to collect enough information to help determine common exposures and possible causes. She stated that at present, she is unable in most cases, to give her patients the answer as to why they have the disease. She also noted that there is an umbrella registry called the Euromyositis Registry in which 3500 patients are involved and they are only now able to draw relevant data on aspects of the condition including causation. She expects that it will be at least 10 years before they are able to determine a clear link between environmental triggers and most forms of myositis, particularly the rarer forms such as PMScl associated overlap myositis. Prof Needham noted that collecting enough data to be more certain of causation requires much larger numbers than are currently available and at present she believes that it is only ‘possible ‘that the Mine fire was a trigger of Mr Briggs condition.

During her evidence, Prof Needham told the court that she has been practising as a neuromuscular neurologist, specialising in neuromuscular diseases since 2009. She also told the court that she is currently a consultant neurologist at the Fiona Stanley Hospital and head of the Department of Neurology at Fiona Stanley Hospital as well as holding positions at Murdoch University, Notre Dame University and Fiona Stanley Hospital as the Foundation Chair in neurology. Additionally, she said that she commenced and leads the myositis discovery program which is a research translational program in the field of myositis.

Prof Needham confirmed that after reviewing the medical records from St George Hospital, his treating general practitioner records, letters from Dr Boers, the report of Mr Kottek and based on Mr Briggs symptoms, signs, blood tests and investigation results, that it is clear to her that he suffers from an autoimmune disorder associated with the PM/Scl antibody that is referred to as overlap myositis associated with PM/Scl. Prof Needham stated that pulmonary physicians refer to the condition as connective tissue disease- interstitial lung disease which in this case is an idiopathic inflammatory myositis. She said that PM/Scl is how they manage antibodies. It is an antibody associated with polymyositis (PM) which literally means lots of inflamed muscles and Scl is short for scleroderma or systemic sclerosis. She said that it is an antibody that is seen in a clinical syndrome where there is an overlap between a muscle disease and systemic inflammation but particularly those features associated with scleroderma or systemic sclerosis being interstitial lung disease, arthritis, sclerodactyly and other features.

Prof Needham stated that it has been verified on three occasions that Mr Briggs has the PM/Scl antibody. In relation to other diagnoses indicating that Mr Briggs has amyopathic dermatomyositis, she said that it is really a matter of the classification of that myositis. She told the court that in her opinion there was enough evidence to suggest that Mr Briggs probably had muscle involvement even at the onset of his condition, so that amyopathic dermatomyositis literally means – amyopathic (no muscle disease) and dermatomyositis (inflammation of the skin). Prof Needham told the court that throughout the clinical records, Mr Briggs had quite widespread muscle aches and pains and during his St George Hospital admission he had elevated muscle enzymes being the creatine kinase and the lactate dehydrogenase enzyme. She also noted that on the EMG, where only 3 muscles were sampled, the biceps EMG suggested myopathic potentials. She said that because an MRI scan, physiological examination and muscle biopsy was not performed she cannot conclude in retrospect whether Mr Briggs had myositis at that time. However, she reported that she suspected he did and therefore he did not satisfy the definition for amyopathic dermatomyositis and the PM/Scl antibody is not associated with that clinical syndrome. Prof Needham gave evidence that she is in no doubt that Mr Briggs has overlap myositis as his clinical symptoms and signs all match that antibody.

On the question of causation, Prof Needham said that in her opinion the suggested temporal connection is tenuous as there was a gap of 5 months between the exposure and onset of symptoms. She told the court that for such a short and sharp exposure to cause an imminent onset of the disease she would have expected that Mr Briggs would have experienced respiratory symptoms being a cough or shortness of breath at the time indicating there was some form of inflammation occurring in the lung. Prof Needham told the court that causation is a very vexed question in medicine and that temporal association only raises possibilities and that to prove causation you need to have strength of association. She said that Mr Briggs has a very rare disease and she does not know of any literature or studies relating to a 12-week exposure with a lag in symptoms for five months for this autoimmune condition. She told the court there are no studies applicable to Mr Briggs condition because he has a rare subtype of overlap myositis and there has not been enough cases to ascertain what the cause or causes are.

Prof Needham told the court that the Myositis Registry is an attempt to capture case details across the world of the different forms of myositis, possible occupational viruses, to see if the medical profession can better understand the causes of the diseases, the natural history of the diseases and to help to classify the conditions better in order to provide better treatment and to prevent conditions from occurring in the first place. She told the court that she runs a weekly myositis clinic and in the last 12 months would have seen approximately 250 myositis patients of which only five have the PM/Scl antibody.

Prof Needham confirmed the opinion she expressed in her report concerning the reference to and reliance on the report by Labirua-Iturburu & Others. She told the court that none of the 32 cases referred to in the report had a PM/Scl antibody (as Mr Briggs) and he does not have antisynthetase syndrome. Prof Needham told the court that if she had been asked to peer review the report she doubted that it would have been published because of what she highlighted during her evidence were its failings. In her opinion, that Study only raised the “possibility” of occupational exposure being a cause of anti-synthetase antibodies without proof.

Prof Needham told the court that it is very difficult in the present case to come to any kind of definite conclusion around causation because of the very short duration of exposure by Mr Briggs. She noted that most of the exposures or occupational exposures or environmental triggers are accumulated over many years. She told the court that because of Mr Briggs symptoms on presentation at the doctors in December 2014, it is equally as likely, perhaps even more likely, that whatever infection he had was the trigger rather than the occupational exposure. However, she said, “you can never be sure”.

During cross examination, Prof Needham whilst acknowledging that infection can be a trigger said that the medical profession is not at the point yet where they are able to identify which type of infection may be the trigger for autoimmune conditions. She also told the court that in the Hopkins Myositis group only 21 of the 949 patients (4%) have PM/Scl of which she has treated 5. She said that the PM/Scl overlap myositis group has a very high proportion of extra muscular manifestations (arthritis, cracking of the skin and hands) with their myositis being usually quite mild but their interstitial lung disease being a much larger problem. She stated that in her opinion, Mr Briggs did experience muscle symptoms in the form of aches and pains, but his bigger problem related to his lungs.

Prof Needham agreed that she is looking for scientific causation/biological plausibility and wants more scientific evidence to support causation and, more case reports. She also agreed that at present the medical profession are still uncertain as to the triggers for autoimmune conditions and in this case, she is unable to find a scientific basis to draw any firm conclusion as to what triggered the condition although, she does not rule out environmental factors or triggers as a “possibility”. When questioned about ‘environmental triggers’ she said they could mean anything from drugs, toxin exposure, viruses or anything “outside the body”.

Prof Needham told the court that she is aware of the opinion by Prof Hall to the effect that Mr Briggs exposure was a significant contributing factor to the onset of his condition. She told the court that she disagreed with his opinion, “as would every world expert”, because Mr Briggs does not have antisynthetase syndrome as PM/Scl is not an antisynthetase antibody.

Summary

Mr Briggs bears the onus of proving on the balance of probabilities that his employment with the defendant between 3 March 2014 and 27 May 2014 was a cause of his lung/auto immune condition resulting in his incapacity for employment from January 2015. Mr Briggs must prove that his ‘injury’ arose out of or in the course of his employment or due to the ‘nature’ of his employment. There is no dispute that his condition renders him incapacitated for pre-injury and suitable employment.

On the basis that the medical evidence was voluminous and complex, the court ordered that a transcript of the evidence be provided to the court and the parties in order to assist in understanding the medical evidence and in the preparation and filing of written submissions.

Although Mr Briggs evidence was largely uncontested, there was a divergence in medical opinion as to the exact nature and diagnosis of his condition and on the central issue of causation. In relation to diagnosis: Dr Levin and Dr Hoy believed he has interstitial lung disease and associated amyopathic dermatomyositis as did Dr Boers, albeit with some uncertainty; Prof Hall diagnosed him as having myositis associated with an underlying autoimmune condition-amyopathic dermatomyositis; Associate Prof Sasse’ diagnosed him as suffering from non-specific interstitial pneumonitis; Prof Pain stated that he has a connective tissue disorder with interstitial lung disease (an autoimmune disorder); Dr Burdon diagnosed him as having dermatomyositis related to pulmonary fibrosis; and, Prof Needham is of the opinion that he suffers from interstitial lung disease-connective tissue disease associated with the anti-PM/Scl antibody and overlap myositis and disputed the diagnosis of amyopathic dermatomyositis based on her opinion that Mr Briggs “probably had muscle involvement even at the outset”.

In relation to the issue of causation: Dr Levin stated that there is a ‘temporal relationship’ and it is “reasonable to assume” that work contributed to his illness; Prof Hall stated that employment was a ‘possible cause’, that the “temporal connection was tantalising” and ultimately, that employment was a significant contributor to the condition because such exposure “statistically put him at increased risk”; Associate Prof Sasse’ stated that his exposure to toxins contributed to his lung condition because “the key fact is the timing” based on the fact that he had good lung function prior to his employment and 6 months later his condition developed with the only change being his work environment; Prof Pain was ‘persuaded’ that his exposure probably caused the onset of his condition based on his normal pre-employment spirometry results and the development of his condition shortly thereafter in conjunction with the literature referred to by Dr Hoy allegedly linking the onset of autoimmune diseases to chronic bronchial irritation; Dr Hoy stated that it is “more likely than not” that exposure was “a factor contributing towards” his lung condition; Dr Boers stated that there is a causal link between his exposure and his condition on the basis of monitoring him over a period of time, after obtaining the opinions of Dr Hoy and Prof Hall, his pre-employment lung function results and the development of symptoms 5 months later; Dr Burdon expressed an opinion that his condition is not work related; and Prof Needham considered his condition is multi-factorial and that his occupational exposure was a “possible trigger” on the basis of temporal association.

The submissions filed on behalf of Mr Briggs focussed on the evidence given by the witnesses and noted that all of the medical evidence acknowledged the ‘possibility’ that Mr Briggs exposure during the period of his employment with the defendant was a possible cause of his condition notwithstanding the exact diagnosis. Mr Briggs referred to and relied on the Full Court of the Supreme Court decision in Dahl v Grice[5] where he submitted that the court rejected the contention that expert evidence between the act and the particular injury was required to the requisite degree of probability. He noted that the court held this was because it was for the tribunal to decide this question considering the evidence of the experts as to the existence of a link between the medical condition (the injury) and the act. Mr Briggs submitted that the case of Dahl stands for the proposition that it was sufficient to establish causation (in the legal sense) if there were events or features whose character and sequential order suggested a causal rather than merely temporal connection.
[5] [1981] VR 513.

Mr Briggs submitted that doctors who supported a causal relationship between his exposure and his condition (Prof Hall, Assoc Prof Sasse’, Prof Pain, Dr Hoy, Dr Boers) as opposed to a ‘possible cause’, based their opinions on all of the facts and did not rely on a temporal connection based on;

- his excellent health prior to his exposure and in particular his pre-employment lung function test;

- his high level of exposure between 3 March 2014 and 27 May 2014;

- the lack of appropriate breathing protection during his employment;

- the study linking environmental exposure to autoimmune conditions;

- the fact that he never smoked;

- the fact that he was not a bird keeper;

- the lack of prior toxin exposure;

- that he has never been involved in spreading fertiliser on his farm; and

- the gap between the last exposure and the onset of symptoms which strengthen the temporal connection.

Mr Briggs also submitted that the court should give less weight to the opinion of Professor Needham on the basis that;

- her diagnosis of ‘overlap myositis’ is contrary to the diagnosis made by all other experts;

- the other experts were of the opinion that he did not have any muscle involvement and hence a neurologist was not an appropriate expert to proffer an opinion or treat him; and

- it was unrealistic of her to expect to find others who had exactly the same condition as he to meet her test of ‘scientific certainty’ regarding causation.

Mr Briggs contended that he has discharged the onus of proving, on the balance of probabilities, that his exposure in the course of his employment was a cause of his lung and autoimmune condition and that his incapacity results from or is materially contributed to by the injury.

The defendant’s submissions referred to the fact that Mr Briggs has pleaded injury by, firstly asserting he suffered injury ‘simpliciter’ and that his injury arose out of or in the course of his employment, or secondly, by asserting his injury arose ‘due to the nature’ of his employment. In relation to the latter, the defendant quite correctly noted that if Mr Briggs sought to rely on the concept of gradual process injury in accordance with s 82(6) of the Accident Compensation Act 1985, it was incumbent on him to adduce evidence that the risks to which he was exposed by virtue of the nature of his employment gave rise to an increased risk in the development of his condition in accordance with the principles in ACC v Botezatu[6], which he has failed to do. The defendant also noted that Mr Briggs reliance on s 82(6) was a ground for him to oppose a Medical Panel referral.
[6] (1993) 1 VR 304 at 305, 311, 312 and 313 noting that the case dealt with the test under s 86 and not s 82(6).

The defendant submitted that the court is therefore required to determine the issue of causation on the basis of whether Mr Briggs condition arose out of or in the course of his employment.[7] Furthermore, it submits that the court must determine whether Mr Briggs employment was a significant contributing factor to the extent that it is suggested that the relevant injury was a disease or a recurrence, aggravation, acceleration, exacerbation or deterioration of the injury. Applying those tests it submitted that notwithstanding whether the court determines that Mr Briggs suffers from an ‘overlap myositis’ associated with the PM/Scl antibody (as diagnosed by Prof Needham) or amyopathic dermatomyositis with secondary interstitial lung disease (as diagnosed by Dr Levin, Dr Hoy, Dr Boers, Prof Hall), it contends the condition did not arise out of or in the course of his employment, that employment was not a significant contributing factor to him contracting the disease, or the recurrence, aggravation, acceleration, exacerbation or deterioration of his condition. The defendant submits that on the evidence presented, the court should not be satisfied, on the balance of probabilities, that Mr Briggs condition was caused by his occupational exposure and the evidentiary basis on which the ‘possibility’ of this connection is founded in the expert medical evidence is inherently flawed.
[7] Zlateska v Consolidated Cleaning Services Pty Ltd (2006) VSCA 141.

Conclusion

The medical evidence indicates that whatever the correct diagnosis, the condition from which Mr Briggs suffers, is a rare one. After considering the evidence of all experts, the court was particularly impressed with the evidence given by Prof Needham and accepts her conclusion that Mr Briggs is suffering from an autoimmune condition categorised as ‘overlap myositis associated with the PM/Scl antibody leading to interstitial lung disease-connective tissue disease. Her qualifications and experience, together with the fact that she had an opportunity to consider all medical records and expert opinions, in addition to her presentation in court, has led the court to accept her opinion as being highly persuasive that Mr Briggs does not suffer from amyopathic dermatomyositis. Accordingly, the court does not accept the submission of Mr Briggs that as a Neurologist she was not appropriately qualified to express an opinion in this matter as the other medical experts were of the opinion that he did not have muscle involvement and a Neurologist has never been assigned to his multi discipline treatment team.

The court also accepts her evidence that there is no literature ‘directly relevant’ to his condition, his exposure in the course of his employment with the defendant and on the issue of causation. Accordingly, the court does not place any evidentiary weight on the study relied on by Mr Briggs and accepts the conclusion of Prof Needham that he does not have the antisynthetase antibody referred to in the study and that it is not appropriate to draw any evidentiary conclusions from it.

Having accepted the opinion of Prof Needham on the question of diagnosis, the issue to be determined is whether Mr Briggs condition was caused or contributed to by his exposures in the period of his employment with the defendant. From a medical perspective, Prof Needham is of the opinion that the temporal connection between his employment period (3 March 2014 to 27 May 2014) and the onset of symptoms in November 2014 (5 months) is “tenuous”. In her opinion, for such a short, sharp exposure, that if it was to cause an imminent onset of the disease, she would have expected him to have experienced respiratory symptoms in the form of a cough or shortness of breath at the time of his exposure to indicate inflammation occurring in the lung. Furthermore, she opined that it is very difficult to come to any kind of definite conclusion because of Mr Briggs short duration of exposure. Ultimately, Prof Needham concluded that because of the nature of the symptoms of which he was experiencing in November 2014 (dry cough/sore throat) and that on examination by Dr Quamar on 5 December (red throat/enlarged tonsils), that it was “equally as likely, perhaps even more likely” that whatever infection he had was the ‘trigger’ rather than his occupational exposure but did add, “you can never be sure”.

When giving evidence, Prof Needham conceded that the medical profession is still uncertain as to the ‘triggers’ and she is unable to draw any firm conclusion as to what ‘triggered’ his condition. The other medical experts, whilst supporting causation, albeit reaching a different conclusion on diagnosis, also conceded that infection was a ‘possible’ trigger. As indicated a number of the other medical experts (Dr Levin, Ass Prof Sasse’, Prof Hall, Prof Pain, Dr Hoy & Dr Boers) supported causation on the basis of temporal connection.

The court is therefore left with expert evidence indicating that occupational exposure is a ‘possible trigger’ as is an infection. The court is required to make a determination considering this expert evidence and having regards to the totality of the evidence.

In Zlateska v Consolidated Cleaning Services Pty Ltd & Anor, the Court of Appeal (Maxwell ACJ, Eames and Redlich JJA) said:

The words “arising out of” the employment have long been recognised as requiring a causal connection between the employment or its incident and the injury. For the reasons set out below, where it can be shown on the balance of probabilities that the act or omission of the employer was a cause of the injury, the worker will have established a sufficient connection to their employment to characterise the injury as “arising out of” their employment. The question of causation is a matter of common sense. It is not necessary for the worker to establish that the act or omission of the employer was the sole or dominant cause of the injury, or that the employment itself created any “special risk” of or “special exposure” to injury…In determining whether the act or omission of the employer was a cause of the injury, the employer must take the worker as it finds him/her. Any special susceptibility or vulnerability on the part of the worker may explain why the particular act or omission is of causal significance. The fact that the act or omission would not have caused injury to a worker who did not have the susceptibility or vulnerability of the injured worker does not alter the causal character of the act or omission.[8] At paragraph 72, the court said; As her Honour noted, Ashley J in Popovski agreed with the magistrate that “the proper test” as to whether injury arose out of employment was that it be the real, the effective or the proximate cause of the injury.

[8] Paragraphs 7-11.

In other words, the proximate cause need not be the sole cause of the injury, but it must be greater than merely ‘not negligible’. As this case involved ‘competing’ medical opinions on the issues of diagnosis and causation, it is appropriate to consider what Gobbo J said in Dahl v Grice;

The review of the authorities leads me to reject the appellants argument that in matters of bodily health, even outside common experience, it is incumbent on a plaintiff to prove the causal connection to the requisite degree of probability by evidence from the expert. It is plain that in such matters the courts have recognised that a possible cause may be elevated to a probable cause. There are a number of reasons why it is undesirable that the opinion as to causal connection be stated in terms of probabilities. In the first place, this is the role of the tribunal of fact and the ultimate task rests with the judge or jury, as the case may be. Secondly, it is inadmissible in the ordinary course for an expert to give evidence in a form that takes up the very ultimate issue that is the responsibility of the tribunal of fact. Though there are many exceptions in practice to the general rule as to not asking questions that by their terms call for an answer to the ultimate issue, it is a rule that is soundly based in its endeavour to reserve to the tribunal of fact the actual responsibility for the resolution of the ultimate issue. A third consideration is that there is inevitably much difference in the views of expert witnesses as to what constitutes a probability as opposed to a possibility, whether in terms of a particular case or simply as a matter of logic. There is the obvious danger that an expert when asked to provide an opinion as to whether a causal link exists may do so in terms of scientific proof that may be altogether too exacting for the degree of satisfaction necessary in a legal proceeding. In the vast majority of personal injury cases the medical expert is not called upon to go any further than to confirm that the injuries are consistent with injury suffered in a certain class of accident and that the plaintiff’s medical condition and symptoms are consistent with such injuries. Where there is a real contest as to causation, this is not resolved by compelling the witness to express his opinion as to the probability of such causation. The tribunal of fact will gain far more assistance if the expert devotes himself primarily to an exposition of the hypothesis that may support a link between the medical condition and the class of accident or injury in question.

It is never easy to state how the tribunal of fact is to proceed from expert opinion as to medical hypothesis or medical experience of known causal links to decision in the particular case. This was the problem referred to by Lord Loreburn in Woods v Thomas Wilson Sons and Co. Ltd. (1915) 8 BWCC 288, at p. 296: “it is quite true that every case must be proved, and something more is needed than a state of facts which is consistent with one view or the other. That something more is supplied if the facts show a probability one way or other. No one can frame a formula by which you can measure probabilities. We must judge in each case as we would in other affairs of life”.

The problem was the subject of what was in my respectful opinion a clear and helpful analysis in the judgement of Mahoney, JA in Fernandez v Tubemakers of Australia Ltd, {1975} NSWLR 190, at pp. 198 and 199-200. His Honour said:

“Problems of causality arise in different forms: thus, in one case it may be whether one of two possible causes can positively be excluded: in another case, it may be whether, of several possible causes, any one can be regarded as more probable than the other” – Ramsay v Watson [1961] HCA 65.

Turning now to the evidence in the present case, there was plainly evidence that the injury suffered in the motor car accident was a possible cause of the respondents’ medical condition following her cerebral haemorrhage in January 1975. Was there, however, evidence that showed that the connection between the accident and the haemorrhage was sufficiently close to warrant a reasonable mind, faced with the problem of determining the question upon the evidence before it, concluding that one of the possible causes was the actual cause? Or, to use the enquiry suggested by Taylor, J in Australian Iron and Steel Ltd v Connell (1959) 102 CLR 525, at 531 adopted by Stephen, J in Tubemakers v Fernandez (1976) 50 ALJR 720, at p.722: were there event whose character and sequential order suggested a causal rather than a merely temporal connection?

In Transport Industries Insurance Co Ltd v Longmuir[9], Tadgell JA stated: the evidence is to be evaluated as a whole in order to consider whether the party bearing the onus of proof has established what is ultimately sought to be proved. The object of the exercise of evaluation is to discover whether the evidence paints a picture reflecting real-life, rather than to place a tick or a cross against paragraph after paragraph of torpid pleading. A true picture is to be derived from an accumulation of detail. The overall effect of the detailed picture can sometimes be best appreciated by standing back and viewing it from a distance, making an informed, considered, qualitative appreciation of the whole. The overall effect of the detail is not necessarily the same as the sum total of the individual details…
[9] [1997] 1 VR 125.

More recently, when referring to what was said by Gobbo J in Dahl v Grice, the Court of Appeal (Nettle, Ashley & Redlich JJA) stated[10] : the question then became whether, on consideration of all the evidence, the jury was satisfied that the respondent had established causation by route (a) or (c) - in the latter case by establishing that factory exposure in breach of duty materially contributed to the contraction of the disease. We say ‘consideration of all the evidence’ because the submissions for the appellant often seemed to imply that the respondent’s case required probability as adjudged by a medical witness, and that in the absence of such probability the respondent’s case must fail. That is not so. Consideration of the entirety of the plaintiff’s case may persuade the tribunal of fact that a sufficient causal link is established although expert medical witnesses gave evidence in the language of possibility only.
[10] Amaca Pty Ltd v King [2011] VSCA 447 at paragraph 83.

The medical evidence relied on by the defendant from Prof Needham on the question of causation essentially is that she was unable to draw any firm conclusion as to what triggered Mr Briggs condition, that of an autoimmune disorder associated with the PM/Scl antibody that in the myositis world we would refer to it as overlap myositis associated with the PM/Scl. The pulmonary physicians refer to it as CTD-ILD which means interstitial lung disease associated with the connective tissue disease. So, the connective tissue disease in this case is an idiopathic inflammatory myositis. Although Prof Needham considered the temporal connection between employment and symptoms to be tenuous and that infection was “equally as likely, perhaps even more likely” than Mr Briggs occupational exposure in the course of his employment with the defendant, she stated that, “you can never be sure”.

The evidence in this case is not confined to the “cause”, because it is apparent that there may be more than one cause, occupational exposure and infection to name two. I have concluded, on the balance of probabilities, that Mr Briggs exposure to smoke, dust, fumes and substances in the course of his employment as an excavator operator between 3 March 2014 and 27 May 2014 materially contributed to the ‘injury’ suffered by him. In reaching this conclusion, I have had regard to the totality of the evidence and on the basis of a reasoned analysis of that evidence having regard to the authorities to which I have referred. In doing so, I have placed weight on:

· the reliability and credibility of Mr Briggs as a witness;

· the nature, extent and duration of his exposure during the relevant period;

· the absence of any prior history of relevant exposures;

· the pre-employment lung function test;

· the conflicting medical opinions as to diagnosis and ‘possible’ cause; and

· the short period between the exposure and development of his condition.

Ultimately, I have been persuaded that there is a causal link between his exposure and his condition.

Accordingly, Mr Briggs is entitled to weekly payments of compensation and reasonable medical and the like expenses in accordance with the provisions of the Accident Compensation Act 1985. I have also determined that he suffers an injury which entitles him to compensation for permanent impairment pursuant to s 98C of the Act.

[2019] VMC 4

1 AUGUST 2019