Nonconformist Pty Ltd v Fisher - [2021] NSWPICPD 26

DETERMINATION OF APPEAL AGAINST A DECISION OF THE COMMISSION CONSTITUTED BY A MEMBER
CITATION:	Nonconformist Pty Ltd v Fisher [2021] NSWPICPD 26
APPELLANT:	Nonconformist Pty Ltd
FIRST RESPONDENT:	Kerry Lillian May Fisher
SECOND RESPONDENT:	Mark Barry Clifford
THIRD RESPONDENT:	Nicole Megan Clifford
INSURER:	AAI Limited t/as GIO
FILE NUMBER:	A1-948/20
MEMBER:	Mr G Edwards
DATE OF MEMBER’S DECISION:	18 December 2020
DATE OF APPEAL DECISION:	19 August 2021
CATCHWORDS:	WORKERS COMPENSATION – epidemiological evidence and the question of causation – Amaca Pty Ltd v Booth [2011] HCA 53; Seltsam Pty Limited v McGuiness; James Hardie & Coy Pty Limited v McGuiness [2000] NSWCA 29; 49 NSWLR 262; 19 NSWCCR 385 discussed and applied – principles applicable to establishing error in accordance with s 352(5) of the Workplace Injury Management and Workers Compensation Act 1998 – Raulstonv Toll Pty Ltd [2011] NSWWCCPD 25; Henderson v Foxworth Investments Ltd [2014] UKSC 41; SLT 775; 1 WLR 2600 applied
PRESIDENTIAL MEMBER:	Deputy President Elizabeth Wood
HEARING:	On the papers

REPRESENTATION:	Appellant:
Mr S McMahon, counsel
Hicksons Lawyers
First Respondent:
Mr D Adhikary, counsel
Shanahan Tudhope Lawyers
Second Respondent:
Mr A J Parker, counsel
Stacks/Goudkamp
Third Respondent:
Mr T Hickey, counsel
Slater & Gordon
ORDERS MADE ON APPEAL:	1. The Certificate of Determination dated 18 December 2020 is revoked. 2. The matter is remitted to a different member for re-determination.

INTRODUCTION AND BACKGROUND

Mr Terry Clifford (the deceased) was employed by Nonconformist Pty Ltd (the appellant) as a courier driver. He was the sole director of that company and performed courier services through a sub-contract arrangement between the appellant and Direct Couriers (Aust) Services Pty Ltd (Direct Couriers). On 22 January 2016, in the course of his employment, the deceased died while driving his van through Campvale, New South Wales during his last delivery run for that day.
The death certificate issued on 18 February 2016 listed the cause of death as ischaemic heart disease and coronary artery atherosclerosis.[1] The autopsy report prepared for the coroner listed the direct cause of death as ischaemic heart disease with an underlying condition of coronary artery atherosclerosis as an antecedent cause.[2]
[1] Application in Respect of the Death of a Worker (ARDW), p 10.
[2] ARDW, pp 11–13.
Ms Kerry Fisher, the wife of the deceased, lodged a claim for workers compensation on the basis that she was dependent upon the deceased. The claim was denied by the appellant. The appellant disputed that:
(a) the deceased’s death resulted from an injury in the course of his employment within the meaning of s 4 of the Workers Compensation Act 1987 (the 1987 Act);
(b) the deceased’s employment was a substantial contributing factor to any injury as required by s 9A of the 1987 Act;
(c) the nature of the deceased’s employment gave rise to a significantly greater risk of injury than if he had not been employed in employment of that nature, as required by s 9B of the 1987 Act, and
(d) if the injury was a disease within the meaning of s 4 of the 1987 Act, the disease was not contracted in the course of employment and the deceased’s employment was not the main contributing factor to the injury or the aggravation of the injury.[3]
[3] Appellant’s notice issued pursuant to s 74 of the Workplace Injury Management and Workers Compensation Act 1998 (the 1998 Act), ARDW, pp 39–42.
Ms Fisher commenced proceedings against the appellant in the Workers Compensation Commission, claiming lump sum compensation in respect of her dependency upon the deceased, in accordance with s 25(1)(a) of the 1987 Act. The deceased’s two adult children, Mr Mark Clifford (the second respondent) and Ms Nicole Clifford (the third respondent), also claimed they were partly dependent upon the deceased, and were joined to the proceedings, claiming apportionment of the lump sum in accordance with s 29 of the 1987 Act.
The matter proceeded to arbitration on 30 October 2020. The question of apportionment was deferred until after the Arbitrator had determined whether the appellant was liable to pay the compensation claimed. The Arbitrator issued a Certificate of Determination on 18 December 2020, in which he found that the appellant was liable to pay the compensation claimed. The outstanding issues of dependency and apportionment were remitted to the Registrar in order for the Registrar to fix a date for further arbitration.
The appellant appeals from the decision of the Arbitrator.

ON THE PAPERS

Section 52(3) of the Personal Injury Commission Act 2020 (the 2020 Act) provides:
“(3) If the Commission is satisfied that sufficient information has been supplied to it in connection with proceedings, the Commission may exercise functions under this Act and enabling legislation without holding any conference or formal hearing.”
The appellant, the first respondent, and the third respondent submit that it is appropriate for the appeal to be determined ‘on the papers.’ The second respondent indicates that the appeal can be decided on the papers but, given the nature of the matter, if it is determined that it is appropriate to conduct an oral hearing, it consents to that course.
I have had regard to Procedural Directions PIC2 and WC3, the documents that are before me, and the submissions made by the parties in this appeal. I note that the appellant, the first respondent and the third respondent submit that the appeal can proceed to be determined on the basis of the documents and the submissions before me and that the second respondent does not object to that approach. I see no reason why an oral hearing is required. I am satisfied that I have sufficient information to proceed ‘on the papers’ without holding any conference or formal hearing and that this is the appropriate course in the circumstances.

TRANSITIONAL MATTERS

After this case had been heard and determined and before the appeal in this matter was allocated to me, the New South Wales Workers Compensation Commission was abolished.[4] The matter became a matter within the Workers Compensation Division of the Personal Injury Commission by operation of the 2020 Act, from 1 March 2021.[5] The 2020 Act amended certain parts of the 1998 Act. Relevantly, the Arbitrators of the former Workers Compensation Commission became non-presidential members of the Personal Injury Commission, and thus the decision-maker involved in these proceedings became a member of the Personal Injury Commission. However, as at the time of the various orders made in the proceedings, the decision maker bore the title of Arbitrator, in this decision he will be referred to by his former title of “Arbitrator”.
[4] Clause 3 of Div 2 of Pt 2 of Sch 1 to the 2020 Act.
[5] Clause 12(1) of Div 2.3 of Pt 2 of the 2020 Act.

THRESHOLD MATTERS

There is no dispute between the parties that the threshold requirements as to quantum and time pursuant to ss 352(3) and 352(4) of the 1998 Act have been met.
Subsection 352(3A) of the 1998 Act provides:
“There is no appeal under this section against an interlocutory decision except with the leave of the Commission. The Commission is not to grant leave unless of the opinion that determining the appeal is necessary or desirable for the proper and effective determination of the dispute.”
The parties are of the view that the Arbitrator’s determination is (at least probably) not interlocutory in nature. The Arbitrator’s determination was conclusive of the issue between the parties in relation to the appellant’s liability to pay compensation. The issues of dependency and apportionment are yet to be determined. There are, therefore, further issues between the parties which are outstanding.
At the relevant time, subsection 352(1) of the 1998 Act provided for an appeal “against a decision in respect of the dispute by the Commission constituted by an Arbitrator” (emphasis added). A “decision” is defined in subs 352(8) to include “an award, interim award, order, determination, ruling and direction”.
The meaning of “interlocutory” in subs 352(3A) of the 1998 Act is undefined.
In Licul v Corney, Gibbs J (as his Honour then was) said (footnotes omitted):
“The distinction between final and interlocutory judgments is not always easy to draw and there has been disagreement as to the test by which the question whether a judgment is final or interlocutory is to be determined. One view - which was preferred by the Court of Appeal in Salter Rex and Co v Ghosh - is that the test depends on the nature of the application made to the Court. The other view which, since Hall v Nominal Defendant, should, I think, be regarded as established in Australia, depends on the nature of the order made; the test is: Does the judgment or order, as made, finally dispose of the rights of the parties?”[6]
[6] [1976] HCA 6; 180 CLR 213, [11].
The observations of the High Court as to what constitutes an interlocutory order provide some guidance but need to be considered in the context of the legislative and procedural framework of the Commission.
There are a number of presidential decisions in which the distinction between an interlocutory decision and a final decision is discussed. The observations made by Deputy President Roche in EdmundDiab v Salem Naji,[7] in which the Arbitrator determined the liability issues and then remitted the matter to the Registrar for referral to an approved medical specialist, are relevant, He said:
“The Arbitrator’s order concerning remitter has been made following his determination of a question concerning liability, that is, the occurrence of injury to both the neck and back. The determination of those issues was made as required by the provisions of section 293(3) of the 1998 Act ...
The Arbitrator’s determination concerning the dispute as to the nature of the injury received by Mr Naji is such that, in the words of Gibbs J, it does ‘... finally dispose of the rights of the parties.’ Those findings are conclusive, and bind the parties and define the rights and liabilities of each concerning the various heads of entitlement to compensation benefits as provided by the Acts. The Appellant, on this appeal, challenges those findings of fact made by the Arbitrator concerning injury. In the circumstances, I conclude that the Arbitrator’s decision, including those findings of fact, is not one of an interlocutory nature within the meaning of section 352(8).”[8]
[7] [2010] NSWWCCPD 33 (Naji).
[8] Naji, [20]–[21].
I am of the view that, given the nature of the determination made by the Arbitrator, the appellant’s liability has been conclusively determined and is final and binding in respect of its obligation to pay the lump sum entitlement under s 25(1)(a) of the 1987 Act to either those who are dependents of the deceased or the deceased’s legal representative. I conclude that the determination the subject of this appeal is not interlocutory in nature. Leave to appeal is therefore not required.

THE EVIDENCE

The lay evidence

Ms Judith Hannah

The human resources manager from Direct Couriers, Ms Judith Hannah, wrote to the appellant’s claims adviser on 3 February 2016.[9] Ms Hannah informed the claims adviser that:
(a)    the deceased resided in Woy Woy, NSW, and drove a one tonne van performing courier work for Direct Couriers on a sub-contract basis;
(b)    on 22 January 2016, the deceased logged on for work at his home at 5.59 am;
(c)    pursuant to that contract, on that day, the deceased proceeded straight to the first pick up for the day, collected a package from Banksmeadow, Sydney at 8.34 am, and a package from Botany. He then travelled to Silverwater and proceeded to Arndell Park, arriving there at 11.17 am. Ms Hannah said that the deceased then had a break (probably for lunch), following which he proceeded to Medowie on the Central Coast to deliver his last job, and
(d)    the accident occurred at 2.56 pm, when the deceased was in the process of delivering that parcel.
[9] ARDW, pp 2–3.

Mr Simon Ross

Mr Simon Ross, the step-son of the deceased, provided a statement dated 15 March 2018.[10] He advised that, for the period of three months from July 2015, he agreed to take on the deceased’s deliveries while the deceased travelled overseas.
[10] ARDW, pp 49–50.
Mr Ross confirmed that part of the role required pick up of animal body parts in coolers from abattoirs in Scone and Aberdeen NSW and delivery of them to Sydney Airport for export to the United States of America. He said he would start the day at 4.30 am, arrive at the airport by 7 am, return home and sleep until midday. He would then travel to the abattoirs to collect the deliveries for the next day and finish at 7 or 8 pm.
Mr Ross advised that other jobs would come through during that time, which he was required to accept, and the work was demanding and stressful, with some of the jobs in places that were difficult to locate.

Ms Kerry Fisher

Ms Fisher provided a statement dated 13 July 2018.[11] She confirmed the working arrangements between the appellant and Direct Couriers and that on the date of the accident, the deceased left for work at 6 am. She advised that, prior to that day, the deceased had no known serious health conditions and was not diagnosed with any disease.
[11] ARDW, pp 51–54.
Ms Fisher said that she spoke with the deceased at about midday that day when she expressed her concerns about the deceased’s long hours and pressure of work. The deceased indicated that he would be home earlier than usual at 4 pm that day. Ms Fisher referred to the police coming to her home at about 4 pm to advise that her husband was killed in the motor vehicle accident. She further referred to a conversation with the coroner the following day, in which she was advised that the cause of death was ischaemic heart disease.
Ms Fisher confirmed that part of the deceased’s role was to pick up animal parts from the abattoirs and deliver them to the airport and he would leave for work at 5 or 5.30 am and return home at 10.30 am. She said he would leave again at 1 pm. She said:
“Terry spent many hours on the road. He did a lot of driving and was sedentary for most of the time. He spent on average approximately 11 to 12 hours per day driving between locations and back home. … he was on the road a long time alone. He couldn't say no to a job, he was expected to complete every delivery.”[12]
[12] Ms Fisher’s statement, [14]–[16], ARDW, p 52.
In a short supplementary statement dated 6 February 2019, Ms Fisher confirmed that the deceased was a non-smoker, rarely consumed alcohol and that there was no history of heart disease in the deceased’s family.[13]
[13] ARDW, p 55.
Ms Fisher provided a further statement dated 30 July 2020, following review of the letter from Ms Hannah of Direct Couriers.[14] Ms Fisher stated that, prior to the first parcel pickup at Banksmeadow mentioned by Ms Hannah, the deceased was required to deliver animal body parts (which he had picked up the day before) to Sydney Airport and then proceed to Banksmeadow. Ms Fisher explained that the reason that this trip was not recorded in the deceased’s duties on the date of his death was that, because the delivery had been picked up on the day prior to 22 January 2016, that delivery was logged as a collection for 21 January 2016. Ms Fisher added that, from her knowledge of the deceased’s practices, he was most likely to have stopped for coffee after the pickup at Banksmeadow.

The medical evidence

[14] Application to Admit Late Documents (AALD) dated 28 July 2020, unpaginated.

Dr Garry Helprin, consultant physician and cardiologist

Ms Fisher’s legal representatives qualified Dr Garry Helprin to provide an opinion in relation to any potential connection between the deceased’s employment and his death. Dr Helprin provided a number of reports.
In his report dated 5 December 2019, Dr Helprin reviewed the deceased’s medical records and job description, together with the statements of Ms Fisher and Mr Ross.[15] Dr Helprin observed that it was agreed that the autopsy report disclosed an old myocardial infarct and narrowing of the artery but that this pathology was not the direct cause of death, and that the deceased most likely suffered a ventricular fibrillation and cardiac arrest. He explained that ventricular fibrillation is a highly lethal abnormal heart rhythm, which was a new injury or condition superimposed on the deceased’s pre-existing coronary heart disease, and which caused the death.
[15] ARDW, pp 56–58
Dr Helprin referred to eight documented scientific studies about the association between ventricular fibrillation, ventricular arrhythmia, or cardiac arrest, and the association with air pollution. He observed that:
(a) one of those studies demonstrated an increased risk of ventricular arrhythmias on short term exposure to air;[16]
(b) two studies demonstrated the association between air pollutants and out of hospital cardiac arrest after short term exposure, the first after one to two days of exposure which was dose dependant, noting that patients with conventional cardiovascular risk factors were more susceptible[17] and the second describing the risk of cardiac arrest as “high;”[18]

(c) one study concluded that larger studies had “suggested” an increased risk of out of hospital cardiac arrest with air pollution exposure,[19] and
(d) a further study found that there appeared to be an association after moderate levels of exposure, where the patients were fitted with an implantable defibrillator, but suggested larger studies were required to confirm the findings.[20]
[16] Rich et. al. in American Journal of Epidemiology Volume 161, No. 12, 2005, pp 1123–1132, ARDW, pp 100–109.
[17] Kang et. at. in International Journal of Cardiology Volume 203 (2016) pp 1086–1092, ARDW, pp 86–92.
[18] Zhao et. al. in International Journal of Cardiology Volume 226 (2017) pp 110–117, ARDW, pp 70–77.
[19] Teng et. al. published in Journal of Epidemiology and Community Health, Volume 68, No. 1, January 2014 pp 37–43, ARDW, pp 78–85.
[20] Ljungman et. al. published in European Heart Journal 2008, Volume 29, pp 2894–2901, ARDW, pp 59–66.

The remaining studies were:
(a)    a study of the association between air pollution and ventricular tachyarrhythmias in an East Asian city;
(b)    an experimental study on animals, and
(c)    a study about stress induced cardiac arrhythmias.
He said that it was important to note that people with cardiovascular risk factors were more susceptible to harm and that nobody could deny that working as a courier driver in the Sydney environs was highly stressful. He noted that, of the various studies provided, studies done in the United States and in metropolitan East Asia (Seoul, Korea) showed a connection between exposure to air pollution and increased incidents of ventricular tachyarrhythmia or ventricular fibrillation. He further noted that one study concluded that there was an association between short term exposure to pollutants and a higher risk of cardiac arrest.
Dr Helprin addressed several queries put to him by Ms Fisher’s legal representatives. He responded that:
(a)    while the sedentary nature of the deceased’s work was not a main factor in causing an aggravation of the deceased’s heart disease, it could be an additional aggravating factor;
(b)    the deceased’s workplace was prone to pollution;
(c)    the deceased had not previously suffered ventricular fibrillation, and
(d)    the scientific studies discussed certainly showed that ambient air pollution in metropolitan areas is a direct cause of ventricular fibrillation, particularly where there is an existing vulnerability.
On the basis of those observations, Dr Helprin formed the view that it was undoubtable that the deceased was exposed to environmental air pollution as well as stress in his work as a courier driver, which factors were the predominant cause of the deceased’s ventricular fibrillation and death. Copies of the scientific literature discussed were attached to Dr Heprin’s report.

Dr Helprin provided a supplementary report dated 17 February 2020 in response to further questions posed by Ms Fisher’s legal representatives.[21] He confirmed that, in his opinion, the ventricular fibrillation was a separate injury. That is, the heart muscle damage caused by the blocked artery was pre-existing, and the ventricular fibrillation was a separate condition because it was an electrical disturbance to the heart, rather than a vascular injury. Dr Helprin further confirmed his opinion that the deceased’s employment as a long-distance courier driver exposed the deceased to ambient air pollution that most likely triggered the electrical disturbance, which would otherwise not have occurred. He considered that the exposure constituted a substantial contributing factor to the ventricular fibrillation, which occurred in the course of the deceased’s employment. He added that the cardiological scientific literature discussed “quite widely and internationally recognises that ventricular fibrillation is causely [sic] related to exposure to ambient pollution.”[22]
[21] ARDW, pp 116–117.
[22] ARDW, p 117.

Dr Mark Herman, cardiologist

The appellant arranged for Dr Mark Herman to provide a file review and opinion on its behalf. He was provided with documentation relating to the deceased’s employment, as well as the clinical notes and report from Dr Ivits (the deceased’s treating general practitioner), the autopsy report, the ambulance report and the coroner’s brief of evidence. Dr Herman reported to the appellant on 4 March 2019.[23]
[23] Appellant’s Reply to ARDW (reply), pp 8–13.
Dr Herman noted the clinical history of hypercholesterolaemia, hypertension, impaired fasting glucose and depression, which were conditions strongly associated with cardiovascular risk. He further noted that, at autopsy, the deceased was found to have significant coronary artery disease and myocardial infarction associated with left ventricular hypertrophy. Significant disease in the left and right arteries was also found. Dr Herman referred to the clinical notes that disclosed that, on 17 March 2012, the deceased complained of chest pain which was thought to be musculoskeletal. Dr Herman considered that the symptoms may have been due to cardiovascular disease.
Dr Herman described the circumstances of the motor vehicle accident and the observations made by police shortly thereafter. He was of the view that it was likely that the deceased suffered a sudden cardiac event prior to his accident, which was probably due to ventricular fibrillation occurring on a background of the existing prior conditions. Dr Herman observed that, in the context of those pre-existing conditions, the annual mortality rates ranged from 3%–10%, of which half are sudden and resulted from a cardiac arrhythmia.
Dr Herman confirmed that the medical cause of death was cardiac arrhythmia (ventricular tachycardia and fibrillation), which is not uncommon in people who have suffered previous myocardial infarcts, and particularly, as in the deceased’s case, if the infarct involved the anterior wall. He said that it was most likely that the arrhythmia occurred while the deceased was driving and, on the basis of the extent of the observations made shortly afterwards, the deceased would not have been able to be saved before the vehicle hit the tree.
Dr Herman concluded that the deceased’s significant coronary artery disease, together with the prior myocardial infarction was a disease contracted in the course of his employment, but the deceased’s employment was not a significant contributing factor to the contraction of the disease. Dr Herman also considered that the deceased’s employment did not cause an aggravation, acceleration, exacerbation or deterioration of the disease. He said that, because of the deceased’s age, the pre-existing pathology and the evidence of a prior myocardial infarction, there was a substantial risk of the sudden arrhythmic cardiac death.
Dr Herman was of the firm view that the deceased’s employment did not contribute in any way to his pre-existing coronary heart disease or the ischaemic event that provoked the fatal arrhythmia on the date of death. Dr Herman said that the deceased’s sedentary lifestyle was not the main contributing factor to the aggravation of the disease. He explained that that proposition would mean that any sedentary worker would be at risk, and employers would be responsible in circumstances where a worker working alone suffered an arrhythmic event. He said that that was a proposition with which he did not agree. Nor did Dr Herman believe that driving provoked the arrhythmia.
Dr Herman maintained that, given all of the potential relevant factors, he did not believe that the nature of the deceased’s employment as a courier driver, driving alone, would give rise to a significantly greater risk of suffering the injury than he would have had if he was employed in employment of a different nature.
Dr Herman provided a supplementary report dated 16 April 2020, following receipt of the reports of Dr Helprin, together with the “journal articles” referred to by Dr Helprin in his report.[24] Dr Herman conceded that there was an association between air pollution and “out of hospital” cardiac arrest or, in the alternative, the onset of ventricular fibrillation, which he described as “modest” in comparison to the conventional risk factors. He commented that the pathophysiological mechanism of how air pollution impacts upon cardiovascular disease was unclear.
[24] Appellant’s AALD dated 11 June 2020, pp 1–5.
Dr Herman reviewed the scientific documentation, identifying that:
(a)    the conclusion reached by Teng et al in Journal of Epidemiology and Community Health 2014 was that the association between out of hospital cardiac arrest and short term exposure to ambient minute separate particles (particulate) matter was inconsistent, and larger studies were required;
(b)    most of the evidence from that study appeared to relate to particulate matter of 2.5 (PM2.5) micrograms per cubic metre;
(c)    the study presented in the Journal of Cardiology Volume 203 (2016) was performed in Korea, where the median PM2.5 in Seoul was 22.6 micrograms per cubic metre, as opposed to 4.8 micrograms per cubic metre in Melbourne and 6.8 micrograms per cubic metre in Perth;
(d)    all of the studies relied upon by Dr Helprin were heterogenous and could be distinguished from the factors present in this case, and
(e)     the nature of the exposure estimates in the studies was imprecise.
In relation to the study be Teng et al, Dr Herman observed:
“In a systematic review of air pollution and incidents, of out of hospital cardiac arrests reported by Tang et al. Journal J Epidemiology Community Health 2014; 68: 37-43, the conclusion is that the association between out of hospital cardiac arrest and short-term exposure to ambient particulate matter is inconsistent and that larger studies are required for more definitive data. … Moreover, it appears to be particulate matter of 2.5 [micrograms per cubic metre] which has the most evidence.”[25]
[25] Report dated 16 April 2020, AALD dated 11 June 2020, p 2.
He quoted the following passage from the conclusion in that study:
“There has been increasing evidence that support[s] the association of ambient air pollution with overall cardiovascular mortality and morbidity. However, inconsistent results have been found in the relationship between out of hospital cardiac arrest and air pollution.”[26]
And:
“large studies using similar sampling techniques are needed. Research is also needed to identify patients who are at most risk and to quantify personal exposure and risk”.[27]
[26] AALD dated 11 June 2020, p 6.
[27] AALD dated 11 June 2020, p 6.
Dr Herman observed that one would expect the levels in regional New South Wales to be even lower than the overseas studies. He was of the opinion that, given the level of exposure, the location where the deceased lived and areas where he worked, it was unlikely that the deceased would have had the same or similar level of exposure as those referred to in the studies relied upon by Dr Helprin. Dr Herman reiterated that the strength of the connection between the exposure and the cardiac arrest was, at best, modest.
Dr Herman concluded that the data providing the link between air pollution and arrhythmic events was a hypothesis, and should be the subject of larger scale, more accurate studies. He pointed out that, in the toxicology report generated in this case, the deceased was noted to have quinine present, which was of some concern and more likely to provoke cardiac arrhythmia than exposure to environmental toxins. Further, in people with ischaemic cardiomyopathy, the vast majority of the sudden cardiac deaths occur without an identified trigger, often during the early hours of the morning.
Dr Herman stated that if the deceased had not previously suffered a heart attack causing myocardial damage, he would not have suffered the arrhythmia which caused the cardiac arrest. He said it was very rare that a ‘de novo’ cardiac arrhythmia would occur in a structurally normal heart.
Dr Herman opined:
“In my opinion, air pollution was not the main contributing factor to his out of hospital cardiac arrest or ventricular fibrillation.
It is very unlikely that Mr Clifford was exposed to a significant level of PM 2.5 [micrograms per cubic metre] and it would be important, if this is deemed likely, to accurately assess the exposure at the time of his sudden cardiac arrest.
In ischaemic cardiomyopathy (previous heart attack involving anterior wall) the annual mortality rates frequently range from 5-10%; half of which is arrhythmic and sudden. Furthermore, the majority of arrhythmic death occurs in the early morning hours and is unrelated to exposure to environmental toxins.
Mr Clifford was permanently at a substantial risk of a sudden cardiac arrest (and arrhythmic death) whether or not he had environmental exposure to toxins.”[28] (emphasis in original)
[28] AALD dated 11 June 2020, p 7.
Dr Herman indicated that the studies relied upon by Dr Helprin did not cause him to alter his opinion, observing that there were material differences between exposure levels in different cities and most of the studies that revealed high levels of toxins were not conducted in Australia. He reiterated that the deceased’s employment did not put him at a significantly greater risk of a heart attack injury than he would have been if not employed.

The occupational hygiene experts

Mr Bradley Prezant, occupational hygienist

Mr Bradley Prezant was qualified by Ms Fisher’s legal representatives to provide an opinion about the issue of exposure to air pollution.[29] Mr Prezant was provided with copies of the reports of Dr Helprin and Dr Herman, the letter from Direct Couriers dated 3 February 2016, as well as the police and ambulance reports.
[29] First respondent’s AALD dated 28 July 2020.
Mr Prezant advised that, taking into account a review of the scientific literature, including those cited by Dr Helprin, he agreed with the opinion of Dr Helprin that there was a causal connection between ambient air pollution and sudden cardiac events, including ventricular fibrillation. He said that the literature demonstrated a significant association between PM2.5 and ultra-fine particulate matter and sudden cardiac events.
Mr Prezant referred to a technical report published by the World Health Organisation European Centre for Health in 2013,[30] which reviewed studies of incidents of mortality associated with PM2.5 in various cities in Europe, Canada and the United States of America (USA) and a large study in the USA, and which reported a significant association between exposure to PM2.5 and admissions to hospitals for treatment of various cardiovascular diseases.
[30] Review of evidence on health aspects of air pollution – REVIHAAP Project Technical Report, World Health Organisation 2013, First Respondent’s AALD dated 28 July 2020.
Mr Prezant quoted from the report’s summary, which recorded that:
(a)    road traffic, especially where vehicles were powered by diesel fuel, was a major source of black carbon in urban areas and there was evidence that short term and long-term exposures to particles in vehicle exhausts was harmful;
(b)    in the smaller short-term studies, it was found that, typically, PM2.5 was associated with cardiovascular conditions;
(c)    diesel engine exhaust had a high content of PM, mostly below 2.5 micrograms, which was found to have numerous adverse effects on healthy volunteers, including inflammation of the airways and reduced vascular function;
(d)    in patients with stable myocardial infarction, exposure to diesel engine exhaust caused myocardial ischaemia;
(e)    epidemiological and clinical studies showed that exposure for less than a day at elevated levels could lead to adverse physiological changes, including changes to cardiovascular systems, and
(f)    there was an unexplained association between exposure to air pollution from traffic and adverse cardiovascular events, however the connection may be explained by the results of brief exposure to diluted diesel exhaust, which promoted myocardial ischaemia.
Mr Prezant noted that the report also recorded observations from experimental studies and the conclusions that might be drawn from those.
Mr Prezant quoted from a different study which recorded that patients who were treated in hospital for coronary heart disease and then exposed to particulate pollution and road traffic after their discharge experienced a decrease in heart rate variability.[31] He referred to a further study addressing the exposure to air pollution on motorways.[32] He quoted three passages from that study, which can be summarised as follows:
(a)    pollutant concentrations from motor vehicle traffic on roadways are typically much higher than ambient concentrations but on arterial roads, ultrafine particle concentrations were generally higher if in proximity to accelerating gasoline powered vehicles;
(b)    the size of the airborne particulate is an important factor because ultrafine particulate of PM less than 0.1mm has greater toxicity than larger particles in an equivalent mass;
(c)    because of the high levels of air exchange in moving vehicles, concentrations within vehicles are close to those on the roadway, and
(d)    measured freeway concentrations of various particulates in Los Angeles, which appeared to be related to truck density, were in the vicinity of a higher magnitude than ambient levels and were higher than on arterial roads.
[31] Zanobetti A et al. (2010). Reduction in heart rate variability with traffic and air pollution in patients with
coronary artery disease. Environmental Health Perspectives, 118(3):324–330, First Respondent’s AALD dated 28 July 2020.
[32] Fruin, S., Westerdahl, D., Sax, T., Sioutas, C., & Fine, P. M. (2008) Measurements and predictors of on-road ultrafine particle concentrations and associated pollutants in Los Angeles. Atmospheric Environment, 42(2), 207–219, First Respondent’s AALD dated 28 July 2020.
Mr Prezant said that travelling within a vehicle offers some reduction in the level of exposure because of the filtration system, generally in the range of 20%–50%, which varies according to the size of the particulate. He provided a graph of indoor/outdoor ratios, which showed a reduction of effect in the order of 50% for PM2.5 and about 20% for ultrafine particles, noting that smaller particulates infiltrate buildings and vehicles more efficiently than larger particulates.
Mr Prezant indicated that, on the basis of the studies reviewed by the World Health Organisation, he was of the opinion that there are significant health impacts associated with exposure to fine particulate and that experimental research shows that there is an increased risk of myocardial infarction for people with pre-existing heart disease. He concluded that a greater exposure to PM2.5 and other airborne fine particulates occurs near highways and roadways and is only partially reduced while inside a vehicle.
Mr Prezant turned to the particular circumstances of the deceased’s travel on the day of his death, noting that the deceased resided in Woy Woy, New South Wales, approximately 25.7 kilometres from an air monitoring station located in Wyong. He said that the monitoring station was in a residential area away from major highways, and ambient conditions around the monitoring station were similar to those surrounding the deceased’s home. On that basis, Mr Prezant considered that the deceased, when in his home, would experience about 80% to 90% of the outdoor levels of exposure to PM2.5 and ultrafine particulate.
Mr Prezant reported the average of the levels of PM2.5 from 6 pm on the evening of 21 January 2016 through to 6 am on 22 January 2016 to be 7.0 micrograms per cubic metre, and thus his estimate of indoor exposure, in the absence of indoor activities that would increase the level, would be 6.3 micrograms per cubic metre. Mr Prezant provided a spreadsheet of the deceased’s movements from the time the deceased left his residence until the time of his death, taking into account the type of road travelled and the estimated time of travel, as indicated in Google Maps. He estimated that the deceased spent 4 hours and 15 minutes travelling in his car, which consisted of:
(a)    21 minutes on rural highways;
(b)    37 minutes on rural streets;
(c)    3 hours and 4 minutes on highways, and
(d)    13 minutes on suburban streets.
Mr Prezant provided copies of road maps on which the deceased travelled, which also showed where the air monitoring stations were situated in the vicinity of the deceased’s journey. Mr Prezant calculated that the deceased would not have travelled during lunch and other breaks from driving for a total time of 3 hours and 44 minutes. Relying on the various studies discussed and, taking into account the assessments of ambient air pollution provided by the relevant monitoring stations, Mr Prezant assessed the “inside vehicle exposure factor.” He also applied the exposure while not driving, in accordance with the ambient air values taken from the monitoring stations. He calculated a value of 25.7 micrograms per cubic metre, which indicated that, as a courier on that day, the deceased had four times greater exposure than a person who was not driving a vehicle.
Mr Prezant pointed out that ambient ultrafine particle data was not (at the date of death or at the time of writing the report) available. He commented that ultrafine particles are produced by vehicles, especially heavy vehicles, and exposures are greatly elevated near highways, so that the assessment using PM2.5 data was an underestimation of the health risks associated with the deceased’s exposure.
Mr Prezant was asked to comment on the opinion of Dr Helprin. Mr Prezant advised that he was not a physician and could not comment upon the susceptibility of a particular individual in respect of identified environmental conditions, but that he was qualified to give evidence about the risk to public health from hazardous exposure, as discussed in the scientific literature. He advised that the deceased’s level of exposure was consistent with the degree of exposure that scientific studies associated with both fatal and non-fatal coronary events. Mr Prezant cited a further study which found the occurrence of myocardial infarction was 2.9 times greater for exposure to ultrafine and PM2.5 particles in one hour of traffic. Mr Prezant also cited studies that showed that six hours of exposure resulted in an increased risk of myocardial infarction in the order of 3.3% to 5.8%. Mr Prezant added that the researchers concluded that ultrafine particulate increased when in proximity to roadways.
Mr Prezant concluded that, in his opinion, courier drivers experience increased exposure in their employment to air pollution caused by traffic compared to workers in indoor locations who do not spend their time driving on roads, particularly where the vehicles on the roads are heavy, diesel fuelled vehicles.

Mr Prezant annexed a copy of the World Health Organisations’ review referred to in his report.[33]
[33] First respondent’s AALD dated 28 July 2020 (review).

Mr Carl Strautins, occupational hygienist and materials scientist

The appellant qualified Mr Carl Strautins to provide an opinion as to the level and type of exposure experienced by the deceased and its association with cardiovascular disorders. Mr Strautins provided a report dated 11 September 2020,[34] which was prepared on the basis of a review of the first respondent’s ARDW and attachments, the appellant’s reply and attachments, Dr Herman’s supplementary report and Mr Prezant’s initial report.
[34] Appellant’s AALD dated 7 October 2020, pp 2–17.
Mr Strautins identified the issue as a consideration of whether particulate matter was the main contributing factor to the cause of the deceased’s cardiac event. He noted Mr Prezant’s opinion as to the increased risk of such an event, which was arrived at by considering the studies that supported an association between PM2.5 and the increased risk of a cardiac event. Mr Strautins stated that, from his experience, the method for assessment of such risk is that outlined by the Australian Institute of Occupational Hygienists (AIOH). He said the risk management strategy was to:
(a)    identify the workplace exposure to the chemical substances and the severity of the adverse health outcome associated with that exposure;
(b)    assess the likely level of exposure required which may result in an adverse health outcome, that level being known as the Workplace Exposure Standard;
(c)    measure or estimate the concentration of the airborne substance in order to confidently make a decision as to whether the risk requires intervention, and
(d)    compare the worker’s exposure from airborne concentrations within the worker’s breathing zones to the workplace standard.
Mr Strautins identified the standards he considered applicable, which were the standards for determination of adverse exposure to inhalable and respirable dusts. He explained that the workplace exposure standard was the maximum level of airborne concentrations that should be considered not sufficient to cause adverse health issues or undue discomfort to workers exposed at that level for the entirety of the person’s working life. He said that the question of whether a level is safe was a contentious issue, and that some experts were of the view that there was no safe level.
Mr Strautins pointed to a practical approach commonly adopted to a consideration of what might be considered a safe level of exposure, namely:
(a)    applying the upper threshold of what would be considered safe in accordance with the workplace exposure standard, and regarding consistent exposure above that level as unsafe;
(b)    considering exposures of greater than 50% of the workplace exposure standard as marginally safe, with industry practice being to initiate controlling action below this level because of the uncertainty surrounding safe exposure, and
(c)    where exposure was less than 10%, determining that the risk was not significant and no action was necessary.
Mr Strautins said that this approach was common, and consistent with the AIOH industry guidelines (which he identified). He said that Safe Work Australia sets out the standard for assessing exposure to airborne contaminants and that, contrary to Ms Fisher’s allegation, that document did not provide a prescriptive requirement for general non-toxic particulate, which was considered a nuisance dust or dust which was not otherwise classified. Mr Strautins quoted from the Guidance on the Interpretation of Workplace Exposure Standards for Airborne Contaminants. The guide provides that, where there is no specific assigned exposure standard, and the inherent toxicity of the substance is low, together with the substance being free from toxic impurities, the exposure should be measured at 10 milligrams per cubic metre and measured as an inhalable dust.
Mr Strautins reported that the AIOH undertook a review of exposure to airborne particulate matter with non-specific toxicological properties (otherwise known as dusts not specified or nuisance dusts) in 2014, which identified Chronic Obstructive Pulmonary Disease as the adverse outcome. The conclusion of the report also made recommendations in relation to adequate control of the exposure and protection of workers from serious side effects. Mr Strautins observed that, while there may be a connection between Chronic Obstructive Pulmonary Disease and cardiovascular function, there was no direct link between exposure and cardiac events.
Mr Strautins expressed the view that, if the exposure modelling calculated by Mr Prezant was accepted and was compared to the AIOH recommended action for respiratory dust, the exposure was about two orders of magnitude less than what would be considered safe for the purposes of preventing Chronic Obstructive Pulmonary Disease. He said that the concentration was so low that it did not require further assessment and no adverse health outcome would be anticipated, in the context of other established risk factors, which he listed.
Mr Strautins pointed to guidelines published by the Stroke Foundation in relation to assessment and management of cardiovascular disease, which indicated that the disease was largely preventable and the risk factors listed could be modified. He observed that particulate matter was not listed as a risk factor, particulate matter had not been assessed in comparison to established risk factors in order to suggest that it was significant, or a main contributing risk of the occurrence of the cardiac event suffered by the deceased. Mr Strautins drew the conclusion that there was no indication of substantial exposure to particulate matter and thus, in the context of the established risk factors, no intervention would have made any meaningful difference to the occurrence of the cardiac event.
Mr Strautins responded to specific questions put to him by the appellant. He commented that the methodology adopted by Mr Prezant seemed to be a risk assessment based on studies that were more related to general air pollution and air quality guidelines applicable globally, rather than an actual workplace exposure assessment. Mr Strautins acknowledged that Mr Prezant had attempted to best estimate the likely exposure to particulate matter on the day of death, however there was a great deal of uncertainty because the level was unknown and had not been evaluated, or meaningfully compared to the exposure an ordinary worker would have experienced.
Mr Strautins asserted that, in order to properly assess the level of exposure to small respirable particulate matter, the workplace exposure standards should be applied. He said that, although the standard measured different sized particles to PM2.5, the difference was not remarkable and the standard could be used as an indicator for the purpose of characterisation and estimation of exposure. Mr Strautins asserted that this information justified a determination that the exposure was so low that it complied with workplace exposure standards and did not require further assessment.
Mr Strautins was of the opinion that conducting respirable dust measurements in accordance with the relevant standard, the exposure to particulate matter would not be measurably, statistically or meaningfully different to a wide range of other employments. He was of the view that Mr Prezant had not properly considered the probable daily exposures that would normally arise in any employment, which is very significant when assessing whether employment was the main contributing factor to the cardiac event. He added that it was more probable than not that any working person will, at some stages, be exposed to greater than ambient levels of air pollution concentrations of particulate matter. He observed that if the proposition was accepted that a cardiac event resulted from exposure to particulate matter in comparison to ambient levels of pollution, then no worker in Australia would be safe from a cardiac event caused by their employment.
Mr Strautins advised that there was no Australian standard for respirable dust, but for inhalable dust the standard was 10 milligrams per cubic metre in an averaged airborne concentration over an eight hour day. He re-iterated that the AIOH recommended a level of exposure to respirable dust be kept below 1 milligram per cubic metre in order to prevent Chronic Obstructive Pulmonary Disease, but there was no workplace exposure linked to cardiac events. He said that the exposure calculated by Mr Prezant was negligible in the consideration of airborne particulate matter as a factor in the assessment of causation of the cardiac event, when compared to the established risk factors for such an event.
Mr Strautins was critical of Mr Prezant’s reliance on the cited studies. He observed that the evidence identified an increase in risk relevant to global health in respect of air pollution and the studies lacked specificity, applicability and could include spectrum bias. Further, Mr Prezant did not take into account, or make a comparison with, other exposures the deceased would have encountered in his non-work life. He concluded that Mr Prezant’s assumption that the deceased would only be exposed to ambient background concentrations of particulate matter outside of his employment as a courier driver was an unreasonable assumption. He said that increased particulate was likely to be present in all types of work activities and the levels of exposure presented were unavoidable.

Mr Prezant’s response to Mr Strautins’ opinion

Mr Prezant was asked to provide a further report, addressing the opinion of Mr Strautins. Mr Prezant responded in his report dated 4 October 2020.[35] He asserted that Mr Strautins’ description of PM2.5 as “nuisance dust or dust not otherwise classified” was incorrect. He offered the following reasons:
(a) PM2.5 near highways is mostly comprised of substances which are formed by condensation of high temperature diesel exhaust containing carcinogens, heavy metals and other toxic substances, and
(b) diesel emissions do not satisfy the Australian definition of “nuisance dust” put forward by Mr Strautins, which was defined as “dust of inherently low toxicity and free from toxic impurities,” and do not satisfy the definition proffered by the United States American Conference of Governmental Hygienists or that of Safe Work Australia. Mr Prezant quoted the various definitions and also quoted from a review article that supported his contention that Mr Strautins was wrong.
[35] First respondent’s AALD dated 6 October 2020, pp 1–13.
Mr Prezant asserted that the standard proposed by Mr Strautins should not be applied where the particulate material contains substances which may be toxic or might cause physiological harm and, for those such substances, the higher standard should be applied when assessing maximum exposure levels. He referred to the history of the classification of “nuisance dust” in the mining industry, where it was used to describe dust that was free of silica or other toxic substances. He said that the term is not typically applied to smaller particulates formed by condensation such as the recommendation made about diesel particulate by the AIOH, of which Mr Strautins was a member.
Mr Prezant explained the term “dust” as used in occupational settings, which was generally used to describe large masses of the same material and characterised by widely variable particle size. He said that the particle sizes in PM2.5 are less than 2.5 microns, which are formed by the process of condensation and the size is critically important in its impact on health. He further explained how and why the size of the particle was critical.
Mr Prezant was also critical of Dr Strautins approach in considering PM2.5 in isolation from other toxins, which he said was inappropriate because the research showed that traffic related air pollution contained a wide variety of other chemicals and was different from PM2.5 produced from other toxins. He said that traffic related air pollution and PM2.5 were as different as “chalk and cheese.”
Mr Prezant agreed with Mr Strautins’ mathematical conversion of 23.7 micrograms per cubic metre to 0.026 mg per cubic metre of PM2.5 but disagreed with his comparison to the AIOH recommended value. He said this was because Mr Strautins inappropriately aggregated the composition of the traffic related air pollution as respirable dust. Mr Prezant also asserted that the standards and guidelines relied upon by Mr Strautins were not applicable. He said that the Safe Work Australia documents were generic documents related to work health and the methods of sampling airborne particulate in the guidelines were also generic methods applicable to sampling respirable or inhalable dusts, which are different from PM2.5. Mr Prezant added that the nuisance dust standard specifies measurement of inhalable dust and not respirable dust. He explained the measuring methods and the differences. He pointed out that the absence of specific workplace standards did not mean that the nuisance dust standard is automatically applied and would only be potentially appropriate where the substance is of inherently low toxicity and free from toxic impurities.
Mr Prezant referred to Mr Strautins’ conclusion that the respirable dust measurements which the deceased was exposed to would not have been any different to the general population across a number of employment categories. Mr Prezant pointed to numerous types of employment where the worker was required to drive on highways and stated that epidemiological studies for many of those occupations showed elevations in cardiovascular outcomes.
Mr Prezant agreed with Mr Strautins’ observation that middle aged male drivers in a big Korean city had a higher likelihood of developing cardiovascular events than men of the same age in other professions, noting that the observation was based on respirable dust, which encompasses a much larger proportion of airborne particulate, larger than PM2.5. Mr Prezant provided a comparative table of the measurements. He said that an enormous difference would be apparent if PM2.5 was considered, rather than respirable particulate.

Mr Strautins’ response to Mr Prezant’s opinion

In a report dated 23 October 2020, Mr Strautins responded to the further evidence of Mr Prezant.[36] Mr Strautins asserted that Mr Prezant had not addressed the question of whether the deceased’s exposure to the particles was the main contributing factor to the cardiac event. Mr Strautins said that Mr Prezant had focussed on the size and toxicity of the particles, rather than the more relevant risk factors. He asserted that the connection to environmental pollution in other cities put forward by Mr Prezant was weak, adding that, although the studies were important, they did not address individual circumstances and to use the outcomes in isolation was misleading. Mr Strautins described the link suggested by Mr Prezant as tenuous and speculative because of the lack of comparison between that link and other well established risk factors.
[36] Appellant’s AALD dated 23 October 2020, pp 6–15.
Mr Strautins referred to his earlier report in which he performed a measure of respirable dust as a test to measure whether the exposure may be significant. He said the assessment is commonly performed in accordance with the measures set out in the workplace exposure standards, and no further tests were required because the risk was so low that intervention would be meaningless. He noted that Mr Prezant conceded that it was unlikely that there would be any measurable differences in the particulate matter when he said that there were no differences in measurements of respirable particulate between highways and other workplaces.
Mr Strautins added that Mr Prezant had not measured the level of the deceased’s likely exposure to diesel particulate, which Mr Prezant was correct in saying was a significant component of traffic related air pollution. Mr Strautins observed that, in making his calculations, Mr Prezant used his professional judgment and made unverifiable and unvalidated assumptions. He explained, however, that, assuming that Mr Prezant’s calculation was correct, even though it was an overestimation of the risk, the exposure was still significantly lower than the AIOH recommended limit value, no action was required and the risk of an adverse health outcome was negligible.
Mr Strautins observed that Mr Prezant did not undertake the normal and expected practice of measuring the exposure to total dust and diesel particulate fractions to which a courier driver may have been exposed in order to verify his estimates of exposure. Mr Strautins commented that it was not clear how Mr Prezant arrived at the conclusion that the deceased’s exposure was the main contributing factor to the deceased’s cardiac event, despite being given the opportunity to respond to Mr Strautins’ earlier report. Mr Strautins said that Mr Prezant’s focus was on a generalised comparison between environmental pollution between cities, which was irrelevant to a discussion about what the main contributing factors were to the deceased’s cardiac event.
Mr Strautins referred to the Australian paper relied upon by Mr Prezant which specifically considered the traffic related exposures to fine and ultrafine particles of professional drivers. He pointed out the observation made by the researchers was that there was no substantive evidence that particles can be attributed to being a significant or the main contributing factor to professional drivers suffering a cardiac event. Mr Strautins describes Mr Prezant’s evidence as a distraction form the principle issue, namely whether the deceased’s exposure to particulate matter was the main contributing factor in the cause of the cardiac event.
Mr Strautins said that Mr Prezant compared the deceased’s exposure at work to the exposure he would have experienced at home. Mr Strautins asserted that this was not a proper comparison because it should have been measured against the likely exposure in other employments, which would have been higher than in the deceased’s home. Mr Strautins calculated that the risk level when taking into account blood pressure, age, smoking status, gender and cholesterol was much greater, so that the deceased had a significant risk of a cardiac event regardless of workplace exposure.
Mr Strautins confirmed his earlier expressed opinion that the deceased’s exposure to particulate matter in his employment did not lead to a significantly greater risk of cardiac injury, irrespective of how the particulate matter was categorised or which methodology was used.

European Heart Journal entitled “Rapid effects of air pollution on ventricular arrhythmias”

This study, which was annexed to Dr Helprin’s report dated 5 December 2019, was undertaken in Stockholm and Gothenburg, Sweden, and used 88 participants, 87 of whom had implantable cardioverter defibrillators due to earlier episodes of ventricular tachyarrhythmias. The study assessed the risk associated with exposure for less than 24 hours. The research produced different results between Stockholm and Gothenburg and the conclusion reached was that:
“Moderate increases in air pollution appear to be associated with ventricular arrhythmias in ICD patients already after 2 h, although future studies including larger numbers of events are required to confirm these findings. Representative geographical exposure classification seems important in studies of these effects.”[37]
[37] Rapid effects of air pollution on ventricular arrhythmias, p 1, ARDW, p 59.

The World Health Organisation review

The World Health Organisation’s review, which was compiled by the organisation’s Europe Office, consisted of a summary of numerous studies and research articles undertaken throughout Europe, Canada, the USA and Asia. The review is voluminous and not all sections pertain to the issues in dispute in this appeal. The evidence provides details of some of the relevant findings which form the basis for the scientific opinions put forward by those experts. The following extracts from the World Health Organisation review are of relevance:
(a) “… an authoritative review of the evidence for cardiovascular effects, conducted by cardiologists, epidemiologists, toxicologists and other public health experts, concluded that long-term exposure to PM2.5 is a cause of both cardiovascular mortality and morbidity.”[38]
[38] Review, p 6.
(b) “The risk of ischaemic heart disease, which includes heart attacks, has particularly strong and consistent associations with PM2.5.”[39]
[39] Review, p 8.

(c) “There is increasing, though as yet limited, epidemiological evidence on the association between short-term exposures to ultrafine … particles and cardiorespiratory health, as well as the health of the central nervous system. Clinical and toxicological studies have shown that ultrafine particles (in part) act through mechanisms not shared with larger particles that dominate mass-based metrics, such as PM2.5 or PM10.”[40]
(d) “… road traffic (especially vehicles powered by diesel fuel) is a major source of black carbon in most urban environments. Consequently, evidence accumulated after 2005 on the health effects of black carbon indicates that both short-term and long-term exposures to particles in vehicle exhausts are harmful. In the more limited number of short-term studies that have been based on source apportionment, PM2.5 from traffic has typically been found associated with cardiovascular health.”[41]

(e)    “Diesel engine exhaust is rich in PM, mostly below 2.5 [micrograms]. A large database describes all sorts of adverse health effects due to exposure to diesel engine exhaust. Exposure to diesel engine exhaust in healthy volunteers causes inflammation of the airways … and reduces vascular function … In patients with heart problems (stable myocardial infarction), diesel engine exhaust causes myocardial ischaemia …”.[42]
(f)    “Single and multicity studies from the United States report associations between 24-hour average exposures to PM2.5 and both mortality and hospital admissions due to cardiorespiratory health problems. Because of the absence of monitoring PM2.5 in Europe until recently, the evidence from Europe is more limited; but where there are studies, the results are less consistent.”[43]
(g)    “There is a lack of data on the effects of short-term exposures to ultrafine particles, and there are no epidemiological studies of long-term exposure to ultrafine particles.”[44]

[40] Review, p 11.

[41] Review, p 22.

[42] Review, p 23.

[43] Review, p 32.

[44] Review, p 168.

THE ARBITRATOR’S REASONS

The Arbitrator identified the first respondent’s case as pleaded in the ARDW and the defence raised by the appellant. He summarised the submissions made by all parties. He provided a detailed account of the non-contentious facts, the lay evidence surrounding the deceased’s employment, and the requirements of that position, including the evidence from Mr Ross about the work being stressful and demanding. He reviewed the deceased’s activities on the day of his death. The Arbitrator concluded that he was satisfied, on the basis of the unchallenged evidence given by the first respondent, that the collection from the abattoirs in Scone recorded on 20 and 21 January 2016 related to a delivery to Sydney Airport undertaken by the deceased on 22 January 2016. He noted the unchallenged evidence that the deceased died of ischaemic heart disease secondary to coronary artery sclerosis while driving his van in the course of his employment. The Arbitrator summarised the evidence contained in the reports of Dr Helprin, Dr Herman, Mr Prezant and Mr Strautins.
The Arbitrator turned to the first issue for determination, which he said was whether the deceased suffered a personal injury within the meaning of s 4(b) or a disease injury within the meaning of s 4(b)(ii) of the 1987 Act. He noted that the deceased suffered from a pre-existing coronary disease in the form of an old myocardial infarction, severe narrowing of the descending artery, on a background of hypercholesterolaemia, hypertension, impaired fasting glucose and associated depression. The Arbitrator accepted the opinions of Dr Helprin and Dr Herman that the deceased suffered a cardiac event while driving his van in the course of employment, that the cardiac event was due to cardiac arrhythmia, and that that event resulted in the deceased’s death. On the basis of that evidence, he made the finding that the deceased died of a cardiac event in the course of his employment, caused by ventricular fibrillation. He also found that the deceased suffered from pre-existing coronary artery disease, namely an old myocardial infarction and severe narrowing of the descending artery, which conditions contributed to the cardiac event, that is the ventricular fibrillation.
The Arbitrator noted that Dr Helprin was of the opinion that the ventricular fibrillation was a “new condition,” not previously suffered by the deceased, which was triggered by exposure to ambient air pollution while driving through regional and metropolitan areas and especially in the Sydney Airport area. The Arbitrator further noted that Dr Helprin explained that the ventricular fibrillation was a separate or new injury because it was an electrical disturbance of the heart, rather than a “vascular injury contributed to by the pre-existent coronary artery disease.”[45] The Arbitrator observed that Dr Helprin’s conclusion that the ventricular fibrillation was caused by the deceased’s exposure to air pollution was based upon the exercise of his medical knowledge and by reference to the scientific literature referred to in his report dated 5 December 2019, including the article in the European Heart Journal.
[45] Reasons, [118].
The Arbitrator referred to Dr Herman’s opinion that the fatal ventricular fibrillation was caused by ischaemic cardiomyopathy on the background of the various underlying conditions which contributed to coronary artery disease. The Arbitrator noted that Dr Herman considered that the deceased’s employment:
(a)    was not the main contributing factor to the aggravation, acceleration, exacerbation or deterioration of the underlying coronary artery disease;
(b)    did not contribute at all to the pre-existing coronary artery disease, and
(c)    did not provoke an ischaemic event triggering the fatal arrhythmia.
The Arbitrator considered that Dr Herman’s use of the words “provocation” and “provoked” were used in the sense of being “caused.” He observed that Dr Herman did not opine whether the ventricular fibrillation was a “new injury.” The Arbitrator took the view that Dr Herman’s opinion was that the cause of the ventricular fibrillation was the underlying coronary artery disease, together with the deceased’s pre-existing risk factors for cardiovascular heart disease.
The Arbitrator noted that Dr Herman agreed with Dr Helprin’s review and analysis of the scientific literature that there was, in fact, an association between either ‘out of hospital’ cardiac arrest or the onset of ventricular fibrillation, and exposure to air pollution. The Arbitrator observed, however, that Dr Herman considered that the association considered in the studies between ‘out of hospital’ and short term exposure to ambient particulate matter was inconsistent and that larger studies were required in order to establish more definitive data.
The Arbitrator formed the conclusion that, prior to the date of death, the deceased provided courier services for a period of six years, which included:
(a) collecting refrigerated containers from the Hunter Valley and delivering them to Sydney Airport, and
(b) driving for considerable periods of time throughout the day, on highways and regional and metropolitan roads throughout Sydney, the Central Coast and the Hunter Valley.
The Arbitrator accepted Mr Prezant’s evidence as to the periods of time the deceased spent driving on the various types of roads and as to the time unaccounted for, and he rejected Dr Herman’s assertion that the deceased’s exposure on 22 January 2016 was “short term” in nature. The Arbitrator also accepted the evidence of Mr Prezant, noting his specialist scientific knowledge and depth of experience in Australia and America in the field of exposure to diesel engine exhaust. That is, exposure to particulate matter (PM2.5) and ultrafine particulate on highways and roads in metropolitan and regional areas. The Arbitrator also accepted Mr Prezant’s method of calculation of the deceased’s exposure, noting the basis upon which Mr Prezant relied to arrive at his conclusion that the deceased, on the day of his death, was exposed to air pollutants four times greater than a person who was not driving a vehicle would have been exposed. He accepted that the greater exposures to PM2.5 and ultrafine particulate were a direct result of driving on roadways, in particular populated by heavy, diesel powered traffic, and that the exposure was significantly higher than in other places of employment, such as offices, schools, retail shops, wholesalers, or other indoor locations.
The Arbitrator rejected Mr Strautins’ criticism of Mr Prezant’s methodology of calculating the “ambient” air pollution because it appeared that Mr Strautins had based his assumption on the association between chronic obstructive airways disease and cardiovascular function and that exposure to “nuisance dusts” was not significant or a main contributing factor to a cardiac event. The Arbitrator formed the view that Mr Strautins:
(a)    had not addressed the issue of exposure to PM2.5, ultrafine particulate and other ambient air pollution when the deceased was driving on the various roads;
(b)    had not addressed the deceased’s level of exposure, and
(c)    did not provide reasons why the assessment and calculation of the exposure was so low that intervention was not warranted.
The Arbitrator considered that Dr Strautins’ reasons for asserting that the exposure was so low that intervention was not required was inconsistent with the World Health Organisation findings that exposure to PM2.5, ultrafine particulate and other toxins significantly increases the likelihood of ventricular fibrillation. He observed that Mr Strautins appeared to be critical of Mr Prezant’s methodology because Mr Prezant should have undertaken a calculation of air pollutants on the roads upon which the deceased travelled and compared the results to the working population as well as established risk factors for cardiac events. The Arbitrator agreed with the submission that Mr Strautins had “missed the point” because he did not deal with the health hazard caused by exposure to air pollution caused by traffic.
The Arbitrator rejected Mr Strautins’ opinion that Mr Prezant’s calculation of the deceased’s exposure to particulate matter was negligible when compared with established risk factors. The Arbitrator reasoned that Mr Strautins did not consider the level and duration of exposure or whether the exposure contributed to the cause of ventricular fibrillation or the coronary artery disease. The Arbitrator concluded that, for those reasons, he preferred Mr Prezant’s opinion as to the level and duration of exposure by the deceased to air pollutants.
The Arbitrator referred to the evidence of Dr Helprin and Dr Herman and observed that there could be no doubt that the deceased’s pre-existing condition of an old myocardial infarction, severe narrowing of the left descending artery and coronary artery disease was a disease. He accordingly made that finding. The Arbitrator quoted from the judgments of Kitto J and Windeyer J in Federal Broom Co Pty Ltd v Semlitch[46] in relation to the meaning of a “disease” and what needed to be considered in order to determine whether a worker suffered from an aggravation of a disease. That is, that there was an aggravation of a disease if it was made more grave or more serious in its effects on the patient.
[46] [1964] HCA 34; 110 CLR 626.
On the basis of Dr Helprin’s opinion and in the context of Dr Helprin’s specialist medical knowledge and reliance on the scientific literature upon which Dr Helprin formed his view, the Arbitrator accepted that the deceased’s coronary artery disease was aggravated, accelerated, exacerbated or deteriorated by exposure to ambient air pollution consisting of PM2.5 and ultrafine particulate, as well as environmental toxins, in the course of his employment on 22 January 2016.
The Arbitrator noted that, while Dr Herman agreed that the study referred to by Dr Helprin established that increased ambient levels of PM2.5 were associated with the increased risk of ‘out of hospital’ cardiac arrest shortly after exposure, Dr Herman pointed out that the studies were performed in Korea, which would be expected to result in comparatively higher levels of PM2.5. The Arbitrator observed that Dr Herman considered that:
(a)    it would be unlikely that the deceased’s exposure would have been similar to the air pollution recorded in the studies relied upon by Dr Helprin;
(b)    the data associating air pollution to arrhythmia was a hypothesis;
(c)    larger scale studies were required in order to provide an accurate assessment of the levels of exposure, and
(d)    it was unlikely that the deceased was exposed to a significant level of PM2.5.
The Arbitrator said that Dr Herman did not provide any reasons as to how he reached his conclusion. Further, Dr Herman’s conclusion that the link between air pollution and arrhythmia was a hypothesis, requiring larger scale studies to prove the link was not supported by the extensive research conducted by the World Health Organisation. The Arbitrator said that the World Health Organisation review, which was of published research, showed the hazardous effect of exposure to PM2.5, as well as other pollutants, that would be likely to cause an increase in the risk of sudden coronary events.
The Arbitrator cited authority for the proposition that a tribunal of fact, having regard to the whole of the evidence, can conclude that a proposition regarded by medical experts as being possible has been made out on the balance of probabilities. He referred to Kirby P’s observation in Kooragang Cement Pty Ltd v Bates[47] that, in order to establish an injury in the course of employment, a common sense evaluation of the causal chain is required.
[47] (1994) 35 NSWLR 452; 10 NSWCCR 796 (Kooragang).
The Arbitrator pointed to Dr Helprin’s reference to “trigger” and “triggering,” and indicated that he considered that Dr Helprin intended those words to mean “aggravated” or “aggravation” of the deceased’s coronary artery disease.
The Arbitrator concluded that, having regard to all of the evidence, the deceased was exposed to ambient air pollution consisting of PM2.5, ultrafine particulate and other environmental toxins in the course of his employment as a courier driver on 22 January 2016. He further concluded that such exposure aggravated, accelerated, exacerbated or deteriorated the deceased’s coronary artery disease, which materially contributed to the ventricular fibrillation, resulting in the death of the deceased.
The Arbitrator turned to the question of whether the deceased’s employment was the main contributing factor to the aggravation, acceleration exacerbation or deterioration of the deceased’s coronary artery disease, in accordance with s 4(b)(ii) of the 1987 Act. He referred to the Court of Appeal decision in Murray v Shillingsworth[48] as authority to say that the decision-maker’s enquiry should be directed to the main contributing factor to the injury, and not the contribution to the overall pathology.
[48] [2006] NSWCA 367; 68 NSWLR 451; 4 DDCR 313, [63]–[64] per Einstein JA.
The Arbitrator referred to various further authorities in respect of what was required in determining the main contributing factor. The Arbitrator noted the observations of Snell DP in AV v AW,[49] in which the Deputy President said that:
(a)    the test is one of causation;
(b)    a more stringent connection with employment was required than that required in s 9A of the 1987 Act, which required the connection to be a substantial contributing factor;
(c)    the test involved a consideration of whether there were competing work and non-work related factors and, following an evaluation of the causal factors, the employment was the main contributing factor;
(d)    medical evidence of whether the test is satisfied is both relevant and desirable, and
(e)    as observed by Roche DP in State Transit Authority of New South Wales v El‑Achi,[50] if an expert does not address the ultimate legal question requiring determination, it is not fatal and the Arbitrator must determine the issue of injury using an evaluative process and having regard to the whole of the evidence.
[49] [2020] NSWWCCPD 9 (AV v AW).
[50] [2015] NSWWCCPD 71.
The Arbitrator accepted the history provided by the first respondent that the deceased was a non-smoker, rarely drank alcohol, had no family history of heart disease and his general health was good. The Arbitrator referred to the possibility expressed by Dr Herman that the deceased suffered a myocardial infarction in 2012. The Arbitrator observed that there had been no “further” investigation of chest pain undertaken, and there was no evidence to conclude that the deceased suffered a myocardial infarction in 2012. The Arbitrator added that, while the deceased may have had risk factors for the development of heart disease, there was no evidence of treatment undertaken for a heart condition prior to the event on 22 January 2016.
The Arbitrator again referred to Snell DP’s observations in AV v AW that what is required in determining whether the employment was the main contributing factor was an evaluative process, having regard to the whole of the evidence. He determined that:
“Having regard to the whole of the evidence, including both work and non-work casual [sic, causal] factors (hypercholesterolaemia, hypertension, impaired fasting glucose and depression), I feel an actual persuasion of the existence of the fact that the employment was the main contributing factor to the aggravation, acceleration, exacerbation or deterioration of the disease within the meaning of s 4(b)(ii) of the 1987 Act.
I find on the balance of probabilities that the worker suffered a disease injury within the meaning of s 4(b)(ii) of the 1987 Act, and that the employment was the main contributing factor to the aggravation, acceleration, exacerbation or deterioration of the disease as a result of exposure to ambient air pollution in the course of employment as a courier driver on 22 January 2016 causing the ventricular fibrillation resulting in death.”[51]
[51] Reasons, [169]–[170].

The Arbitrator concluded that he was satisfied on the balance of probabilities that the deceased’s underlying coronary artery disease was aggravated by exposure to air pollutants during the course of his employment as a courier driver, which caused the ventricular fibrillation, resulting in the deceased’s death.
The Arbitrator turned to the issue of whether s 9B of the 1987 Act was satisfied. That is, whether the nature of the deceased’s employment gave rise to a significantly greater risk of suffering the injury (in this case, ventricular fibrillation, arrhythmia and tachycardia) than had the deceased not been employed in employment of that nature.
The Arbitrator referred to decision of Snell DP in Renew God’s Program Pty Ltd v Kim,[52] in which the Deputy President adopted the observation he made in his own decision while in the role of Senior Arbitrator, of De Silva v Secretary, Department of Finance, Services and Innovation[53] that:
“Section 9B(1) does not require a significant risk. It requires a comparison of (1) the risk to which the nature of the employment concerned gives rise and (2) the risk had the worker not been employed in employment of that nature. It is necessary that the first of these be ‘significantly greater’ than the second, if compensation is to be payable.”[54]
[52] [2019] NSWWCCPD 45 (Kim).
[53] [2015] NSWWCC 279 (De Silva).
[54] De Silva, [105].
Applying those decisions, the Arbitrator said that:
(a)    the exercise involved a comparison of the level of risk;
(b)    the “employment concerned” was the particular work the worker in fact did in the employment and not a class or classification of employment;
(c)    what is required is that the risk in that employment was significantly greater than the risk the worker would have been exposed to had he not been employed in work of that nature;
(d)    the task is an evaluative one, requiring an assessment of the comparative risk, which is not a test of true causation;
(e)    medical evidence as to some particular effect is not required, and
(f)    it is necessary to determine whether the test is satisfied on the basis of all of the evidence.

The appellant submits that, for those reasons, the Arbitrator erred in fact by preferring the opinion of Dr Helprin over that of Dr Herman, and that error materially affected the outcome of the case. Thus, the appellant submits, this ground of appeal should be upheld.

The first respondent’s submissions

The first respondent contends that the appellant’s submissions do not accurately reflect the evidence or the Arbitrator’s reasons. She refers to Dr Herman’s opinion that it was unlikely that the deceased would have been exposed at the same or similar level to the exposure level referred to in the literature relied upon by Dr Helprin, taking into account where the deceased lived, where he worked and the period of exposure.
The first respondent concedes that Dr Herman predicated this statement with a reference to the levels of exposure in Seoul, Korea before expressing the view that:
(a)    the levels of exposure would likely be less in Melbourne and Perth;
(b)    it was likely that the deceased was not exposed to a significant level of PM2.5, and
(c)    an accurate assessment of the deceased’s exposure at the time of death was required.
The first respondent contends, therefore, that the appellant’s assertion that Dr Herman provided a proper basis for his opinion that the deceased would not have been exposed to the significant levels of pollution discussed in the Korean study cannot be accepted. She says that this was not the opinion provided by Dr Herman. The first respondent says that Dr Herman did not, at any point, explain why he was of the opinion that the deceased’s exposure was not significant and just because Dr Herman thought that the exposure levels in Korea and Australia would be different, that did not constitute reasons for his conclusion. The first respondent submits that the Arbitrator’s observation that Dr Herman did not provide reasons for his opinion was, therefore, correct.
The first respondent submits that the Arbitrator did not accept that the connection between air toxicity and a cardiac event constituted a hypothesis and submits that classing it as such was not consistent with the World Health Organisation review. She points to the Arbitrator’s reasons for rejecting that notion, which were that the World Health Organisation had undertaken extensive research and reported on the hazardous effect of exposure to air pollutants, in particular PM2.5, which was likely to cause an increase in the risk of sudden coronary events. The first respondent adds that, in accordance with Christensen and her earlier submissions, where a medical expert regards something as possible, a tribunal of fact can determine that, on the balance of probabilities, it is probable. Thus, she submits, notwithstanding Dr Herman’s opinion, the Arbitrator was entitled to make a determination in respect of causation.
The first respondent maintains that, even if the Arbitrator’s remarks were not factually correct, it would not make a difference to the outcome because the Arbitrator indicated that, in any event, he could determine the matter on the balance of probabilities.
The first respondent contends that the appellant has taken an unduly narrow approach to the World Health Organisation review. She explains that, although the authors expressed reservations in relation to the link between exposure to particulate matter and a cardiac event, the authors also indicated that studies had shown that there was a link and Mr Prezant referred to those studies in his report. The first respondent asserts, therefore, that the limitations expressed in the publication could not be taken to mean that Dr Herman’s comments were entirely consistent with the research, because the scientific literature did not consider that the causal link was a mere hypothesis.
The first respondent submits that the appellant has failed to establish error as alleged and this ground of appeal should be dismissed.

THE RELIEF SOUGHT

The appellant seeks to have the Arbitrator’s Certificate of Determination revoked and an award entered in its favour.
The first respondent submits that the Arbitrator’s decision ought to be affirmed, or, in the alternative, if error on the part of the Arbitartor is established, the matter should be remitted to a different arbitrator for re-determination. The second and third respondents seek to have the appeal dismissed.

CONSIDERATION

The appellant asserts that the Arbitrator made incorrect findings about the medical and scientific literature and gave undue weight to that literature (Ground Two), thus erring in relation to his preference for the opinion of Dr Helprin over that of Dr Herman (Ground Five). The appellant submits that the Arbitrator erred in finding that the literature supported a causal connection between exposure to air pollutants and ventricular fibrillation or cardiac arrest. It is convenient to deal with both grounds together.

The scientific literature

The appellant says that Dr Helprin’s opinion, which the Arbitrator accepted, was that the literature established as a certainty that ambient air pollution in metropolitan areas was a direct cause of ventricular fibrillation, in the presence of a cardiac condition. The appellant says that the literature fell short of establishing the connection as a “certainty.”
Dr Helprin expressed his view as:
“There’s certainty from the scientific literature that I’ve described that ambient air pollution in metropolitan areas is a direct cause of ventricular fibrillation, particularly in the vulnerable heart.”[67]
[67] ARDW, p 58.
The appellant asserts that there were no such conclusions in the literature, and the highest the scientific literature could be put is that there was an “association” between exposure to air pollutants and ventricular fibrillation. Both Dr Helprin and Dr Herman agreed that there was an “association,” but ultimately arrived at differing conclusions about the scientific literature. As an example, there was a complete divergence of opinion between Dr Helprin and Dr Herman as to the conclusion reached in the study “A systematic review of air pollution and incidence of out-of-hospital cardiac arrest” by Teng et al.
The scientific literature relied upon by Dr Helprin consisted of the eight studies summarised at [31]–[32] above. On the basis of those eight studies, Dr Helprin concluded that the nature of the deceased’s work posed a greater risk of the deceased suffering a ventricular fibrillation. Not all of those studies supported an association between exposure to air pollutants and cardiac events because potentially they were either:
(a)    equivocal in their conclusions;
(b)    could possibly be distinguished from this case because of their location or because of the medical condition of the participants, or
(c)    might not be referrable to the relevant enquiry.
The Arbitrator reasoned that:
“Dr Helprin reached his conclusion that the ventricular fibrillation was caused by exposure to ambient air pollution in the exercise of his medical knowledge and scientific literature referred to [in] his report dated 5 December 2019, including a clinical research publication of the European Heart Journal entitled ‘Rapid effects of air pollution on ventricular arrhythmias,’ attached to his report.”[68]
[68] Reasons, [119].
Dr Helprin observed that the study entitled “Rapid effects of air pollution on ventricular arrhythmias” found that there appeared to be an association following moderate levels of exposure, where the patients were fitted with an implantable defibrillator, but suggested larger studies were required to confirm the findings. Thus, Dr Helprin recognised that the deceased did not have an implanted defibrillator, the cohort was too small to be indicative, and the particular study of short-term exposure was inconclusive.
The Arbitrator did not explain why he included reference to that particular research study as a basis for his acceptance of Dr Helprin’s opinion. Dr Helprin’s observations about that study do not appear to be indicative of the study being supportive of his opinion on causation. The Arbitrator also did not address the divergent opinion of each of these medical experts as to the conclusion reached in the study by Teng et al.
The studies relied upon by Dr Helprin in arriving at his conclusion that there was a “certainty” that there was a direct causal connection were limited to those discussed above and did not involve consideration of the World Health Organisation review.
The appellant raised a significant issue as to what conclusions were arrived at in both the World Health Organisation review and the studies relied upon by Dr Helprin. The appellant asserted that the World Health Organisation review specifically noted that there were critical gaps in the studies that needed further research in order to assess the contribution of air toxicity to adverse health outcomes. The appellant submits that the many points made in the studies about the limitations indicated that the outcomes were consistent with Dr Herman’s conclusion that the scientific studies remained a hypothesis.
The Arbitrator acknowledged the appellant’s submissions about the World Health Organisation review and the other studies relied upon by the occupational and medical experts at [23(vv)]–[23(ww)] of his reasons. The Arbitrator did not go so far as to say that the report from the World Health Organisation stated with certainty what the cause and effect exposure to air pollutants would have been. However, he rejected the evidence of Dr Herman in part because it was, in his view, inconsistent with the World Health Organisation review and also because the association between exposure to air pollutants and cardiac events could not be classed as a hypothesis. The Arbitrator did not engage with the appellant’s submissions about the limitations of the findings other than to say that, in any event, in circumstances where science can only assert possibilities, a tribunal can determine, on the basis of the whole of the evidence, that the causal link is established on the balance of probabilities.
The difficulty with that approach is that the Arbitrator proceeded to reject the opinion of Dr Herman without having considered the submissions about the alleged inconsistency between the findings in the research and the opinion of Dr Helprin and without identifying what he determined the status of the findings in the research to be. Of note was the inconsistency between Dr Helprin’s assertion of the conclusion reached in the study undertaken by Teng et al and that recorded by Dr Herman in respect of the same study.
The observations by Spigelman CJ in McGuiness are relevant to the issue of the status of the scientific literature. As his Honour observed (with Stein JA and Davies AJA agreeing):
“Epidemiology … is concerned with the study of disease in human populations. It is not, of itself, directed to the circumstances of an individual case.
Evidence of possibility, including expert evidence of possibility expressed in opinion form and evidence of possibility from epidemiological research or other statistical indicators, is admissible and must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn. Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference is not open to be drawn.”[69]
And:
“Some of the epidemiological evidence suggests some increase in risk. On the approach I believe to be appropriate, that evidence and that conclusion are circumstantial facts which may be taken into account as ‘strands in the cable’ for the purpose of drawing the inference that the particular exposure caused or materially contributed to the injury in the specific case.”[70]
[69] McGuiness, [78]–[79].
[70] McGuiness, [102].
The epidemiological evidence about the association between exposure to air pollutants and cardiac events constituted “strands” in the causal chain of connection consistent with Kirby P’s observations in Kooragang but were not, of themselves, evidence establishing the necessary causal connection between the exposure to air pollution, if accepted, and the deceased’s ventricular fibrillation resulting in death. An assessment of the competing expert evidence of Mr Prezant and Mr Strautins, and that of Dr Herman and Dr Helprin as to the question of causation was a further step in the consideration of the question of causation and an assessment of the evidence of those experts required an examination of whether the opinions were properly founded upon the facts and the conclusions in the scientific literature.
Thus the “strands in the cable” which formed the circumstantial facts upon which the Arbitrator could draw the necessary inference that the exposure to air pollutants materially contributed to the injury were not sufficiently exposed. Without having dealt with that issue, the Arbitrator was not in a position to reject the opinion of Dr Herman on the basis that it was inconsistent with the findings in the research.
Dr Helprin’s opinion was based upon an assumption that the deceased was in fact exposed to air pollutants in the course of his employment and upon his review of the scientific literature produced with his report and summarised by him. Although the Arbitrator, in his reasons, referred to the appellant’s submissions that Dr Helprin’s opinion lacked a proper analysis and was speculative, the Arbitrator did not address those purported shortcomings when providing his reasons for affording greater weight to the opinion of Dr Helprin over that of Dr Herman.
The Arbitrator reviewed Dr Herman’s evidence, noting that he agreed with Dr Helprin that the scientific literature indicated that there was “indeed” an association between air pollution and the onset of ventricular fibrillation. The Arbitrator further noted that Dr Herman said that the association between out of hospital care and short-term exposure to ambient particulate matter was inconsistent and required larger studies to be undertaken in order to collect more definitive data.
The appellant asserted that Dr Helprin’s opinion was flawed because he overstated the conclusions reached in the scientific literature and did not provide a properly reasoned basis for his assertions. The Arbitrator did not deal with those submissions when assessing the evidence and before accepting Dr Helprin’s opinion. Further, he rejected Dr Herman’s opinion because of its “inconsistency” with the World Health Organisation conclusions without having assessed what those conclusions were and without identifying the inconsistency.

Rejection of Dr Herman’s opinion over that of Dr Helprin on the basis that Dr Herman failed to provide reasons for his conclusions

The appellant is critical of the Arbitrator for taking into account Dr Helprin’s medical speciality when Dr Herman was of the same expertise. I do not consider that the Arbitrator was referring to Dr Helprin’s expertise as being a reason to prefer his opinion over that of Dr Herman. In Amaca Pty Ltd v Booth,[71] Gummow, Hayne and Crennan JJ considered the status of scientific research as evidence in relation to the test of causation. Their Honours said (citation omitted):
“The discipline of epidemiology, and its application in answering issues of causation in litigation, was described by Lord Phillips in Sienkiewicz as follows:
‘Epidemiology is the study of the occurrence and distribution of events (such as disease) over human populations. It seeks to determine whether statistical associations between these events and supposed determinants can be demonstrated. Whether those associations if proved demonstrate an underlying biological causal relationship is a further and different question from the question of statistical association on which the epidemiology is initially engaged.’”[72]
[71] [2011] HCA 53 (Amaca).
[72] Amaca, [86].
That is, while the scientific literature formed a basis upon which a medical opinion could be arrived at, the medical opinion as to the cause of the deceased’s ventricular fibrillation and death must be expressed by an appropriately qualified expert. In this case, both Dr Helprin and Dr Herman held appropriate qualifications, and the Arbitrator was simply observing that Dr Helprin was suitably qualified to offer a medical opinion on causation. He did not reject Dr Herman’s opinion on the basis of lesser qualifications.
The Arbitrator reviewed Dr Herman’s evidence, noting that he agreed with Dr Helprin that the scientific literature indicated that there was “indeed” an association between air pollution and the onset of ventricular fibrillation. The Arbitrator further noted that Dr Herman said that the association between out of hospital care and short-term exposure to ambient particulate matter was inconsistent and required larger studies to be undertaken in order to collect more definitive data.

The Arbitrator further noted Dr Herman’s opinion that:
(a)    it was unlikely the worker was exposed to a significant level of PM2.5;
(b)    given where the deceased lived and worked, and the period of exposure, it was unlikely the worker would have had the same or similar exposure to air pollutants as the exposure presented in the literature, and
(c)    the data linking air pollution to arrhythmia was a hypothesis requiring further large scale studies to accurately assess the levels of pollution exposure.
The Arbitrator rejected Dr Herman’s opinion on the basis that:
(a) Dr Herman did not provide reasons for his conclusion that the deceased would not have been sufficiently exposed to air pollutants, and
(b) Dr Herman’s conclusion that the data linking air pollution to arrhythmia was a “hypothesis,” and larger scale studies were required, was not supported by the extensive research undertaken and reviewed by the World Health Organisation.
Dr Herman based his assertion that the scientific studies were a hypothesis on the rationale that:
“The systematic review of air pollution incidents and out of hospital cardiac arrest had
several limitations including a high degree of heterogeneity between studies and
reporting methods and very few eligible studies being available for review. There were
furthermore potential confounders including diurnal patterns, imprecision of
exposure estimates and the economic deprivation that increases the rates of
morbidity mortality attributed to air pollution were not considered.”[73] (emphasis in the original)
[73] Report dated 16 April 2020, p 3, AALD dated 11 June 2020.
Thus, Dr Herman did provide reasons for his conclusion that the studies were limited to the level of hypotheses. Dr Herman also reasoned that:
“In the paper presented by Kang et al, International Journal of Cardiology Volume 203 (2016) pages 1086-1092, this study showed that increased ambient levels of PM 2.5 [micrograms per cubic metre] were significantly associated with increased risk of OHCA within 1-2 days of exposure. However, in that study performed in Korea, the median of PM 2.5 in Seoul was 22.6 [micrograms per cubic metre] in contrast to 4.8 [micrograms per cubic metre] in Melbourne and 6.8 [micrograms per cubic metre] in Perth. [emphasis in the original]
One would expect even lower levels in regional NSW.
In my opinion, it is unlikely that [the deceased] would have had the same or similar exposure to those presented in the literature (by Dr Helprin) given where he lived and worked and indeed, the period he was subjected to it.”[74]
[74] Report dated 16 April 2020, pp 2–3, AALD dated 11 June 2020.
The above reasoning also points to Dr Herman’s conclusion that the deceased’s exposure levels would have been less than those recorded in the scientific literature. In concluding that Dr Herman did not provide reasons for his opinion in relation to the status of the scientific literature and in relation to the likelihood that the deceased’s exposure would be less than that asserted by Dr Helprin, the Arbitrator did not address those reasons. In failing to do so, the Arbitrator fell into further error in his preference for the opinion of Dr Helprin over that of the evidence of Dr Herman.

CONCLUSION

As the respondents submitted, the authorities are settled on what is required in order to establish error on the part of the Arbitrator in an appeal to a Presidential member. Of relevance to this appeal, the requisite error can be established if it can be shown that the Arbitrator was wrong by:
(a) overlooking material facts, or giving undue or too little weight in deciding the inference to be drawn,[75] or
(b) showing a demonstrable misunderstanding of relevant evidence, or demonstrably failed to consider relevant evidence.[76]
[75] Raulston, [19].
[76] Henderson v Foxworth Investments Ltd [2014] UKSC 41; SLT 775; 1 WLR 2600, [67].
The Arbitrator was required to assess the status to be given and weight to be afforded to the scientific literature, which was evidence taken into account by Mr Prezant, Dr Helprin and Dr Herman in forming their views as to causation. In accepting the opinion of Dr Helprin over that of Dr Herman without considering the matters raised by the appellant and without assessing the status of the conclusions reached in the scientific literature, the Arbitrator overlooked material evidence and fell into what constitutes appealable error. The Arbitrator erred in rejecting the opinion of Dr Herman on the basis that it was inconsistent with the scientific literature and unsupported by reasons.
The Arbitrator’s finding as to causation was affected by error. That finding underpinned the Arbitrator’s consequent findings that the deceased’s employment was a significant contributing factor to the injury (s 9A of the 1987 Act), the employment was the main contributing factor to the aggravation of the deceased’s pre-existing coronary disease (s 4(b)(ii) of the 1987 Act) and that s 9B of the 1987 Act were satisfied. In the circumstances of the appellant having established error of the kind that materially affected the Arbitrator’s ultimate conclusions, it is not necessary nor is it appropriate to consider the remaining grounds of appeal. The Arbitrator’s Certificate of Determination is revoked, and in the circumstances of this case, it is appropriate for the matter to be remitted to another member for re-determination.

DECISION

The Arbitrator’s Certificate of Determination dated 18 December 2020 is revoked.
The matter is remitted for re-determination by another member.

Elizabeth Wood
DEPUTY PRESIDENT

19 August 2021