Pillay v Pacific Coast Christian School Limited

CERTIFICATE OF DETERMINATION OF MEMBER
Citation:	Pillay v Pacific Coast Christian School Limited [2023] NSWPIC 74
APPLICANT:	Vanitha Pillay
RESPONDENT:	Pacific Coast Christian School Ltd
Member:	Cameron Burge
DATE OF DECISION:	28 February 2023
CATCHWORDS:	WORKERS COMPENSATION - Weekly payments and medical expenses claim in relation to an alleged work-related respiratory condition in the nature of a disease said to be caused by an infestation of mould in the workplace; the applicant alleged she was exposed to mould in her workplace which in turn caused a respiratory condition known as chronic inflammatory response syndrome; the respondent disputes the applicant suffered a work-related injury and denied her employment was the main contributing factor to the development of her respiratory illness; Held – award for the respondent.
determinations made:	1. Award for the respondent.

STATEMENT OF REASONS

BACKGROUND

Mrs Vanitha Pillay (the applicant) claims medical expenses and weekly compensation in respect of an alleged respiratory illness said to have been suffered due to exposure to air borne mould in the course of her employment up to and including the deemed date of alleged injury on 21 July 2017.
From December 2015, the applicant worked two days per week in an accounts-payable role with Pacific Coast Christian School Ltd (the respondent) in its administration block. According to the applicant, in July 2017, she began having flu-like respiratory symptoms and consulted her general practitioner (GP) in August 2017.
The applicant states she suffered a further respiratory attack in mid-September 2017 and was treated with oxygen and a nebulizer at Pottsville Medical Centre. She alleges her health continued to deteriorate, requiring referral to an ear, nose, and throat (ENT) specialist, a respiratory physician, gastroenterologist and immunologist/allergist. There is no serious challenge to the nature of the symptoms which the applicant suffered.
In December 2017, the applicant underwent a CT scan which showed sinus inflammation. On 7 March 2018, the applicant underwent endoscopic sinus surgery at the hands of
Dr Busby, ENT specialist. The applicant’s problems persisted, and in March 2019, she consulted an immunologist and allergist, Dr Tan. In June 2019, blood tests diagnosed the presence of eosinophilia (a higher than usual white blood cell count).
According to the applicant, Dr Tan recommended investigation of the respondent’s air-conditioning system. In February 2019, an investigation of that system allegedly discovered mould contamination. The applicant alleges subsequent blood tests revealed the presence of fungi and mould to which the applicant attributes the development of chronic inflammatory response syndrome (CIRS).
The responded disputes the applicant's condition was caused by her employment by way of any work-related exposure to mould.

ISSUE FOR DETERMINATION

The parties agree that the only issue in dispute is whether the applicant suffered an injury in the course of her employment (ss 4,4 (b), 9A of the Workers Compensation Act 1987 (the 1987 Act)).
The parties agree the period of weekly payments in dispute is from 13 February 2020 to 23 December 2021, and that the applicant's pre-injury average weekly earnings (PIAWE) were $873.82 per week.

PROCEDURE BEFORE THE PERSONAL INJURY COMMISSION

I am satisfied that the parties to the dispute understand the nature of the application and the legal implications of any assertion made in the information supplied. I have used my best endeavours in attempting to bring the parties to the dispute to a settlement acceptable to all of them. I am satisfied that the parties have had sufficient opportunity to explore settlement and that they have been unable to reach an agreed resolution of the dispute. The parties attended a hearing on 8 December 2022. At the hearing, the applicant was represented by Mr Carney of counsel instructed by Mr Kreveld. The respondent was represented by Mr Stockley of counsel instructed by Mr Lee.

EVIDENCE

Documentary evidence

The following documents were in evidence before the Personal Injury Commission (Commission) and considered in making this determination:
(a)    Application to Resolve a Dispute (the Application) and attached documents;
(b)    Reply and attached documents, and
(c)    respondent’s Application to Admit Late Documents (AALD) and attached documents dated 2 December 2022.

Oral evidence

There was no oral evidence called at the hearing.

FINDINGS AND REASONS

Whether the applicant suffered a workplace injury

The applicant carries the onus of proving she has suffered a work-related injury. As the applicant alleges her injury was by way of a disease process caused by the nature and conditions of her employment, she must demonstrate the employment was the main contributing factor to contracting the disease (s 4(b)(i) of the 1987 Act).
The authorities make it clear that in order to prove injury, the applicant must demonstrate a “sudden or identifiable pathological change”: see Castro v State Transit Authority (NSW) (2000) 19 NSWCCR 496 (Castro).
The applicant does not argue her employment caused an aggravation of a disease. Rather, her case is the employment caused the contraction of the illness. In either instance, the requirement is to prove employment was the main contributing factor.
The determination of main contributing factor (or indeed substantial contributing factor in the case of a frank injury) is an exercise in causation. In determining the cause of an injury, the Commission must apply a commonsense test of causation. In the workers compensation context, that test was set out by Kirby P (as he then was) in Kooragang Cement Pty Ltd v Bates (1994) 35 NSWLR 452 (Kooragang).
In that matter, his Honour said at [810]:
“The result of the cases is that each case where causation is an issue in a workers compensation claim, must be determined on its own facts. Whether death or incapacity results from a relevant work injury is a question of fact. The importation of notion approximates caused by the use of the phrase 'results from', is now not accepted. By the same token, the mere proof that certain events occurred which predisposed a worker to subsequent death or injury, will not, of itself, be sufficient to establish that such incapacity or death 'results from' a work injury. What is required is a common sense evaluation of the causal chain. As the early cases demonstrate, the mere passage of time between a work incident and subsequent incapacity or death, is not determinative of the entitlement compensation.”
There is a significant difference between the notion of “main contributing factor” and “substantial contributing factor”.
There can be many substantial contributing factors to an injury, however, there can only be one main contributing factor. In AV v AW [2020] NSWWCCPD 9, Deputy President Snell dealt with the nature of the test for establishing main contributing factor, and said:
“66. I have previously expressed the view that the test of ‘main contributing factor’, inserted into the definition of ‘injury’ in s 4(b) by the 2012 amendments, is more stringent than the test applicable pursuant to s 4(b) in its previous form, which was subject to s 9A of the 1987 Act. There may be more than one 'substantial contributing factor'. Section 9A requires that the employment concerned be a substantial contributing factor to the injury. That use of the indefinite article admits of the possibility of other, and possibly non-employment -related, substantial contributing factors. On the other hand, the requirement in s 4(b) inserted by the 2012 amendments, that employment be the 'main contributing factor' permits the existence of only one such factor. The requirement of the 'main contributing factor' involves a more stringent connection with the employment than the requirement of a 'substantial contributing factor' that applied to disease injuries prior to the 2012 amendments…
70. In Awder Pty Ltd t/as Peninsular Nursing Home v Kernick, I expressed the view that whether ‘substantial contributing factor', for the purposes of s9A of the 1987 Act, was satisfied was 'a question to be decided on the evidence overall, including a consideration of the matters described in s 9A(2). It is not purely a medical question. That view was applied by Keating P in Hogno v Fairfax Regional Printers Pty Ltd and by Roach DP in Villar v Tubemakers of Australia Pty Ltd. The test of 'main contributing factor', like that of 'substantial contributing factor', involves a broad evaluative consideration of potential competing causative factors. It should be decided on the evidence overall and is not purely a medical question.
71. In El-Achi Roche DP, considering the application of the test in s 4(b)(ii) in its current form, said:
‘That a doctor does not address the ultimate legal question to be decided is not fatal (Guthrie v Spence (2009) 78 NSWLR 225 @ [194] to [199] and [203]). In the Commission, an Arbitrator must determine, having regard to the whole of the evidence, the issue of injury, and whether employment is the main contributing factor to the injury. That involves an evaluative process’ (emphasis added).
72. I agree with the above passage from El-Achi. The Deputy President in El‑Achi also referred, in my view correctly, to the 'main contributing factor' test as 'one of causation'. This is consistent with the discussion of s 9A of the 1987 Act by the Court of Appeal in Badawi v Nixon Asia Pacific Pty Ltd. The owners referred to the 'causative element' of the test in s9A. It is consistent with the discussion in State of New South Wales v Rattenbury in which Roche DP, dealing with s4 (b) after the 2012 amendments, discussed whether 'main contributing factor' was satisfied, by reference to whether there were competing causal factors to the relevant 'disease' injury.
73. In Bradley a case involving s4 (b) (ii) in its current form, King SC ADP referred to the question posed by an Arbitrator, 'Whether or not… the [workers] work throughout his working life as a painter and decorator had been the main contributing factor to the aggravation of his shoulder disease'. The acting deputy president described this question as the correct one.”
As the Deputy President noted at [76] in AV v AW, where a relevant disease potentially involves both employment and non-employment factors, the evaluative process involves consideration of the causative role of both. It is necessary to consider firstly whether there were competing causal factors (employment and non-employment related) of the disease, and in considering those relevant contributing factors, whether employment represented the main one.
In this matter, the first step in establishing the chain of causation is to determine whether there was mould present in the workplace. If there was not, the applicant’s claim must fail.
By report dated 23 February 2019, Mr Mark Smith conducted a mould contamination validation report at the respondent's premises. The results of that testing are found at page 99 of the Application where Mr Smith says, “based on the results of the works conducted, it is also OCTIEF's opinion that active mould growth is present and may be a health risk”.
Samples were then taken from the respondent's premises including the area where the applicant worked and sent to NSS Environmental Services where they were analysed by
Mr David Lark, mycologist. In his report dated 27 February 2019, Mr Lark concluded:
“The evidence of mould detected in the samples submitted for analysis were rated at [reference to table contained within Mr Lark's report].
It was noted that the mould concentration and outside air sample was elevated and the outside air sample was high.
Genera of mould were detected in the indoor air samples that were detected in the outside air sample.
Fungal hyphae were detected – the presence of fungal hyphae is indicative of recent active mould growth and therefore constitutes a potential health hazard.
With reference to the types and levels of mould detected in the samples submitted from within the above site, genera of mould were detected which include species which, as reported by references one, three, five, seven [in Mr Lark's report] have been shown to be either:
·       Immuno-compromising; and/or
·       Allogeneic and/or
·       Mycotoxin producers."
Following these reports, remedial works were carried out at the respondent's premises, and subsequent testing indicated there was no further active mould growth.
The respondent has offered no evidence to contradict the findings of Messrs Smith and Lark. Accordingly, I am satisfied on the balance of probabilities that there was active mould growth in the area of the applicant's workplace.
Having found there was mould present in the workplace, the applicant must next demonstrate on a commonsense evaluation of the evidence that the mould was the main contributing factor to the onset of her respiratory disease. That is to say, the mere presence of mould does not establish a causal link, as correlation is not causation.
In this matter, the issue of whether the mould found in the workplace was causative of the applicant's complaints is extremely contentious.
The applicant’s original GP, Dr Balin provided two reports to the applicant's solicitors. In the first, dated 15 June 2021, Dr Balin noted:
“Vanitha Pillay’s blood serology result showed reactivity to another type of mould. Further, samples from her were sent overseas for mycotoxin testing; I am not aware of these results. There was speculation that her diagnosis was mycotoxin induced chronic illness.
Michael, the answer to whether ambient mould exposure contributed or caused her symptoms or illness is difficult. The several symptoms and signs she was having appeared diverse and not easily related to one cause. Certainly, this patient became very unwell….
Vanitha Pillay was referred by me to Dr Michael Busby, ENT specialist [at] Tugun, who treated her nose and sinus infection. She was also seen and treated by Dr Das Mutalithas, a respiratory specialist also at Tugun, who investigated and tried to control her unstable asthma. There were temporary and minimal improvements in her symptoms on these two specialist treatments.
Then Vanitha Pillay went to see Dr Sarah Wong in Chatswood who has an interest in the treatment of auto-immune disorders.
I believe treatment was started with vitamins, antioxidants and prescription medications.
On this regimen, the asthma and the reflux/stomach irritation settled. The sinusitis was under better control with regular nasal douching.
…Finally, Vanitha Pillay attended Dr Sandeep Gupta at Maroochydore. He does practice holistic medicine with a focus on environmental medicine. He added to the then current treatment and there was further improvement in energy and mood. Only occasionally would there be any sinus infection and her asthma remain controlled.
Michael, I am led to believe that the two doctors thought that Vanitha Pillay was suffering from CIRS (Chronic Inflammatory Response Syndrome).
…Although mould is an immune-system stressor and in some patients can lead to multiple symptoms and signs as well as chronic ill-health, I am unable to confirm that mould at her workplace caused her to become ill and then not recover fully or is likely to have done so. Further CIRS, (which may be in its early stages of medical understanding) could be caused by mould, but also by other agents, toxins, other substances, as well as autoimmune disorders, stress et cetera. Further confusing the question of causality, is that the mould reaction that was observed in her serology test is different to the species that was not isolated in the laboratories attempts to grow it in culture, but often the microorganism is just not detected when culture is attempted, even under ideal conditions.”
In his second report dated 8 September 2021, Dr Balin noted the applicant received ongoing treatment and nutritional support to control and/or eliminate mould. He noted aspergillus fumigatus mould was identified in the applicant's bronchoscopy in February 2019. Dr Balin continued:
“Since then, blood test reactivity to aspergillus fumigatus shows ongoing marker antibodies to this, but overall test results in the last two years also show that there is no current presence of this mould, suggesting this infection has been eradicated (negative IgE), but with persistently raised marker antibodies (IgG) to aspergillus fumigatus. In CIRS it is postulated that it is one's own antibodies that continued the inflammation and disease process.”
Mr Carney sought to rely on the findings in Dr Balin's second report as proof of a causal link between the presence of mould and the applicant's condition, however, it should be noted that Dr Balin, quite appropriately in my view, refers to nothing higher than a postulation that there is a link between the applicant’s symptoms and the alleged disease process. Moreover, Dr Balin specifically stated he was unable to confirm mould at the workplace caused the applicant to become ill.
The applicant submitted her treating respiratory physician Dr Mutalithas was attempting to treat what he thought was an infection in the applicant's nasal passages and sinus. The applicant sought to rely on the positive aspergillus serology of 12 February 2019 as an indication of the presence of organisms in the body which could have produced the relevant mycotoxin.
That proposition was, Mr Carney submitted supported by the report of Dr Gupta, who is described as a “specialist general practitioner”. There is no question that Dr Gupta has an interest in respiratory illness, however, it must be noted that he is by his own admission a vocationally registered general practitioner with postgraduate qualifications in integrative medicine and is a member of the Royal Australian College of general practitioner’s special interest group in integrative medicine.
In his report dated 21 September 2020, Dr Gupta indicates he had completed training in assessment and management of biotoxin related illness, including (CIRS) through the Centre for Research in Biotoxin Related Illness in the USA in 2017.
Dr Gupta noted he first examined the applicant on 3 July 2020 and listed her symptoms (at page 27 of the Application). Dr Gupta took a detailed history from the applicant including her employment with the respondent as a payroll officer from December 2016 to June 2020. He noted the referral of the applicant for a CT scan of the sinuses which demonstrated bilateral congestion, which was followed by referral to ENT surgeon, Dr Busby who started a new regime of oral antibiotics. In March 2018, Dr Busby undertook functional endoscopy sinus surgery.
Dr Gupta recorded that in or around September 2018 it was reported several staff members of the respondent became unwell with rashes, shortness of breath, middle ear infections and other complaints. He noted the applicant was hospitalised with severe shortness of breath and uncontrollable coughing. Around this time, the applicant was referred to a respiratory physician Dr Mutalithas. Dr Mutalithas diagnosed asthma and allergic rhinitis and started the applicant on prednisone for management.
Dr Gupta noted the aspergillus serology performed by Dr Mutalithas on 12 February 2019 was positive. Dr Gupta said “this likely indicates the presence of aspergillus organisms in the body which could have produced the ochratoxin mycotoxin. This is consistent also with aspergillus in the biotype specimens collected by total ventilation and hygiene services”.
Dr Gupta found the applicant fulfilled the criteria of potential chronic and current exposure to mould and stated there was an absence of other possible causes of illness using a differential diagnosis.
I do not accept that aspect of Dr Gupta's report. It is apparent from the treating medical material which will be discussed later in these reasons that there were other potential causes referred to by treating specialists. These included a sinus infection and inflammation, together with upper respiratory tract issues. Given the presence of these potential other causes, in my view it is necessary to give consideration to the potential competing causative factors to determine whether the applicant's exposure to mould in the workplace was the main contributing factor to her condition.

In any event, Dr Gupta’s conclusion was:
“In summary, on the basis of my thorough assessment, I conclude that the patient,
Ms Vanitha Pillay, is suffering from chronic inflammatory response syndrome due to exposure to the interior of water damaged buildings (CIRS – WDB) related to the exposure to microbial contamination at Pacific Coast Christian School, and as evidenced by history, positive cluster analysis of symptoms, positive visual contrast sensitivity, positive testing in the blood and urine and a partial response to therapy. She additionally has aspergillus rhinosinusitis on the basis of history and positive aspergillus serology and Ochratoxin A in the urine.”
Dr Gupta’s opinion stands in contrast with those of treating specialists Dr Busby,
Dr Mutalithas, and Dr Tan. Mr Carney submitted that those specialists were looking to treat the applicant’s symptoms rather than diagnosing the underlying cause.
Dr Gupta’s opinion is supported by that of Dr Sarah Wong, GP in her report dated
25 July 2019. In that document, Dr Wong noted the applicant's pathology investigations showed certain results consistent with a diagnosis of CIRS. They included DQ/DR gene type indicating a genetic susceptibility to CIRS, a high leptin level and positive urinary mycotoxins. Dr Wong stated:
“These results, along with your history, suggest the possible diagnosis of chronic inflammatory response syndrome (CIRS) as described by Dr Richie Shoemaker, MD in Maryland USA."
Dr Wong sent the applicant’s serology for testing at the Great Plains Laboratory in the United States.
There is no follow up report from Dr Wong confirming the outcome of those serology results. However, the pathology results are attached to the Application, and at page 180, the presence of eosinophilia is noted. As previously pointed out, that is the presence of greater than normal white blood cells. The pathology results note eosinophilia may occur in association with allergic and atopic disorders, parasitic infections and prosthetic devices. Less commonly, it is seen in autoimmune disease.
Dr Robertson, pharmacologist and forensic toxicologist IME W5675-22 Pillay Headnotenoted the findings of the various medical experts in his report found at page 41 of the Application.
Dr Robertson noted a urine sample collected on 23 June 2019 from the applicant was found to contain elevated concentration of Ochratoxin A, which is a mycotoxin produced by Aspergillus and Penicillium. Dr Robertson noted that the elevated concentrations of Ochratoxin in the applicant’s urine does not provide evidence of the source of Ochratoxin A, dietary or otherwise but does corroborate evidence of exposure to mould such as Aspergillus. Dr Robertson then assumes for the purposes of his findings and opinions that the applicant was exposed to mould including Aspergillus in the workplace. At page 47 of the Application, Dr Robertson noted:
“Mould and other fungi; dust mites; bacteria et cetera are ubiquitous in the environment but particularly in wet, moist areas lacking adequate inflation resulting in spores, mycotoxins, endotoxins and volatile organic compounds that often give rise to odours associated with damp and/or mouldy rooms. If inhaled or ingested one or more of these may lead to toxicity and associated health implications."
Dr Robertson sets out clearly the assumptions upon which he relied in formulating his opinion. They were:
(a)     the symptoms described the medically verifiable;
(b)     the applicant was exposed to an environment which contained mould and was exposed on a frequent and extended basis over a number of years;
(c)     there was no equal or more likely cause for the symptoms or ongoing recurrence of them, and
(d)     many of the symptoms improved while the applicant was not within the workplace.
Dr Robertson noted that at least on one occasion, the applicant underwent allergen testing which was negative. However, in February 2019 a blood sample had elevated Aspergillus fumigatus IgG levels. Dr Robertson then quite appropriately notes:
“I am not an immunologist or allergist and as such I cannot comment on the significance of these results with respect to ruling out any allergic response to any mould. These results would however appear to suggest that any mould related symptoms were likely due to a combination of mycotoxins and an immune response.”
Dr Robertson’s concession to the expertise of other medical experts is appropriate and well-reasoned. Given Dr Robertson's concession, it is appropriate to consider the views of any immunologist or allergist who have provided opinions in this matter.
The relevant immunologist/allergist report in this matter is from Dr Tan, found at page 155 and following of the Application. Dr Tan provided a report dated 22 March 2019, in which he found the following on examination:
“On examination today, her chest was clear. She was not tender in the sinus and there was mild nasal congestion. She has ongoing concern whether she has allergy to mould or whether this is due to mycotoxin. As far as allergy is concerned, I went through her specific IgE testing result and noted that she had normal total IgE, and her specific IgE were negative to mould mix, the pteronyssinus, grass mix, animal dander mix and trees mix.
Her symptoms and results would suggest chronic rhinosinusitis and eosinophilic asthma. Given her concern, I have asked for specific IgE to the individual mould species tested and also to aureobasidiums which was found at her workplace (I am not certain if this is available though). I am uncertain with the mycotoxins/biotoxin in her illness.”
Dr Tan concluded the applicant’s symptoms and results would suggest chronic rhinosinusitis and eosinophilic asthma. He was at best uncertain of the role of mycotoxins/biotoxins in the applicant's illness. On balance, Dr Tan's opinion in my view does not provide assistance to the applicant in establishing a causal link between the presence of mould at the workplace and the applicant's condition.
Dr Busby, treating ENT specialist provided a number of reports to the applicant’s GP
Dr Balin. During the course of those reports, Dr Busby noted the applicant was of the view her symptoms reported over the course of several years were mould related. They included skin lesions on her upper neck, ongoing “brain fog”, and scattered changes throughout her sinuses and upper respiratory tract. In a report dated 20 May 2019 which also copied in
Dr Mutalithas, Dr Busby noted the applicant had a normal IgE but was “quite convinced that all of her symptoms have been caused by mould in the air-conditioning system at work”.
Dr Busby provided a report to the applicant's solicitors dated 31 August 2022. He recorded the following:
“In March 2018, she underwent sinus and nasal surgery with me at John Flynn Hospital. Initially this helped, but she has seen me multiple times since then with continuing ongoing postnasal drip which bothers her immensely.
Vanitha has also been under the care of a respiratory physician for asthma symptoms.
Vanitha’s nasal symptoms seem to have plateaued. Her CT scan shows that she still has inflammation of the mucosa of her sinuses, and so I have discussed further sinus surgery to both open up some of the remaining sinuses, and to take some biopsies (she has two sisters with sarcoidosis).
Vanitha reports significant exposure to mould at her workplace and is convinced that this is the cause of her symptoms. She has had various blood test organised by her other doctors, but her IgE results that I have seen have been normal.
Vanitha’s counsel for interactions with other health professionals are vast and difficult to follow – as I do not know of many of the people she refers to. It is difficult to ascertain whether all of the advice that she has been given is mainstream or not.”
Dr Busby then diagnosed her clinical history and examination including nasal endoscopy, CT scans for the sinuses, and blood tests. He concluded the applicant’s normal IgE levels would make allergic fungal sinusitis less likely than not. When asked to provide a prognosis and discussion on causation, Dr Busby said:
“Unlikely to resolve without treatment. We have exhausted the usual nonsurgical options. Further limited surgery is still an option – I have suggested this during appointment in the last six months at least – it does have a good chance of providing some improvement, but this is unlikely to completely resolve her symptoms. I would also like to take biopsies at the time of surgery to look for other causes and to assess the likelihood of allergic fungal sinusitis.
In summary, I have not been able to prove that Ms Pillay has fungus/mould causing any of her symptoms, however it is certainly possible. A biopsy of her sinus mucosa may be useful in confirming that or other causes. An adequate biopsy would be best done under anaesthetic and at the same time as further sinus surgery if she decides to proceed with that. I have also suggested that seeing an allergist would be useful. I have done a referral and she is in the process of organising that.”
There is no report from any allergist which postdates the last report of Dr Busby in August 2022. Indeed, the only allergist report in the matter is that of Dr Tan from 2019, which has previously been discussed and which does not provide evidence of a causal connection between the mould at the applicant’s work and her ongoing condition.
Dr Mutalithas, treating respiratory physician tested the applicant for IgG, IgE and RAST antibodies. He concluded he had “done some invitro allergen tests and all have come back negative. Total IgE levels were also not elevated. Blood counts in the past have, however, shown eosinophilia”.
Dr Mutalithas also provided a number of reports in which he discussed the possibility of mould related infection. In September 2018, Dr Mutalithas noted invitro allergen tests for the applicant had all come back negative, while total IgE levels were also not elevated.
On 12 February 2019, Dr Mutalithas noted the applicant's intense treatment for sinus issues arranged by Dr Busby, and commented as follows:
“Things appeared to have flared few weeks ago and this seems to have coincided with the discovery of mould at the workplace. I gather one of her work colleagues was also unwell with it and judging by her description appears to have had an infection of some sort which needed a protracted course of antibiotic therapy.
He had heard her wheezing at your surgery and this was certainly the case here as well. Chest auscultation revealed wheeze from both sides. Strangely I have not been able to demonstrate airflow limitation or response to bronchodilator from the lung function test from her to date.
She was concerned about the fungal exposure and whether she may have an active fungal infection. Clinically, I suspect her sinuses have flared and the postnasal discharge is probably aggravating matters. I have asked her to increase her Pulmicort rinses to everyday and the prednisone to 15 milligrams a day, at least for a week before dropping down to 5 milligrams daily. I have left the Seretide dose as it is.
I am going to order serology looking into sensitisation to a panel of common airborne fungi. I will also include some other specific IgE and blood count as well. She was worried that there might be fungal colonisation in the airways and want this looked into so I will arrange a bronchoscopy and hopefully could provide her with some reassurance.”
In a follow-up report to Dr Balin dated 27 February 2019, Dr Mutalithas noted the investigations which had taken place, particularly with regard to fungal infection within the lungs. He said he was “able to reassure her that the bronchoscopy did not show any abnormality and the bronchial wash aspirate did not show any fungal hyphae”. The other findings in relation to the testing were:
"Total IgE was not elevated and specific IgE to a mixture of moulds including Cladosporium was absent.
The lung function tests this time, however, did show airflow limitation and there is a bronchodilator response.…
It appears that Vanitha has eosinophilic asthma with significant rhinosinusitis as well. I have made some medication changes to optimise the anti-inflammatory therapy as well as bronchodilation….
At this stage she seemed more concerned about finding out what the mould was at the workplace that triggered all of this. She enquired about blood test for myotoxins which I am not very familiar with. She may be seeing you shortly for referral to see an immunologist and possibly even in myotoxologist.”
Dr Mutalithas then saw the applicant again in June 2019 and noted an overall improvement in her symptoms.
Before turning to the IME evidence in this matter, it is worth noting the state of treating medical opinion therefore appears to be that GPs Dr Wong and Dr Gupta are of the view the applicant’s condition relates to workplace mould, whereas treating specialists Dr Tan (immunologist), Dr Mutalithas (respiratory physician) and Dr Busby, (ENT specialist) do not accept that this is the case. Dr Balin, GP states he is unable to state mould exposure was the cause of the applicant’s illness.
Dr Burke, IME for the respondent is an occupational physician who provided reports dated
24 September 2019 and 16 October 2019. Dr Burke noted the presence of mould spores in the air can induce allergic reaction or asthma symptoms if individuals are sensitive and exposed. He noted, however, there are hundreds of types of moulds, and not all of them are responsible for causing allergic symptoms. Dr Burke stated the most common allergy causing moulds include Alternaria, Aspergillus, Cladosporium and Penicillium. He noted there was a possibility that the applicant’s symptoms could be associated with exposure to fungi. Dr Burke indicated, however, the testing which had been done did not specifically point to a specific causation by the mould which had been identified at the respondent's premises. Dr Burke diagnosed probable chronic rhinosinusitis and eosinophilic asthma.
Dr Burke summarised and assessed the applicant’s condition as follows:
“She has been intensively investigated by an ENT specialist, a respiratory physician, a gastroenterologist and an immunologist. There is consensus among her treating specialists that she has developed an eosinophilic asthma (which is now reasonably well-controlled) as well as chronic rhinosinusitis. She continues to report ongoing symptoms associated with this.
Orthodox allergen testing has not revealed any specific allergies, and there is no evidence demonstrated thus far to suggest the fungi to which she may have been exposed have been responsible for the sinusitis or the asthma.”
Dr Burke relied upon the absence of any findings in the tests carried out to opine there is no causal link between the applicant's exposure to any mould at work and her condition.
In a further report dated 19 April 2021, Dr Burke also considered the views of Dr Robertson and Dr Gupta. He considered additional material shown to him provided evidence of exposure to mould, but no evidence to demonstrate a true allergic response, because all of the orthodox assessments by appropriate specialists have not demonstrated a convincing biological link between the condition which the applicant was diagnosed with and her mould exposure. Dr Burke reiterated that paint exposure could have resulted in short-term exacerbation of the applicant’s symptoms but would have ceased within approximately two weeks of the cessation of exposure to the paint fumes.
As noted, Dr Burke's findings were a diagnosis of chronic rhinosinusitis and probable eosinophilia. Dr Burke was of the view that exposure to paint during workplace renovations could possibly have resulted in a short-term exacerbation of respiratory symptoms, but those would have resolved upon the cessation of exposure to the paint fumes. Dr Burke was unable to conclude that mould had resulted in the development of any of the applicant’s symptoms.
The respondent also relied on a report by Dr Howison, ENT surgeon. For his part, Dr Howison concluded the applicant's exposure to mould and paint had not contributed to her current medical problems and that a diagnosis of CIRS is not considered by the Royal Australian College of Physicians to be a valid diagnosis.
In his initial report, Dr Howison commented on Dr Gupta’s remarks concerning a Department of Health investigation as to any causal relationship between exposure to biotoxins and unexplained complex symptoms which make up a diagnosis of CIRS. Dr Howison noted:
“The Department of Health stated evidence, at this stage, is lacking that there is a causal relationship between exposure to environmental biotoxins and the nature of these essentially unexplained symptom complexes.”
The Royal Australian College of Physicians agreed and stated ‘sufficient research has not been conducted nor consensus reached for the term biotoxin related illnesses or CIRS to be used as a valid diagnostic label’.”
Dr Howison agreed with Dr Burke that paint exposure may result in a short-term exacerbation of respiratory symptoms, however, once the applicant was removed from exposure to the paint, the symptoms would not be expected to last for more than two weeks. He said there is no evidence that mould has resulted in the development of chronic rhinosinusitis and therefore he felt that the applicant's work was not a “substantial contributing factor” to Ms Pillay’s ongoing symptoms.
At this point, it is worth reiterating, consistent with the decision in AV v AW, that if something is not a substantial contributing factor to a condition, it by definition cannot be the main contributing factor.
In a supplementary report dated 18 March 2021, Dr Howison specifically noted Dr Gupta’s report in which he diagnosed the applicant is suffering from CIRS due to exposure to microbial contamination in the workplace. He reiterated his view that CIRS is not considered by the Royal Australian College of Physicians to be a valid diagnosis. He also indicated that he had read Dr Robertson’s report and it did not change Dr Howison’s opinion.
Dr Howison then provided a further report dated 13 October 2022. In that document,
he was specifically asked to address the issues raised in the supplementary reports of Dr Gupta, Dr Robertson, and Dr Busby together with the other GP Dr Balin and indicated those documents did not alter his opinion.
For the respondent, Mr Stockley submitted the applicant has consulted self-styled experts in myotoxins, however, the actual qualifications of those doctors go little beyond those of a GP.
Whilst that submission is in my view correct, the fact an opinion is provided by a GP does not disqualify it from being accurate.
Nevertheless, not one specialist opinion in this matter, treating or medicolegal, finds a causal connection between the applicant’s exposure to mould and her ongoing problems. Whilst Dr Robertson’s report was helpful in establishing the toxicity of various moulds in general and clearly stated the assumptions on which he relied, he expressly deferred to the findings of other experts when commenting in his report on questions of causation.
I am unable on the balance of probabilities to find the requisite causal connection between the applicant’s mould exposure in the course of her employment with the respondent and the applicant’s alleged disease injury. The applicant has the onus of proving such a connection and has not done so.
Whilst the applicant has plainly suffered a serious respiratory condition, including inflammation to the sinuses and chest, her condition has been the subject of examination by acknowledged experts in the field such as Dr Mutalithas, Dr Tan and Dr Busby. None of those treating experts conclude the applicant’s condition was caused by exposure to workplace mould.
I accept Mr Stockley’s submission that the approach of Drs Wong and Gupta is to assert the presence of mould is probative of causation, however, the moulds in question are in fact common and ubiquitous. Those doctors have, in my opinion, barely taken into account the treating specialist opinion, including the findings of some improvement following treatment to the applicant’s sinuses – itself suggestive that the cause of the condition was something other than mould.

The applicant must demonstrate some evidence which would be sufficient to ground a common-sense finding of a causal connection between the presence of workplace mould and the applicant’s condition.
In my view, the competing causal explanation is on balance more compelling, namely that the applicant is prone to sinusitis and asthma, and that if a fungal agent had anything to do with the development of her condition (which I find has not been established), that agent is ubiquitous and there is no sufficient causal connection established between the onset of her condition and the mould in the workplace.
On balance, I am not satisfied that the applicant has discharged her onus of proof in establishing exposure to mould in the workplace was causative of her condition. Notwithstanding, Dr Gupta and Dr Wong’s opinions, established treating experts in the field of ear, nose and throat medicine, respiratory medicine, immunology/ allergens and her regular treating GP all support the views espoused by Drs Howison and Burke, namely that there is insufficient evidence of a causal link between mould exposure and the applicant’s condition.
I find those opinions compelling. Given the competing diagnoses between chronic sinusitis and rhinosinusitis against that of CIRS, it is incumbent that the applicant demonstrates the latter is the main contributing factor to her condition.
On balance, I cannot be satisfied this is the case. For the above reasons, there will therefore be an award for the respondent in this matter.

[2023] NSWPIC 74

28 February 2023