Fisher v Nonconformist Pty Ltd

[2023] NSWPICPD 12

DETERMINATION OF APPEAL AGAINST A DECISION OF THE COMMISSION CONSTITUTED BY A MEMBER

CITATION:

Fisher v Nonconformist Pty Ltd [2023] NSWPICPD 12 (Clifford No 4)

FIRST APPELLANT:

Kerry Lillian May Fisher

SECOND APPELLANT:

Mark Barry Clifford

THIRD APPELLANT:

Nicole Megan Clifford

RESPONDENT:

Nonconformist Pty Ltd

INSURER:

AAI Limited t/as GIO

FILE NUMBER:

A2-948/20, A3-948/20, A4-948/20

PRESIDENTIAL MEMBER:

President Judge Phillips

DATE OF APPEAL DECISION:

22 March 2023

ORDERS MADE ON APPEAL:

1.     The third appellant’s time to appeal the Member’s decision of 6 May 2022 is extended to 8 June 2022.

2.     The Member’s Certificate of Determination dated 6 May 2022 is confirmed.

CATCHWORDS:	WORKERS COMPENSATION – heart attack injury – whether injury sustained in accordance with section 4 of the Workers Compensation Act 1987 – whether employment is a substantial contributing factor to the injury – section 9A of the Workers Compensation Act 1987 – consideration of the test in Badawi v Nexon Asia Pacific Pty Ltd t/as Commander Australia Pty Ltd [2009] NSWCA 324 – decision makers not confined to the statutory matters at s 9A(2) – epidemiological studies – Seltsam Pty Ltd v McGuiness [2000] NSWCA 29 referred to – approach to expert evidence – Hancock v East Coast Timber Products Pty Limited [2011] NSWCA 11 applied and considered – alleged error in failure to reply to a clearly articulated argument not established – Dranichnikov v Minister for Immigration and Multicultural Affairs [2003] HCA 26; Wang v State of NSW [2019] NSWCA 263 applied and considered
HEARING:	On the papers
REPRESENTATION:	First appellant:
Mr D Adhikary, counsel
Shanahan Tudhope Lawyers
Second appellant:
Mr A J Parker, counsel
Stacks Goudkamp Lawyers
Third appellant:
Mr A Pryor, solicitor
Slater & Gordon Lawyers
Respondent:
Mr S McMahon, counsel
Hicksons Lawyers
DECISION UNDER APPEAL
MEMBER:	Mr P Sweeney
DATE OF Member’s DECISION:	6 May 2022

INDEX TO DECISION

INDEX TO DECISION

INTRODUCTION

BACKGROUND AND EVIDENCE

Report of Dr Helprin dated 5 December 2019

Scientific literature referred to by Dr Helprin

Report of Dr Helprin dated 17 February 2020

Report of Dr Helprin dated 17 January 2021

Reports of Dr Herman

Mr Prezant’s report dated 28 July 2020

Scientific Literature referred to by Mr Prezant

Mr Strautins’ report dated 11 September 2020

Mr Prezant’s report of 4 October 2020

Mr Strautins’ report of 23 October 2020

Chronology

Clifford No 1

Clifford No 2

Clifford No 3

THE MEMBER’S REASONS

ON THE PAPERS

TRANSITIONAL MATTERS

THRESHOLD MATTERS

Application for extension of time to file appeal

Consideration

LEGISLATION

GROUNDS OF APPEAL

First appellant

Second appellant

Third appellant

PRINCIPLES ON APPEAL

DISCUSSION

First appellant’s appeal

As to Ground One: The Member committed errors of law by misapplying the legal test pursuant to section 9A of the 1987 Act

As to Ground Two: The Member committed an error of law by applying a more onerous standard of proof

As to Ground Three: The Member committed an error of fact by failing to address Dr Helprin’s opinion

As to Ground Four: The Member committed errors of fact and/or of law by making determinations that were not based on the evidence

As to Ground Five: The Member committed an error of law by failing to respond to a substantial, clearly articulated argument

Second appellant’s appeal

As to Ground One: Failing to provide lawful reasons

As to Ground Two: Failing to apply the correct legal test concerning s 9A

Third appellant’s appeal

DECISION

INTRODUCTION

1. Mr Terry Clifford (the deceased) was employed as a working director of Nonconformist Pty Ltd (the respondent), a company which provided contract courier services to Direct Courier (Australia) Services Pty Ltd. The deceased had undertaken this subcontract arrangement for Direct Couriers for approximately six years prior to 22 January 2016. The deceased’s work as a courier driver, in broad terms, involved the deceased in driving his courier van to various places to collect items for delivery and delivering them to the allocated destination. Part of the deceased’s job was to pick up animal parts, which were frozen in eskies, from two abattoirs and deliver them to Sydney airport. This latter type of delivery was time dependent.

2. The deceased lived on the Central Coast and his courier routes were usually undertaken in a mixture of rural and Sydney metropolitan areas.

3. On 22 January 2016, the deceased left home on the Central Coast and commenced work at approximately 6am. At approximately 3pm, the deceased was driving his van on Richardson Road, Campvale when the deceased’s vehicle left the roadway whilst travelling at about 80km/h and drove across a grass verge for about 50m before impacting a steel fence post and a tree. The vehicle sustained significant damage in this incident. The police reported that:

   “There were no indications that any attempt to halt the vehicle or apply brakes had been made.”[1]

   [1] Statement of Senior Constable Mark Williamson, 15 March 2018, Application in Respect of Death of Worker (ARDW), p 26, [6].

4. The police attended upon the deceased’s vehicle and attempted to revive him. Despite attempts by attending police officers and medical crews, the deceased regrettably passed away at the scene of the accident at approximately 3.45pm.[2] The cause of death was not the impact of the accident, but rather a heart attack injury (ventricular fibrillation cardiac arrest) which appeared to take place moments prior to the collision.[3]

   [2] Statement of Senior Constable Mark Williamson, 15 March 2018, ARDW, p 29, [23].

   [3] See [10]–[12] of this decision below.

5. As a result of this event, the deceased’s wife, Ms Kerry Lillian May Fisher (the first appellant), and the deceased’s children (Mr Barry Clifford and Ms Nicole Megan Clifford, the second and third appellants) pursued death benefits under the Workers Compensation Act 1987 (the 1987 Act), alleging that the heart attack injury was causally related to employment, primarily, the exposure to traffic related air pollution (TRAP), including particulate matter with a diameter of 2.5 micrometres or smaller, an indicator of air pollution (PM2.5), whilst in the course of duties as a courier driver. It was not disputed by the respondent that the three appellants in these proceedings are the sole dependants of the deceased and are entitled to pursue this application. Their applications for these benefits have been dealt with in the following determinations. For ease of reference, I have numbered each of the three preceding decisions as follows:

   (a)    Fisher v Nonconformist Pty Ltd (948/20, 18 December 2020), 18 December 2020, Arbitrator G Edwards (Clifford No 1)

   (b)    Nonconformist Pty Ltd v Fisher [2021] NSWPICPD 26, 19 August 2021, Deputy President E Wood (Clifford No 2)

   (c)    Fisher v Nonconformist Pty Limited [2022] NSWPIC 201, 6 May 2022, Member P Sweeney (Clifford No 3).

6. In Clifford No 3, Member Sweeney entered an award for the respondent. It is from this decision that the three appellants appeal.

BACKGROUND AND EVIDENCE

1. The facts of this matter are not greatly in dispute.

2. Prior to the accident on 22 January 2016, it is not disputed that the deceased had pre-existing heart disease.[4]

   [4] Autopsy report, ARDW, pp 11–12.

3. There is no dispute that the deceased was in the course of his employment with the respondent and was driving his van on Richardson Road, Campvale. It is not disputed that the motor vehicle accident did not cause or contribute to the deceased’s death. It is not disputed that the cause of death was a heart attack.

4. The observations of the attending police officers, and in particular Senior Constable Mark Williamson, are stated as follows:

   “4.     Several minutes before 3.00pm on Friday 22nd of January 2016, a white Hyundai iload light goods vehicle was travelling east on Richardson Road at Campvale NSW. This vehicle, NSW registration [redacted] was being driven by the vehicle's owner, a 65 year old male, the deceased Terry Raymond CLIFFORD who used it as a courier van. The deceased worked in this role for Direct Couriers as a contractor.

   5.     Whilst continuing east the vehicle has left the roadway on the nearside whilst travelling at about 80km/h, travelling across the northern grass verge for about 50m before impacting with a steel fence post and then heavily impacting a tree with a diameter of about 40cm. This tree, the catastrophic point of impact is 510 m east of the intersection of Richardson Road and Grahamstown Road.

   6.      The vehicle sustained extreme frontal damage across the centre and offside with both air bags deployed. The tree was felled by the impact and landed across the roadway, blocking traffic in both directions. There were no indications that any attempt to halt the vehicle or apply brakes had been made. At this time there was moderate traffic and the incident was witnessed by a number of persons travelling immediately behind the vehicle driven by the deceased, including;

   WITNESS 1: [C] MCKAY …

   WITNESS 2: [T] MCKAY…

   …

   9.      I ran to the deceased[’s] vehicle and saw the deceased upright in the driver’s seat, slumped forwards with his weight being supported by the seatbelt. The interior of the vehicle was full of what appeared to be smoke or fine powder. It was readily apparent that this was fine powder, of the [kind] released when airbags are explosively deployed. Also at the driver’s door was the above witnesses MCKAY who had immediately stopped their vehicle and rushed to the deceased’s vehicle.

   10.    The deceased appeared to have a blue hue with darker shades to a light purple around the mouth and his tongue was slightly protruding. I felt for a carotid pulse and could not find one, there was no breathing sounds or indications detectable. Accounts of the witnesses MCKAY indicate that these initial observations of the deceased of mine had occurred about 60 seconds after impact with the tree, with a maximum of about 90 seconds possible.

   11.    At this time Senior Constable HOUSTMA was approaching quickly from the police vehicle. I yelled to Constable HOUSTMA to contact police radio and advise them that Ambulance units were requested as a matter of urgency as was the fire brigade in relation to the tree across the roadway.

   12.    I undid the seatbelt across the deceased and began to pull him from the vehicle. As I began [to] move the deceased he appeared to take a single large spasmodic inhalation. I laid the deceased flat on the ground, about 1.5 metres from the driver's door.

   13.    A pulse could still not be detected and there was no further indication of breathing present. I placed the deceased on his side before I cleared his airway. I found that phlegm like frothy discharge was present. While in the recovery position while the airway was being cleared no pulse was found. I began Cardio Pulmonary Resuscitation (CPR) on the deceased. Active compressions were begun at no more than about 120 to 130 seconds after the impact with the tree.

   14.    I continued CPR with Constable HOUSTMA and periodically updated radio and heard a number of police units also acknowledge the job and begin to converge on the location.

   …

   17.    The CPR efforts appeared to be having an effect with some colour returning to the deceased’s extremities and the blue hue somewhat dissipating. About 3.10pm Ambulance unit RT262 arrived with Ambulance officers Kate OWENS and Michael WALMLEY attending.

   …

   19.    At 3.17pm the attending ambulance officer updated their radio network and the police radio network that the Westpac Helicopter had been engaged and was about 5 minutes away from the area. Police continued active compressions with ambulance officers supervising, monitoring and administering various medications.

   20.    Over the course of the next 20 to 25 minutes the deceased was given numerous injections of adrenaline at scene and was shocked using a defibrillator many times. The deceased remained a systolic and unresponsive.

   21.    At 3.25pm the Westpac helicopter landed at the Grahamstown sports ground, which is located several kilometres from the incident site. Highway patrol vehicles conveyed the officers and equipment from that location to the incident site.

   22.    The Westpac Medical Emergency Response Helicopter crew in attendance consisted of Dr Cynthia BIERL and Specialist Ambulance Officer Jeremy VENESS …

   23.    The driver was declared deceased at scene at 3.45pm by the attending Westpac Emergency Response Doctor, Dr Cynthia BIERL. Indications suggest the driver suffered a critical medical incident, most likely a heart attack (myocardial infarction) prior to leaving the roadway.

   …

   30.    The deceased was renowned as a reasonably healthy individual who did not complain of illness or infirmity. The deceased did not take any medications on a regular basis and did not see doctors regularly. His wife had noted a slight degradation in his general condition during the previous six months. On the night before the deceased's day of death the deceased remarked to his wife that he had some back pain. The deceased had travelled extensively in the years preceding his death, visiting about thirty countries in the previous two to three years. The deceased had only recently returned from a trip to Morocco, Spain and the Middle East, where he travelled with his wife.”[5]

   [5] ARDW, pp 25–30.

5. An autopsy was carried out on the deceased at the Department of Forensic Medicine, Newcastle on 27 January 2016.[6] The findings of this report are not in dispute. The opinion expressed by the pathologists (Dr Rexson Tse and Dr Allan Cala) is as follows:

   [6] ARDW, pp 11–18.

   “OPINION

   I acknowledge that I have read the Expert Witness Code of Conduct in Schedule 7 of the NSW Uniform Civil Procedure Rules 2005; and agree to be bound by the code.

   Based on what I have observed, my experience and training, and the information supplied to me:

   Terry CLIFFORD died on the 22nd January 2016 at Richardson Road, Campvale, NSW 2318 and that the cause of death is as follows:

   1. DIRECT CAUSE:

   Disease or condition leading to death:

   (a)     ISCHAEMIC HEART DISEASE

   ANTECEDENT CAUSES:

   Morbid conditions, if any, giving rise to the above cause, stating the underlying condition last:

   (b)     CORONARY ARTERY ATHEROSCLEROSIS

   (c)     ***

   2. Other significant conditions contributing to the death but not relating to the disease or condition causing it:

   [blank].”[7]

   [7] ARDW, p 12.

6. In the comments section of the autopsy report, the doctors note as follows:

   “1.     This man died from ischaemic heart disease secondary to coronary artery atherosclerosis.

   2.      Examination of the heart showed significant ischaemic heart disease. The heart was enlarged (590 grams) with an old myocardial infarction and significant coronary artery atherosclerosis in all the main coronary arteries. The extent of ischaemic heart disease found in this man was such that sudden death would have occurred at any point in time.

   3.      There were no injuries recognised that would have explained his death.”[8]

   [8] ARDW, p 13.

7. The deceased’s stepson, Simon Ross, gave evidence, which was not disputed, that the deceased’s job was demanding and stressful.[9]

   [9] ARDW, pp 49–50.

8. The deceased’s wife (the first appellant) provided two statements[10] which note that prior to the accident the deceased was generally in good health apart from a genetic disorder which is not relevant for these proceedings. The first appellant gives evidence about the long hours worked by the deceased, the time pressure he worked under and the fact that he spent many hours alone on the road.[11]

   [10] ARDW, pp 51–54 (dated 13 July 2018) and p 55 (dated 6 February 2019).

   [11] ARDW, p 52, [12]–[14].

9. In the months following his death, a claim was made by the deceased’s dependants on the respondent’s insurer, AAI Limited t/as GIO. By notice issued under s 74 of the Workplace Injury Management and Workers Compensation Act 1998 (the 1998 Act) on 18 May 2016, and upheld on review on 23 November 2017, the insurer declined the dependants’ claim for death benefits under the 1987 Act.[12]

   [12] ARDW, pp 39­–42.

10. The insurer disputed that the deceased’s death resulted from an injury within the definition of s 4 of the 1987 Act and further disputed that the deceased’s employment was a “substantial contributing factor” as contemplated by s 9A of the 1987 Act. If the injury was a disease, the insurer also disputed that the disease was contracted in the course of employment and that employment was the main contributing factor to the disease or its aggravation pursuant to s 4(b) of the 1987 Act. The insurer disputed that the deceased’s employment gave rise to a significantly greater risk of the deceased suffering a heart attack than had he not been engaged in employment of that nature in accordance with the requirement of s 9B of the 1987 Act.

11. Some four years after the death, proceedings were commenced by the dependants in the former Workers Compensation Commission on 20 February 2020 and the matter was first heard on 30 October 2020 by Arbitrator Edwards who determined the matter in favour of the dependants. This decision was successfully appealed (Clifford No 2). The matter was reheard after an appeal in the Personal Injury Commission on 9 April 2022 by Member Sweeney, who found against the claim made by the dependants. I will summarise these findings later in this decision.

12. The dispute which proceeded on each occasion before the Commission was about whether or not the undoubted heart attack suffered by the deceased whilst driving his van was an injury as contemplated by s 4(a) of the 1987 Act, or whether it was a disease which had been aggravated in the course of his employment in accordance with s 4(b)(ii) of the 1987 Act. If the answer to either or both of these questions is yes, it was then necessary for the appellants to satisfy the requirements found in ss 9A and 9B of the 1987 Act.

13. The dispute is essentially a contest between the opinions of the parties’ respective experts and cardiologists on the question of causation. As stated above, there is no dispute about the fact of the accident, the fact that the deceased had a pre-existing heart condition, nor is there any dispute about the findings on autopsy. The evidence given by the three appellants is also not in dispute for the purposes of this appeal.

14. As I will summarise below, the appellants’ evidence was to the effect that the deceased, in the course of his employment as a courier driver, had been exposed to TRAP and stress, the combination of which was the predominant cause of the deceased’s ventricular fibrillation and death. The appellants’ principal medical evidence comes from Dr Garry A Helprin, consultant cardiologist. This opinion of Dr Helprin,[13] was based upon Dr Helprin’s skills, experience and by reference to various scientific studies about the association between ventricular fibrillation, ventricular arrhythmia (or cardiac arrest) and air pollution. Dr Helprin also relied upon calculations supplied by occupational hygienist, Mr Bradley Prezant, about the deceased’s possible exposure to pollution on 22 January 2016. The respondent disputed this opinion based upon the evidence of cardiologist, Dr Mark Herman, and Mr Carl Strautins, an occupational hygienist.[14]

    [13] ARDW, pp 56–115 (dated 5 December 2019) and pp 116–117 (dated 17 February 2020).

    [14] Reply to ARDW (reply) pp 8–13 (dated 4 March 2019), Application to Admit Late Documents (AALD), 11 June 2020, pp 1–5 (dated 16 April 2020).

Report of Dr Helprin dated 5 December 2019

1. Dr Helprin provided two reports dated 5 December 2019[15] and 17 February 2020.[16] In Dr Helprin’s report of 5 December 2019, he neatly propounds the circumstances of the deceased’s death and the appellants’ claim in the following manner:

   “Agreed Facts

   1.      At autopsy, Mr Clifford had an old anterior myocardial infarction with severe narrowing of the left anterior descending artery. This was not the direct cause of death but a contributing or underlying factor.

   2.      Mr Clifford most likely had a ventricular fibrillation cardiac arrest on the basis of his pre-existing coronary disease. Ventricular fibrillation is a highly lethal abnormal rhythm of the heart and this occurred while he was driving and this caused him to crash his car. In other words, it was not the car crash that caused Mr Clifford's death, it was the ventricular fibrillation which is a new condition or injury on the basis of preexisting old coronary artery disease.

   I think the thing to focus on in this case is the fact that Mr Clifford developed ventricular fibrillation which he’d never had before while he was at work driving his car.”[17] (emphasis in original)

   [15] ARDW, p 56.

   [16] ARDW, p 116.

   [17] ARDW, p 57.

1. Dr Helprin deals with the question raised by s 9B, being whether the nature of employment gave rise to a significantly greater risk of injury had he not been employed in employment of that nature, as follows:

   “Question 2

   ‘Whether the nature of the deceased’s employment gave rise to a significantly greater risk of the worker suffering the injury than had the worker not been employed in employment of that nature.’

   This is really the key question. Everyone agrees that Mr Clifford suffered a ventricular fibrillation cardiac arrest in the context of driving his car at work. Mr Clifford’s work place is prone to environment air pollution especially around the airport. Mr Clifford had never had ventricular fibrillation before.

   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. Therefore, the nature of the employment, i.e. Professional Driver, gave rise to significant greater risk of the worker suffering the injury, i.e. ventricular fibrillation, than had the worker not been employed in employment of that nature. There’s obviously significantly greater risk in the work-related environment of exposure to pollutants which can be the main factor in a case of ventricular fibrillation as well as stress.

   Therefore, it’s my contention that Mr Terry Clifford’s work as a Professional Driver in which he was undoubtedly exposed to environmental air pollution as well as stress was the predominant factor in the causation of the injury of ventricular fibrillation which was the causative factor in death.”[18]

   [18] ARDW, p 58.

2. There is no doubt that the deceased suffered a ventricular fibrillation cardiac arrest whilst driving his car in the course of his employment. Dr Helprin is of the opinion that the injury of ventricular fibrillation was as a result of the deceased’s exposure to environmental air pollution, as well as stress, whilst performing his occupation as a courier driver.

Scientific literature referred to by Dr Helprin

1. Dr Helprin refers to a number of scientific articles that examine the association between air pollution and ventricular arrhythmias or ventricular fibrillation. Given that this literature underpins the opinion of Dr Helprin, it is necessary to refer to it briefly to understand the doctor’s opinion.

2. In a European Heart Journal article titled “Rapid effects of air pollution on ventricular arrhythmias” published on 12 November 2008, a study was conducted on 211 patients with implanted cardioverter defibrillators (ICDs) in Stockholm and Gothenburg, Sweden. [19] Air pollution and meteorological data were obtained from roof-top monitors in each city, although data for PM2.5 were only available for Stockholm. The data from the study showed that 73 of the 211 patients had 114 ventricular arrythmias. In the patients, pre-existing ischaemic heart disease was the most common cardiovascular condition. The study found that the risk of ventricular arrhythmias was associated with increased levels of pollution in the preceding 2-hour exposure period, although there was a stronger association with PM10 in Gothenburg than PM2.5 in Stockholm. The authors note that this is the first European study investigating the association between air pollution and ventricular arrhythmias in patients with ICDs, although some earlier ICD studies have shown mixed results. The authors describe the mechanism by which air pollution can cause sudden cardiac death. They explain that the sudden death, precipitated by ventricular arrhythmias, is a consequence of processes involving ischemia, previously damaged myocardium and fluctuating myocardial vulnerability.

   [19] ARDW, p 59.

3. The study concludes that “ventricular arrhythmias in ICD patients appear to be associated with moderate increases in air pollution already within the 2 preceding hours”, however further research is required to confirm these findings, as “representative geographical exposure classification seems important in studies of these effects”. (emphasis added)

4. An article from the International Journal of Cardiology titled “The impact of short-term exposure to air pollutants on the onset of out-of-hospital cardiac arrest: A systematic review” published on 25 October 2016 reviewed 15 studies to analyse the acute effects of air pollution, including PM2.5, on out of hospital cardiac arrest (OHCA).[20] The studies referred to were located in the USA, Japan, China, Korea, France, and in Melbourne and Perth, Australia. It found an association between short-term exposure to environmental pollution, particularly PM2.5, and OHCA. The authors also considered studies on mice, and asserted that PM2.5 is considered to trigger cardiovascular disease related mortality, including myocardial infarction, stroke and OHCA, but concluded that further research is needed to investigate the association between individual exposure levels and OHCA risk, particularly for people with chronic cardiovascular diseases.

   [20] ARDW, p 70.

5. There is an article from the Journal of Epidemiology and Community Health, entitled “A systematic review of air pollution and incidence of out-of-hospital cardiac arrest”.[21] This report aimed to identify, evaluate and summarise the studies of air pollution and OHCA to examine the hypothesis that air pollution is associated with OHCA. It did this by examining eight studies, five in USA, two in Europe, and one in Melbourne, Australia. It found that larger studies have suggested an increased risk of OHCA with exposure to air pollution, including PM2.5, with five studies finding an association and three not. In discussion of the limitations of this study, the article notes that ambient pollution levels measured at monitoring sites can be different to the individual’s actual exposure. It is also hard to accurately measure an individual’s exposure where they are moving to different locations or if there are fewer monitoring sites covering a larger area. Another limitation was the limited number of studies and the heterogeneity between studies and reporting methods. The article concludes that the association is “inconsistent”, although recent studies have found a positive association. It suggests that further, larger studies are needed.

   [21] ARDW, p 79

6. An article from the International Journal of Cardiology titled “Ambient air pollution and out-of-hospital cardiac arrest” examined the impact of short-term exposure to air pollution (including PM2.5) on the occurrence of OHCA in Seoul between 2006 and 2013.[22] It found that the risk of OHCA increased significantly with even mild elevation of PM2.5, and further increased with higher levels within 1 to 2 days of exposure, a risk higher for males with existing heart disease or hypertension. Although this study found a positive association, it noted that other studies have had inconsistent results. The study reported the strength was in the large sample size, but was limited due to the lack of detailed information on the cause of the cardiac arrests, the weight and smoking status of the patients, details of other underlying diseases in patients, and limited knowledge of meteorological variables.

   [22] ARDW, p 86.

7. Another article from the same journal titled “Association of Short-term Ambient Air Pollution Concentrations and Ventricular Arrhythmias” evaluated the association between ventricular arrhythmias detected by ICD devices and ambient air pollution concentrations in the hours immediately before the arrhythmia.[23] It was conducted on patients in Boston, USA who had an ICD implanted between 1995 and 1999 and followed the subjects until 2002. During this time, there were 595 ventricular arrhythmias in 75 study subjects where PM2.5 was measured. The findings of the study suggest that ambient air pollution is associated with an increased incidence of ventricular arrhythmias among patients with ICD devices.

Report of Dr Helprin dated 17 February 2020

[23] ARDW, p 93.

1. In this supplementary report, Dr Helprin confirms that the deceased’s injury (ventricular fibrillation) was not an aggravation, acceleration, exacerbation or deterioration of his pre-existing heart condition, but a separate injury. He characterises the ventricular fibrillation as a separate condition as it is an electrical disturbance of the heart, as opposed to a vascular injury. The doctor maintains that the deceased’s work as a long-haul courier driver was a substantial contributing factor and the main contributing factor was exposure to ambient pollution which triggered the electrical disturbance, which would not have occurred otherwise. He refers to the scientific literature referred to in his previous report to demonstrate that “ventricular fibrillation is causally related to exposure to ambient pollution.”

Report of Dr Helprin dated 17 January 2021

1. In this report, Dr Helprin notes there are further scientific reports emphasising the association between air pollution and the risk of sudden cardiac death from ventricular arrhythmia, particularly in vulnerable patients. He provides a discussion of their significance.[24]

   [24] AALD, 3 February 2022, p 99.

2. He reviews a 2021 article entitled “Air Pollution and Cardiac Arrhythmias: A Comprehensive Review” where 121 studies were conducted and concluded that “short-term and long-term exposure to the air pollutants can interact with cardiac rhythms through oxidative stress, autonomic dysfunction, coagulation dysfunction, and inflammation. It seems that particulate matter, especially PM2.5, have stronger association with cardiac arrhythmias among all air pollutants.” [25]

   [25] This article is annexed to AALD, 3 February 2022, p 135.

3. He reports on a 2021 article entitled “Cardiovascular Dangers of Air Pollution"[26] which reviewed several studies, including studies conducted in Rome and Sao Paulo, to demonstrate an association between particulate matter and sudden cardiac death.

   [26] This article is annexed to AALD, 3 February 2022, p 114.

4. Dr Helprin refers to a article entitled “Exposure to Air Pollution and Particle Radioactivity with the Risk of Ventricular Arrhythmias”[27] which detailed a study conducted on 176 subjects in Boston, Massachusetts and concluded that particle air pollution and its radioactive components contribute significantly to the risk of acute clinically relevant electrophysiological cardiac outcomes in high-risk patients.

   [27] This article is annexed to AALD, 3 February 2022, p 104.

5. Dr Helprin discusses a 2020 editorial article entitled “Air Pollution, climate and cardiac arrest”[28] that analysed 39,000 OHCA cases in Korea between 2012 to 2016 to link environmental exposure to OHCA. Dr Helprin emphasises the large-scale nature of the study.

   [28] This article is annexed to AALD, 3 February 2022, p 132.

6. The final article, by the National Heart Foundation of Australia, is entitled “Environment, climate change and heart health” from 2021.[29] It says that in Australia in 2015, air pollution caused 2,500 deaths, with people with heart conditions being most at risk. Further, the article recommends those with heart conditions avoid spending a lot of time in places that have higher air pollution levels, such as near busy roads or factories.

   [29] This article is annexed to AALD, 3 February 2022, p 123.

7. Dr Helprin then responds to several questions posed by the first appellant’s legal representative. In response to Dr Herman’s opinion, Dr Helprin opines that the association is no longer a mere hypothesis but an established scientific fact. He notes that the Australian public receives mass communication to stay inside when air pollution increases, particularly those with chronic lung, heart and other health conditions. Dr Helprin relies on the above articles to show the link between exposure to road based atmospheric air pollution and ventricular fibrillation. He says that although Dr Herman takes issue with the use of pollution levels in Seoul, he has now provided studies from Rome, Boston, Houston and Sao Paulo, some of which have similar levels of pollution to Sydney.

8. Dr Helprin maintains his view that the deceased’s employment as a courier driver was the main contributing factor to the ventricular fibrillation. He refers to Mr Prezant’s modelling that shows increased exposure to PM2.5 at work on the roads than compared to at home. He says that the articles clearly indicate a link and explain the fatal ventricular arrythmias, and the deceased’s risk factors do not explain his sudden death from ventricular arrhythmias, only the prior myocardial infarction.

9. Dr Helprin concurs with Dr Herman that most sudden cardiac deaths occur without a documented trigger and in the early hours when patients are not particularly stressed or exposed to environmental toxins. He notes that given those circumstances, the death in question is unusual and requires an explanation. He says that the exposure to environmental pollution provides the most logical and likely explanation for why the death did not occur in those usual circumstances and occurred in the working environment on the road.

10. Dr Helprin notes that Australia cannot replicate every medical study and must rely on international studies. He states that the National Heart Foundation of Australia recognises the international studies he has provided and gives specific advice to avoid busy roads.

Reports of Dr Herman

1. In contrast, the first respondent relies upon the reports of Dr Herman, cardiologist. This doctor provides his initial opinion on 4 March 2019, prior to Dr Helprin’s first report.[30] In this report, the doctor notes the deceased’s history of hypercholesterolaemia, hypertension, impaired fasting glucose and depression, conditions which are strongly associated with cardiovascular risk.

   [30] Reply, p 8.

2. Dr Herman finds that the sudden cardiac event on 22 January 2016 was due to arrhythmia or ventricular fibrillation. Thus, both doctors are in agreement as to the mechanism of the cardiac event. However Dr Herman is of the view that the deceased’s employment was not a significant contributor to either the ventricular fibrillation or the heart disease that the deceased was undoubtedly suffering from. Dr Herman posits the following view:

   “In my opinion, the medical cause of his death was due to a cardiac arrhythmia (ventricular tachycardia with ventricular fibrillation) provoking sudden loss of cardiac output and cardiac death. This is not uncommon in patients with previous myocardial infarctions particularly when involving the anterior wall (as was the case in Mr Clifford at autopsy).”[31]

   [31] Reply, p 10.

3. On 16 April 2020, Dr Herman provides a report in which he was asked to comment upon Dr Helprin’s view about whether air pollution caused the deceased’s heart attack and to consider the literature referred to by Dr Helprin. Dr Herman states as follows:

   “As per the literature referred to by Dr Helprin, there is indeed an association between air pollution and out of hospital cardiac arrest (OHCA), or alternatively the onset of ventricular fibrillation. The association however is modest at worst compared with conventional cardiovascular risk factors and the pathophysiological mechanism by which air pollution exerts its effects on cardiovascular disease remains unclear.”[32]

   [32] AALD, 11 June 2020, p 2.

4. Dr Herman continues, in respect of the report I have summarised at [28] above:

   “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.”[33]

   [33] AALD, 11 June 2020, p 2.

5. Dr Herman then queries the exposure in regional NSW in comparison to the studies, and asserts: “Finally, the strength of the association between exposure and cardiac arrest was modest at best”.[34]

   [34] AALD, 11 June 2020, p 3.

6. Ultimately, Dr Herman was of the view that the data linking air pollution to arrhythmic events is “hypothesis generating requiring further large scale studies”. He also states that the presence of quinine in the deceased, as found in the toxicology report, is relevant in that quinine can promote cardiac arrythmia and is more likely to do so than environmental exposure to toxins.[35]

   [35] AALD, 11 June 2020, p 3.

7. Dr Herman then reaches his ultimate conclusion that air pollution was not the main contributing factor to the deceased’s cardiac arrest or ventricular fibrillation. Dr Herman also opines that the level of exposure to pollution and the type of particulate matter that the deceased was exposed to is “purely speculative”.[36]

   [36] AALD, 11 June 2020, p 4.

8. In a further report dated 9 October 2020, Dr Herman has the opportunity to review Mr Prezant’s reports (referred to below) and maintains his previous opinion that the deceased’s employment was not the main contributing factor to his injury and death. He says that it was a result of multiple traditional cardiac risk factors associated with previous myocardial infarction. He reports that Mr Prezant’s report had not changed his opinion as the association between exposure to air pollution and cardiac events is negligible compared to traditional risk factors and the risk of sudden cardiac death where there has been a previous heart attack causing heart muscle damage (ischaemic cardiomyopathy). For the same reason, Dr Herman confirms that the deceased’s employment was not a substantial contributing factor to the injury causing death, nor did it create a significantly greater risk of him suffering a heart attack injury.[37]

   [37] AALD, 23 October 2020, p 6.

Mr Prezant’s report dated 28 July 2020

1. Mr Prezant is a certified occupational hygienist specialising in epidemiology who was qualified by the first appellant to provide an opinion on TRAP and cardiac events, specifically in respect of the deceased. In this initial report,[38] Mr Prezant agrees with Dr Helprin’s opinion that there is a causal relationship between ambient air pollution and sudden cardiac events, including the ventricular fibrillation suffered by Mr Clifford. This opinion is based on scientific literature to which he refers. I would note, however, that Mr Prezant is not relevantly qualified to posit a view about Dr Helprin’s medical opinion. Mr Prezant accepts this proprosition.[39]

   [38] AALD, 28 July 2020, p 1.

   [39] AALD, 28 July 2020, p 11, [40].

2. Mr Prezant refers to a 2013 report prepared by the World Health Organisation (WHO) “Review of evidence on health aspects of air pollution – REVIHAAP Project” which asserts an increase in daily mortality associated with PM2.5, evidenced in studies performed in the United States, Canada, Stockholm, and Barcelona. Mr Prezant refers to studies within the WHO report indicating the effects of exposure to traffic pollution, including diesel vehicle exhausts, reduce cardiovascular function (worse in patients with heart problems), and that PM2.5 has typically been associated with cardiovascular and respiratory health, but not always. Mr Prezant notes that studies referred to by the WHO suggest that 1–2 hours of exposure may be enough to lead to harmful physiological changes, but the WHO report notes that the biological mechanism by which exposure to air pollution from traffic causes adverse cardiovascular events remains unclear.

3. This report from the WHO is in evidence.[40] It is a technical report that answers 24 questions relevant to reviewing European policies on air pollution and health aspects of these policies. It concludes that there is a considerable amount of new scientific information on the adverse effects on health of particulate matter. Relevantly, it finds that the risk of ischaemic heart disease, which includes heart attacks, has particularly strong and consistent associations with PM2.5. The report also describes the biological mechanisms, stating that studies show exposure to PM2.5 is associated with systemic inflammation, oxidative stress and alteration of the electrical processes of the heart.[41] It has findings in respect of exposure to roads. It notes a limited number of short-term studies that have been based on source apportionment and that “because of limited data and large variability in outcomes and available source indicators and/or categories, traffic cannot be ranked yet relative to other particle sources with respect to harmfulness.” In terms of exposure times, the report notes that no studies have evaluated whether, for example, a high 1-hour exposure would lead to a different response than a similar dose given for 24 hours or for repeated very short-term exposures.

   [40] AALD, 28 July 2020, p 31.

   [41] AALD, 28 July 2020, p 45.

1. Mr Prezant cites another article[42] to support his conclusion that exposure to PM2.5 on freeways is 10 times the ambient levels measured by air pollution stations. This article states that pollutant concentration levels on arterial roads appear to be one-third of those of freeways. Further, due to “the typically high air exchange rates of moving vehicles, in-vehicle concentrations are typically close to roadway concentrations.” He notes that there is some reduction due to the filtration system in the vehicle. These conclusions were used to model the deceased’s exposure levels.

   [42] Scott Fruin ‘Measurements and predictors of on-road ultrafine particle concentrations and associated pollutants in Los Angeles’ (2008) 42(2) Atmospheric Environment 207, AALD 28 July 2020, pp 352–353.

2. Mr Prezant uses data from the closest monitoring station (approximately 25.7km away) to calculate the average level the deceased would have experienced between 6pm and 6am at his home in Woy Woy. He then uses a spreadsheet to track the deceased’s movements on the day of his death, noting the roads he travelled and the estimated time spent on these roads. He estimated that the deceased spent 21 minutes on rural highways, 37 minutes on urban streets, 3 hours and 4 minutes on highways and 13 minutes on suburban roads. He provides a map of these roads and identifies the locations of the monitoring stations. He then calculates the periods when the deceased was not travelling in his vehicle, labelled as “unaccounted time” or “lunch”, which was time where the deceased was likely at the Bankstown depot or dropping off or picking up packages. He estimates these periods to be approximately 3 hours and 44 minutes.

3. Mr Prezant adjusts the deceased’s exposure levels to account for the different street types and the fact that he was in a vehicle. He concludes that the deceased was exposed to higher levels compared to a person not driving a vehicle in those areas.[43] Further, he reports that these calculations are likely an underestimation of Mr Clifford’s exposure on the day of his death.

   [43] Mr Prezant calculates the deceased was exposed to approximately 25.7 µg/m³ compared to typical exposures for a person not driving a vehicle of 7.4 µg/m³ in Earlwood, 7.2 µg/m³ in Chullora, 5.5 µg/m³ in Wyong, and 7.2 µg/m³ in Wallsend.

4. Mr Prezant notes that Dr Helprin is a physician who can comment on the medical issues specific to Mr Clifford, but he is qualified to speak to the exposures and their impact on public health as reflected in literature. The levels Mr Clifford was exposed to are “consistent with those levels of exposure that the scientific literature has associated with increased risk of sudden coronary events”.

5. Mr Prezant concludes that courier drivers, by the nature of their employment on the roads, are exposed to more traffic-related pollution (particularly PM2.5 and ultrafine particles) when compared with other types of workplaces, such as offices, schools, retail, wholesale and other indoor locations. This increased exposure can be up to 10 times that of other workplaces.

Scientific Literature referred to by Mr Prezant

1. Annexed to Mr Prezant’s report is a 2007 article from the New England Journal of Medicine titled “Ischemic and Thrombotic Effects of Dilute Diesel-Exhaust Inhalation in Men with Coronary Heart Disease”.[44] This was a study conducted on 20 men with prior myocardial infarction. The participants were exposed to dilute diesel exhaust or filtered air for 1 hour during periods of rest and moderate exercise. After 6 hours of exposure, the participants were reviewed to determine the direct effects of air pollution on myocardial, vascular and fibrinolytic function.

   [44] AALD, 28 July 2020, p 340.

2. The study found that brief exposure to dilute diesel exhaust (levels occurring in urban road traffic) promotes myocardial ischemia and inhibits the heart’s capacity to break down blood clots in men with stable coronary heart disease. The study documented myocardial ischemia was increased by a factor up to three after inhalation of diesel exhaust.

3. An article titled “Reduction in Heart Rate Variability with Traffic and Air Pollution in Patients with Coronary Artery Disease” from 2010 observed 46 subjects, whose heart rate variability (HRV) was studied in their homes on up to four occasions during the year after a documented coronary artery disease, with 18 having experienced an acute myocardial infarction.[45] The results of the study suggest that short-term traffic exposure and ambient exposure to air pollution are associated with significant reductions in HRV.

   [45] AALD, 28 July 2020, p 348.

4. There is an American article titled “Models for Predicting the Ratio of Particulate Pollutant Concentrations Inside Vehicles to Roadways” wherein a study conducted in 2013 aimed to measure the ratio concentration of different particulate matter (including PM2.5) inside a vehicle compared to on the roadway. It considered ventilation settings, driving speed and vehicle characteristics.[46] Six vehicles were selected to reflect different age, mileage, volume, and manufacturer. These factors have previously been identified as significant determinants of the air exchange rate and ultrafine particle concentrations inside/outside ratios. It concluded that in identical roadway concentrations, differences in ventilation setting, speed, and vehicle characteristics create a 2−5-fold difference in exposure inside vehicles.

   [46] AALD, 28 July 2020, p 368.

5. A research article titled “Hourly Exposure to Ultrafine Particle Metrics and the Onset of Myocardial Infarction in Augsburg, Germany” has been supplied.[47] It investigates the relationship between different particle length, number and surface area and myocardial infarction at an hourly timescale. The article concludes that transient exposure to particle number, length, and surface area concentrations or other potentially related exposures may trigger the onset of nonfatal myocardial infraction.

   [47] AALD, 28 July 2020, p 376.

6. In a UK article titled “Characterisation of nanoparticle emissions and exposure at traffic intersections through fast-response mobile and sequential measurements”,[48] a study aimed to identify traffic conditions under which traffic lights become hot spots for particle concentration, assess the effect of ventilation settings on concentrations inside the vehicle at traffic lights, and quantify the contribution of exposure at traffic lights with respect to exposure during the whole commute. The study found that traffic lights were a hot-spot for particle exposure, particularly due to vehicles accelerating from idle conditions. Particle exposure inside the vehicle compared to outside was reduced (up to 70%) the most during free-flow traffic conditions, when the fan was drawing outdoor air into the vehicle and the heating was switched off. During delay conditions, concentrations were reduced the most (88%) when the fan was drawing outside air at 25% and heating was on 50%. Short term exposure for about 2% of total commuting time in car corresponded to approximately 25% of total exposure during the commute.

   [48] AALD, 28 July 2020, p 386.

7. Finally, there is an Australian article titled “Traffic-related fine and ultrafine particle exposures of professional drivers and illness: An opportunity to better link exposure science and epidemiology to address an occupational hazard?”.[49] This article suggests that the health outcomes of professional drivers provide an area for scientists to examine the effects of TRAP on health. It explores the hazard created by TRAP, the health effects attributable to exposure, determinants of exposure and strategies to reduce exposure. The article reports that it is now increasingly apparent that ultra-fine and fine particles are associated with adverse cardiovascular outcomes. It notes that the causative mechanism behind this requires further research. The article notes the research which shows that exposure to particles for up to 2 hours has been associated with decreased heart rate variability, higher incidence of ectopic beats, and elevated biomarkers of inflammation. However, it also notes research that has shown controlled exposure to dilute diesel did not alter heart rate rhythm or variability. The report states that this area requires further investigation to understand the inconsistent study results.

   [49] AALD, 28 July 2020, p 403.

Mr Strautins’ report dated 11 September 2020

1. Mr Strautins, occupational hygienist, is relied on by the respondent.[50] Mr Strautins first provides an overview to characterise workplace exposure. He considers Mr Prezant’s methodology and reports that Mr Prezant had come to his conclusions by reviewing studies that associate background levels of environmental pollution, being particulate matter about 2.5 microns in diameter, with cardiovascular disease. He reports that Mr Prezant concluded that because Mr Clifford was a courier driver, he was exposed to levels of particulate matter that he otherwise would not be exposed to in the course of his employment and was therefore at an increased risk of a cardiac event.

   [50] AALD, 7 October 2020, p 10.

2. Mr Strautins compares this with his experience and the general methodology occupational hygienists use when assessing workplace exposures and their significance, as outlined in the Australian Institute of Occupational Hygienists (AIOH) Simplified Risk Management Strategies, which is different to the approached used by Mr Prezant. He states that the approach he outlines, although simplified, is industry standard and consistent with professional industry guidelines.

3. Mr Strautins then turns to the deceased’s exposure to particulate matter. He reports that there are no prescriptive requirements in the NSW Work Health and Safety Regulation 2017 for general non-toxic particulate matter. He says the particulate matter is considered a nuisance dust or dust not otherwise classified. Therefore exposure should be maintained as consistent with Safe Work Australia’s Guidance on the Interpretation of Workplace Exposure Standard for Airborne Contaminants.

4. Mr Strautins reports that the Australian Institute of Occupational Hygienists Exposure Standard Committee undertook a review of exposure to nuisance dust or dust not otherwise classified in 2014. The findings identified Chronic Obstructive Pulmonary Disease (COPD) as an adverse health outcome. Mr Strautins writes that although there may be an association between COPD and cardiovascular function, cardiac events are not linked as a health outcome. Therefore the exposure to nuisance dust is not a significant or main contributing factor to a cardiac event. He states that if Mr Prezant’s exposure modelling is accepted, Mr Clifford’s exposure would have been about two orders of magnitude less than what is considered reasonably safe to prevent COPD.

5. Mr Strautins considers that based on these calculations, the risk of injury was not unacceptable considering the other established risk factors, being smoking status, blood pressure, cholesterol, BMI, nutrition, physical activity, alcohol intake, age and sex, family history, social history, and other potential conditions such as diabetes, chronic kidney disease, familial hypercholesterolaemia and evidence of atrial fibrillation. He notes that exposure to particulate matter is not presented as a risk factor in a publication by the Stroke Foundation, which was endorsed by the Royal Australian College of General Practitioners. He opines that in this case, there is no indication exposure to particulate matter is substantial and no intervention would have made any meaningful difference to the outcome when considering established risk factors.

6. He says that Mr Prezant provided the best estimate of the deceased’s exposure to particulate matter on the day of his death, however there remains a high degree of uncertainty and he did not compare exposure to that of an ordinary worker. Mr Strautins says that the correct methodology is as outlined from the Australian Institute of Occupational Hygienists Simplified Risk Management Strategies. He acknowledges that although this test measures different sized particles than PM2.5, he believes that it could still be used as an indicator test to characterise and estimate exposure. Mr Strautins says that using this test, Mr Clifford would not have been exposed to particulate matter in a way meaningfully different than the general working population. Mr Strautins believes this to be a significant factor when considering whether the deceased’s exposure to particulate matter during the course of his employment was the main contributing factor to his injury. He opines that if Mr Prezant’s opinion were accepted, no Australian would be safe from this injury because of their employment.

7. Mr Strautins considers the deceased’s exposure as a courier driver was negligible when compared to established risk factors.

8. In considering whether exposure to particulate matter was the main contributing factor to death, Mr Strautins says that Mr Prezant has not properly considered other risk factors and has not compared the working population’s exposure to particulate matter to the deceased’s exposure.

9. In considering whether it was a substantial contributing factor, Mr Strautins states that from his experience, the anticipated exposure of a courier driver is so low, it does not warrant consideration as a workplace hazard or a factor in a cardiac event.

10. Mr Strautins concludes by stating that while the evidence relied upon by Mr Prezant is relevant to global health in respect to air pollution, the studies lack specificity and applicability to the deceased’s case. He states that the workplace standards are more applicable in the circumstances.

Mr Prezant’s report of 4 October 2020

1. Mr Prezant responded to Mr Strautins’ report, finding the categorisation of PM2.5 as “nuisance dust or dust not otherwise classified” as incorrect.[51] He notes that PM2.5 adjacent to highways is formed by condensation of high temperature diesel exhaust containing carcinogens, heavy metals and other toxic substances. As such, it could not meet the definition of nuisance dust as cited by Mr Strautins. He provides scientific literature to support his finding that “diesel exhaust is genotoxic, chemically reactive, transported from the lungs via the bloodstream throughout the body, all without creating a dust overload in the lungs.”

   [51] AALD, 6 October 2020, p 8.

2. Mr Prezant also differentiates PM2.5 produced from TRAP to PM2.5 produced from other sources. He opines that Mr Strautins did not consider these contributors to PM2.5 toxicity, which are linked to health effects, including cardiovascular disease and cardiovascular mortality.

3. Mr Prezant argues that although Mr Strautins has correctly calculated the time weighted average exposure, his conclusion that the deceased’s level of exposure was reasonably safe was incorrect as he has based this on safe levels of nuisance dust rather than PM2.5 from TRAP. Further, the standards or guidelines for exposure to nuisance dust provided by Mr Strautins do not apply to the deceased’s exposure.

4. Mr Prezant confirms his opinion that the deceased would have been exposed to more elevated toxic air contaminants than the average worker, as most other workers do not work along highways. He notes that other workers who are, such as truck drivers, toll operators and potentially bus drivers, have shown elevated cardiovascular endpoints. He concludes that as Mr Strautins has used the incorrect method for measuring PM2.5 from TRAP, he has incorrectly concluded that the deceased’s exposure was not different to that of the general working population.

Mr Strautins’ report of 23 October 2020

1. In response to Mr Prezant’s supplementary report, Mr Strautins says that Mr Prezant has made a tenuous and speculative link as he failed to consider other risk factors associated with a cardiac event.[52] He also says that the most appropriate way to assess the main contributing factor to the death is to consider the other risk factors. Mr Strautins says that the risk due to particulate matter is so low that it does not warrant further consideration.

   [52] AALD, 23 October 2020, p 14.

2. Mr Strautins then considers the toxicity of diesel particulate matter as a significant contributor to TRAP. He states that Mr Prezant did not accurately measure the deceased’s exposure to particulate matter, and that his method of calculation provides only an indication of particulate matter levels. It is based on professional judgement and assumptions that have not been verified. Mr Strautins says that exposure is significantly below AIOH recommendations and therefore, no intervention would have provided any meaningful health benefit to the deceased.

3. Mr Strautins refers to papers cited by Mr Prezant to state that there is no substantive evidence that particles are associated as a main or significant contributing factor to a cardiac event in professional drivers.

4. Mr Strautins reports that upon review of the relative risk from multi-city studies and using Mr Prezant’s methodology, there is an average increase in risk of 0.66%. Given this, Mr Strautins concludes that this cannot be the main contributing factor when compared with Australian cardiovascular risk charts, and the deceased was thus at significant risk regardless of workplace exposure.

Chronology

1. I set out below a chronology and my description of the proceedings thus far.

Death of the deceased	22 January 2016
Autopsy report, Drs R Tse and A D Cala	8 March 2016
GIO s 74 Notice declining claim for death benefits	18 May 2016
GIO second s 74 Notice (after internal review) declining claim	23 Nov 2017
Proceedings commenced in the former Workers Compensation Commission (948/20)	20 Feb 2020
Hearing before then Arbitrator Mr G Edwards	30 October 2020
Certificate of Determination issued by the Workers Compensation Commission (Arbitrator Edwards)	18 December 2020
Appeal filed in Workers Compensation Commission (A1-948/20)	15 January 2021
Personal Injury Commission commences (Workers Compensation Commission abolished) 1 March 2021	1 March 2021
Appeal decision of Deputy President Wood, remitting matter to be reheard	19 August 2021
Hearing before Member Sweeney	4 April 2022
Certificate of Determination issued by Personal Injury Commission (Member Sweeney)	6 May 2022

Clifford No 1

1. When this matter was first heard in the then Workers Compensation Commission in 2020, Arbitrator Edwards found that the deceased’s coronary artery disease was aggravated by air pollutants in the course of his employment, causing ventricular fibrillation resulting in sudden death pursuant, pursuant to s 4(b)(ii) of the 1987 Act. The Arbitrator was satisfied that employment was the main contributing factor with reference to the legal test set out by Snell DP in AV v AW,[53] having regard to all factors, including both work and non-work. The Arbitrator also found that s 9B of the 1987 Act was satisfied, applying Snell DP’s decisions of Renew God’s Program Pty Ltd v Kim[54] and De Silva v Secretary, Department of Finance, Services and Innovation.[55] In his Statement of Reasons issued on 18 December 2020, the Arbitrator recounted, in detail, the submissions relied upon by the parties, and the relevant evidence he considered. As the parties rely on those submissions in Clifford No 3 which is on appeal, I will set them out in some detail.

   [53] [2020] NSWWCCPD 9.

   [54] [2019] NSWWCCPD 45.

   [55] [2015] NSWWCC 279.

2. The first appellant’s submissions were recounted by the Arbitrator in some 60 paragraphs.[56] It was submitted that there was a material contribution to the deceased’s heart attack injury by exposure to TRAP. The first appellant relied on Dr Helprin’s opinion that the deceased suffered a new injury by way of ventricular fibrillation, and that the deceased was at a significantly greater risk of injury due to exposure to traffic road (sic, related) air pollution, as required by s 9B of the 1987 Act, with reference to the doctor’s opinion being based on scientific research and his medical knowledge.

   [56] Reasons in Clifford No 1, [20](a)–(nnn).

1. The first appellant referred to the opinion of Mr Prezant, noting he agreed with Dr Helprin’s opinion of a causal relationship between ambient air pollution and cardiac events, such as ventricular fibrillation, and noted that Mr Prezant considered the findings of the WHO in its 2013 article. It was submitted that the article indicated that PM2.5 and ultra-fine particulate matter significantly increased since 2005, with road traffic being a major source of black carbon which is harmful in both short-term and long-term exposure, demonstrating a significant association with cardiac events. The WHO found that diesel engine exhaust is rich in PM2.5 and causes myocardial ischemia, with studies suggesting that one to two hours of exposure to TRAP may be enough to lead to harmful physiological changes. There was reference to the spreadsheet and methodology used by Mr Prezant, his assessment of route and travel times and the calculation of particulate matter in these areas, which supported Mr Prezant’s conclusion that the deceased’s exposure to ambient air pollution was four times greater in the course of employment than a person not travelling.

2. It was submitted that Dr Helprin provided a medical opinion on the question of causation and the causal link between the heart injury and exposure to air pollution in the course of employment, and that opinion together with Mr Prezant’s established on the balance of probabilities that the cardiac injury was caused by the deceased’s exposure, satisfying both injury and aggravation, as well as s 9B of the 1987 Act.

3. In respect of Dr Herman, the first appellant submitted that the doctor’s opinion should be given no weight, particularly the opinion that the association between air pollution and ventricular fibrillation is modest at worst, as he did not consider Mr Prezant’s report. It was submitted that Dr Herman accepted on a scientific basis, the connection between air pollution and the onset of ventricular fibrillation, and that he did not have a proper foundation on which to base this conclusion. The doctor did not focus on the work of the deceased; did not properly consider the case, and disregarded exposure to air pollutants without providing adequate reasons for his conclusion. It was asserted that Dr Herman limited his view to the general population, rather than the specific work of the deceased.

4. In regard to Mr Strautins, the first appellant submitted that the expert did not have proper regard to Mr Prezant’s findings and ignored the deceased’s exposure to particulate matter, rather focusing on issues of safety. It was argued that Mr Strautins “missed the point” on the categorisation of PM2.5 as nuisance dust, which is not relevant in the deceased’s case. It was suggested that Mr Strautins’ criticism of Mr Prezant’s report should be disregarded as Mr Prezant provided reasons and evidence to support his conclusions. Further, the first appellant drew attention to Mr Strautins’ acceptance of the effects of air pollution.

5. The first appellant also made submissions in respect of s 9A, submitting that the connection to employment was “real and of substance”, with reference to Dr Helprin, who considered employment was both a substantial contributing factor triggering ventricular fibrillation, and a main contributing factor. In turning to s 9B, the first appellant submitted that the test was an evaluative test, involving an assessment of comparative risks, and is not a test of true causation. Section 9B was thus satisfied.

6. The second appellant (the deceased’s son) adopted the submissions of the first appellant.[57] He argued that the deceased suffered either a frank personal injury or a disease. It was noted that the deceased had an asymptomatic pre-existing coronary heart disease which made him more susceptible. He considered that there were a number of factors around causation, including the sedentary nature of employment, poor diet, air pollution and stress and all the events must be considered. The second appellant submitted it was not necessary, as suggested by Mr Strautins, to properly consider normal daily exposure in other employment, as the deceased was at work. It was argued that Mr Strautins did not engage with the question as to the extent of the exposure to air pollutants, and that Dr Herman’s reports provided too narrow an interpretation of the causal link. If the deceased had been at home, the risk would be lower, and thus as he was at work, this gave rise to a significantly greater risk of injury.

   [57] Reasons in Clifford No 1, [21](a)–(x).

7. The third appellant (the deceased’s daughter) adopted the above submissions and also submitted that the risk factors of the cardiac event by exposure to air pollutants had not been properly assessed by the respondent’s evidence. It was argued that Dr Herman accepted the increased risk of a cardiac event caused by exposure to pollutants, and that his opinion that employment did not place the deceased at a greater risk was not made out. It was not enough to address causation by way of a “blanket statement” that a previous heart attack increases mortality rates”.[58]

   [58] Reasons in Clifford No 1, [22](a)–(j).

8. In response, the respondent also made lengthy submissions recounted at reasons [23](a)–(hhhh) of Clifford No 1. The respondent argued that the injury was a personal injury pursuant to s 4(a), noting it was a ventricular fibrillation causing death, identified by Dr Helprin as a new, separate injury. Notwithstanding, it was submitted that no weight should be placed on the opinion of Dr Helprin, as the doctor failed to deal with causation as a result of the pre-existing heart disease and other existing risk factors. The respondent submitted that the doctor conducted a simple assessment as to whether the deceased was exposed to air pollutants without considering the actual area where the deceased was driving. In contrast, Dr Herman considered the factor of air pollution, as well as the other conventional risk factors, in finding the risk was modest at best.

9. It was submitted that Mr Prezant relied on overseas research which is of little benefit to determine the deceased’s exposure in Australia. It was unclear what methods were applied to calibrate the exposure to road traffic pollutants on the date of death, and Mr Prezant did not conduct tests around the various areas where the deceased worker drove on the day of exposure. The respondent submits that Mr Prezant’s report is of limited probative value, being based on the research conducted by the WHO which resulted in mixed findings. It noted the difficulties and challenges identified with the modelling and the review of the effects on heath of ambient air pollution. This was not enough to judge causation and the certainty and uncertainty of cardiovascular mortality. Furthermore, the relevance of the WHO study was questionable given the geographical areas.

10. The respondent relied on the report of Mr Strautins. The respondent submitted that in respect of s 9A(2)(d) and (e), the probability that the injury would have occurred at some stage irrespective of employment was considered by Dr Herman, and not the others. If ventricular fibrillation is considered to be a disease injury, it must be proven that employment was the main contributing factor to is aggravation. Dr Herman’s opinion was that that the cause of the ventricular fibrillation was the underlying coronary disease and that employment was not the main contributing factor to its aggravation. The respondent notes that both Dr Herman and Mr Strautins identified work and non-work factors which were required for the assessment of whether employment posed a significant risk.

11. In conclusion, the respondent submits, with reference to Flounders v Millar,[59] that the onus of proof in the commonsense test of causation is upon the appellants, and where reliance on circumstantial evidence to prove the circumstances raises a more probable inference in favour of what is alleged, the choice between conflicting inferences must be more than a matter of conjecture. It submits that the appellants’ case is one of conjecture, leaving the Commission to speculate about possibilities as to the cause of injury.

    [59] [2007] NSWCA 238.

12. In coming to his findings pursuant to ss 4(b)(ii) and 9B, the Arbitrator considered the submissions posited by the parties, and also detailed the medical and expert evidence in the proceedings. The Arbitrator accepted the opinions of Dr Helprin and Dr Herman that the deceased suffered a cardiac event in the course of his employment, caused by ventricular fibrillation. The Arbitrator also accepted that the deceased suffered a pre-existing coronary artery disease, which contributed to the ventricular fibrillation. The Arbitrator accepted the evidence presented by Mr Prezant, based on his scientific knowledge as an occupational hygiene and epidemiology specialist with over 40 years of experience practising in Australia and America, that drivers on highways and roads are exposed to diesel engine exhaust (PM2.5) and ultrafine particular matter. The Arbitrator accepted Mr Prezant’s methodology to calculate the deceased’s exposure, based on the scientific literature and the WHO publication, in respect of the levels of pollution within the deceased’s vehicle, being significantly higher than in other workplaces.[60] The Arbitrator rejected Mr Strautins’ criticism of Mr Prezant’s report and found that Mr Strautins failed to provide reasons supporting his view of a low level of air pollutants. The Arbitrator held that that Mr Strautins’ “reasoning that the worker’s exposure to air pollutants was so low that it did not warrant further assessment is inconsistent with the findings of WHO that the likelihood of ventricular fibrillation is significantly increased by exposure to particulate matter … and other environmental toxins”.[61] The Arbitrator also held that “Dr Herman’s conclusion that the data linking air pollution to arrhythmic [sic] was a ‘hypothesis’ requiring further large scale studies is not supported by the extensive research undertaken by WHO and its publication of the hazardous effect of exposure to air pollutants, especially PM2.5, likely to cause an increased risk of sudden fatal and non-fatal coronary events”.[62]

    [60] Reasons in Clifford No 1, [133].

    [61] Reasons in Clifford No 1, [137].

    [62] Reasons in Clifford No 1, [152].

Clifford No 2

1. An appeal was lodged against the Arbitrator’s decision in Clifford No 1, alleging, amongst other things, that the Arbitrator made incorrect findings about the medical and scientific literature (including the WHO report), thus erring in his preference for the opinion of Dr Helprin over that of Dr Herman noting the doctors diverged in relation to their conclusions about the scientific literature. The appeal was upheld, and the Arbitrator’s decision was revoked by Deputy President Wood on 19 August 2021. Deputy President Wood applied Seltsam Pty Limited v McGuiness; James Hardie & Coy Pty Ltd v McGuiness[63] as relevant to the status of scientific literature, noting that the “epidemiological evidence about the association between exposure to air pollutants and cardiac events constituted ‘strands’ in the causal chain of connection”,[64] and that an examination of the evidence of the experts required an examination of whether their opinions were properly founded upon the facts and conclusions in scientific literature. The Arbitrator did not do this, and thus, was not in a position to reject the opinion of Dr Herman on the basis that his opinion was inconsistent with the research. Contrary to the Arbitrator’s findings, Deputy President Wood considered that Dr Herman did provide reasons as to why his opinion was limited to a hypothesis, and had made reference to the scientific literature to support his conclusion that the deceased’s exposure levels would be less than those recorded in the research, thus falling into error. In failing to address the matters raised by the appellants and assess the status of conclusions reached in the scientific literature, the Arbitrator overlooked material evidence, and erred in rejecting Dr Herman’s opinion on the basis it was not supported by same. The Arbitrator’s findings as to causation were affected by error.

Clifford No 3

[63] [2000] NSWCA 29; 49 NSWLR 262; 19 NSWCCR 385 (Seltsam).

[64] Reasons in Clifford No 2, [176].

1. Following the appeal in Clifford No 2, the proceedings were remitted to Member Sweeney who issued a Certificate of Determination on 6 May 2022 with an award for the respondent. Member Sweeney was satisfied that the appellants had established a personal injury within the meaning of s 4(a) of the 1987 Act (rather than a disease), but was not satisfied employment was a substantial contributing factor to the injury within the meaning of s 9A of the 1987 Act.

2. The parties relied on the submissions made before Arbitrator Edwards which I have detailed above under Clifford No 1. In addition, the first appellant clarified that the injury in question was a “new injury and this new injury was an electrical injury as opposed to a vascular injury.”[65] Reliance was placed on the most recent report of Dr Helprin of 17 January 2022, namely the doctor’s reference to “further major scientific reports synthesising the association between ambient air pollution and the risk of sudden cardiac death from a serious ventricular arrythmia particularly in a vulnerable patient.”[66] The first appellant referred to the report of the National Heart Foundation of Australia, asserting that the risk was no longer “negligible”, and that Dr Helprin was of the opinion that “exposure to small air pollution particles explains fatal ventricular fibrillation on a busy road”.[67] The first appellant traversed the report of Mr Prezant; maintained that Mr Strautins “missed the point”, and argued that Dr Herman failed to refer to research which supported a causal connection. This argument was also adopted by the other two appellants. It was argued that the doctor’s rejection of the causal nexus was a discussion of the general population rather than the specific circumstances of this case. In regard to s 9A of the 1987 Act, the first appellant asserted that the underlying factors were “effectively irrelevant in this matter”, with the second appellant asserting that a finding of substantial contributing factor was “almost inescapable”, noting that “everybody considers that employment was a contributing factor”.[68]

   [65] Reasons in Clifford No 3, [11].

   [66] Reasons in Clifford No 3, [12].

   [67] Reasons in Clifford No 3, [13].

   [68] Reasons in Clifford No 3, [17]–[19].

3. The respondent argued that the appellants’ evidence failed to address the fact that the deceased was always at risk of ventricular fibrillation. The respondent raised the principle known as Occam’s razor, noting that Dr Herman’s opinion was simple as to the cause being the pre-existing condition, and that the studies on which the appellants had built their case did not address local circumstances.[69]

   [69] Reasons in Clifford No 3, [23]–[24].

4. Member Sweeney proceeded to conduct a review of the salient points of the medical evidence relevant to his decision, including the medical reports, the scientific literature, and expert reports.

THE MEMBER’S REASONS

1. Member Sweeney noted that the case pleaded before him required consideration as to whether the heart attack injury was a personal injury in accordance with s 4(a) of the 1987 Act, or alternatively a disease which was aggravated in the course of employment and to which employment was the main contributing factor pursuant to s 4(b)(ii). The characterisation of the heart attack as an injury or a disease was of “more than academic interest”, because if it was an injury, it required the appellants to prove employment was a substantial contributing factor pursuant to s 9A of the 1987 Act. In either event, s 9B must also be proven, that employment gave rise to a significantly greater risk of injury had the deceased not been employed in employment of that nature.[70]

   [70] Reasons in Clifford No 3, [91]–[92].

2. In making this distinction, the Member referred to Zickar v MGH Plastic Industries Pty Ltd[71] and Kennedy Cleaning Services Pty Ltd v Petkoska,[72] wherein Zickar was considered, and Gleeson CJ and Kirby J said at [39]:

   “… If this evidence amounts, relevantly, to something that can be described as a sudden and ascertainable or dramatical physiological change or disturbance of the normal physiological state, it may qualify for the characterisation as an ‘injury’ in the primary sense of that word … If the propounded ‘injury’ is distinct from the underlying pathology that constitutes a ‘disease’ that directly or indirectly caused the sudden event to occur, it is necessary to proceed to the alternative and additional basis whereby, in such cases, compensation may also be recovered for the disease process…”.[73]

   [71] [1996] HCA 31; 187 CLR 310 (Zickar).

   [72] [2000] HCA 45.

   [73] Reasons in Clifford No 3, [94].

3. In adopting this approach, the Member held that ventricular fibrillation was an “injury” which arose in the course of employment, given its “sudden, dramatic and terminal consequences”. It was “sudden and ascertainable” and “distinct from the underlying pathology”.[74]

   [74] Reasons in Clifford No 3, [96]–[97].

4. Finding “injury”, the Member stated it “remains to consider whether employment was a substantial contributing factor to the injury”. This required a connection between injury and employment which is “not less stringent” than “arising out of” employment, with reference to Badawi v Nexon Asia Pacific Pty Ltd t/as Commander Australia Pty Ltd,[75] as well as an evaluation of the matters set out in s 9A(2).[76] The Member considered the test was one of causation, invoking the commonsense test in accordance with the reasoning in Zinc Corporation Ltd & Anor v Scarce[77] and the proof necessary to establish this. The Member referred to Seltsam, and its commentary in relation to epidemiological evidence, the balance of probabilities test not being satisfied by evidence which fails to do more than establish a possibility, and causation, whereby “causation in an individual case can be established by a process of inference from circumstantial evidence which combines primary facts like ‘strands in a cable’. Epidemiological evidence of the effects on populations of exposure to a substance is circumstantial evidence which may form part of the process of inference”.[78]

   [75] [2009] NSWCA 324 (Badawi).

   [76] Reasons in Clifford No 3, [98].

   [77] (1995) 12 NSWCCR 566.

   [78] Reasons in Clifford No 3, [100].

5. The Member then proceeded to make the enquiry on the evidence as to “whether there is a causal connection as envisaged by s 9A” by referring to the autopsy report which indicated that “sudden death could occur at any time”. The Member considered this to be the “logical starting point’.[79]

   [79] Reasons in Clifford No 3, [101]–[102].

6. The Member referred to Dr Herman’s initial report which provided an opinion consistent with the autopsy and concluded that employment did not contribute to the ischaemic event which provoked death, an opinion which was provided before Dr Helprin suggested that exposure to TRAP caused or contributed to death. He referred to the “various attacks” on Dr Herman’s opinion who remained of the view that the deceased was at high risk of death by coronary artery disease, but acknowledged that air pollution may have been a contributing factor, albeit not substantial. The Member noted the explanation provided by Dr Herman in reaching this conclusion, that the link was “a strong association rather than definite proof”, and that Dr Herman was not convinced the increased risk resulting from pollution was “significantly greater than in any other person with ischaemic cardiomyopathy at his age and with the additional cardiac risk factors”.[80]

   [80] Reasons in Clifford No 3, [104]–[107].

7. The Member considered that the language of the cardiologists was not always consistent, with risk and cause sometimes conflated, with Dr Helprin opining that TRAP increased the risk of heart failure, and that this increased risk caused or triggered the injury, and thus the risk of injury “came home” as referred to in Chappel v Hart.[81] The Member noted the basis on which Dr Helprin formed his opinion, being the scientific literature and Mr Prezant’s report.[82]

   [81] (1998) 195 CLR 232.

   [82] Reasons in Clifford No 3, [104]–[108].

1. The Member was not satisfied that Mr Prezant’s evidence was of sufficient quality to provide that satisfactory basis and as a result questioned the provenance of Mr Prezant’s quantification of the deceased’s exposure to PM2.5 on the day of his death. There was no error in this approach.

2. I am fortified in this view by virtue of the fact that this appeal ground is advanced on a very narrow basis which has not been made out, namely, that the respondent’s expert’s opinion had been entirely discounted and as a result the Member was duty bound to accept Mr Prezant’s view. This is not correct in principle. Further, this appeal ground does not direct attention to any salient aspects of Mr Prezant’s opinion which were unchallenged or could be said to have been established to such a degree that the Member had to accept it. It is clear to me that in accordance with the remarks from Rolfe AJA in Hull that I have set out at [205] above, the assumptions upon which Mr Prezant relied, namely the transposition of international studies to Australian conditions, had not been established. This was a rational basis for the Member to reach the conclusion that he did.

3. This ground is not established and is as a consequence dismissed.

As to Ground Five: The Member committed an error of law by failing to respond to a substantial, clearly articulated argument

1. The first appellant contends under this ground that the Member failed to deal with the following aspect of Dr Helprin’s report and, as a consequence, committed an error of law of the type as described in Dranichnikov v Minister for Immigration and Multicultural Affairs[149] and Wang v State of New South Wales.[150]

   [149] [2003] HCA 26 (Dranichnikov), per Gummow and Callinan JJ, [24].

   [150] [2019] NSWCA 263 (Wang), per McCallum JA (Macfarlan and Meagher JJA agreeing).

2. Dr Helprin was the first appellant’s principal expert. The opinion advanced by Dr Helprin was predicated upon two bases, firstly a significant body of scientific research which identified an association between exposure to pollution and cardiovascular events, and in particular ventricular fibrillation, and secondly the calculations or estimations performed by Mr Prezant. The first appellant states that the Member failed to deal with her argument and submissions in as much as they referred to Mr Prezant’s calculations. A secondary submission is advanced that even if the Member made reference to Mr Prezant’s work, the Member failed to address the “materiality of the submissions in his reasons”.[151]

   [151] First appellant’s appeal submissions, 31 May 2022, [91].

3. The respondent counters by saying that no such error was made, pointing to various aspects of the Member’s decision where Mr Prezant’s evidence was dealt with by the Member in terms.[152]

   [152] Respondent’s submissions in opposition to the first appellant’s appeal, [7.27]–[7.29].

4. With respect to the reliance placed upon Dranichnikov by the first appellant, the respondent states that the submission is misconceived as there is no “established fact”, as referred to by Gummow and Callinan JJ in Dranichnikov at [24], in terms of Mr Prezant’s evidence. As a consequence, the respondent states that this ground of appeal has not been established

Consideration

1. The first appellant’s argument under this ground is really advanced on two bases arising from Dranichnikov and Wang. The Dranichnikov point is that the Member, in dealing with Dr Helprin’s expert evidence, failed to deal with the aspect of the first appellant’s submission which relied upon Mr Prezant’s calculations. The alternate proposition advanced by the first appellant is that even if the Member did deal with Mr Prezant’s calculations, the Member failed to address the materiality of that issue in the sense referred to in Wang.

2. Dranichnikov was an immigration case. Mr Dranichnikov was a Russian citizen who sought a protection visa on behalf of himself, his wife and child. The basis on which he sought such a visa was twofold. Firstly, that as a Russian businessman he is at risk from criminal organisations who operate in Russia who have links to the authorities. Secondly, he asserted that he was part of a more limited group consisting of businessmen who had publicly criticised law enforcement authorities for failing to take action against criminals.

3. In dealing with Mr Dranichnikov’s case, the Refugee Review Tribunal at first instance accepted that Mr Dranichnikov was a witness of credit, and therefore accepted the correctness of his account of the situation in Russia.

4. But the Refugee Review Tribunal dismissed his case, and failed to deal with the argument that he was a more limited class of businessman who had taken a public stance against law enforcement authorities for failing to take action against criminals. It is failure to deal with this latter argument which gave rise to the error of law. The decision of the Refugee Review Tribunal was quashed by the High Court, and it was directed to review the delegate’s decision in accordance with law.

5. In Wang, the Court of Appeal was called upon to deal with a Dranichnikov submission in that it was asserted that the primary judge had failed to address written submissions advanced by the appellant. The Court of Appeal said as follows:

   “The submission invoked the decision of the High Court in Dranichnikov v Minister for Immigration & Multicultural Affairs [2003] HCA 26; (2003) 77 ALJR 1088 in which it was stated that a failure to respond to a substantial, clearly articulated argument relying on established facts was a constructive failure to exercise jurisdiction: at [24] to [25] per Gummow and Callinan JJ. The decision is not authority for the proposition that any failure to refer to any argument put to a trial judge amounts to error. It is necessary to engage with the nature and materiality of the argument in the context of the issues in the proceedings. In Dranichnikov, the Refugee Review Tribunal, in considering whether Mr Dranichnikov had a well-founded fear of persecution on the grounds of his status as a member of a particular social group, overlooked or misconceived the particular social group to which he claimed to belong. That was the central question in the proceedings.

   The approach taken in the present case was to list every submission put on behalf of Mr Wang to which the primary judge did not refer in his judgment and to assert error on that basis. That reflects a wrong approach. The primary judge was not required to address every submission advanced during the course of the hearing: Soulemezis v Dudley (Holdings) Pty Ltd (1987) 10 NSWLR 247 at 271.

   As noted in the State’s written submissions, Mr Wang’s written submissions appear to identify only two particular submissions advanced by him which were material to the outcome and which were not addressed by the trial judge, namely, the submissions relating to Mr Wang’s capacity in the English language … and the submissions in relation to wrongful arrest ... Otherwise, the table of alleged omissions does not articulate any cogent basis for challenging the judge’s findings. Nor does it establish a constructive failure to exercise jurisdiction.”[153] (emphasis added)

   [153] Wang, [63]–[65].

6. I do not accept that the Member failed to deal with Mr Prezant’s evidence.

7. The Member dealt with Mr Prezant’s evidence at reasons [50]–[61], and specifically how Mr Prezant reconstructed the deceased’s likely exposure to pollution in the course of his employment on 22 January 2016. He then considered Mr Strautins’ evidence[154] and his criticisms of Mr Prezant’s methodology.[155] Mr Prezant responded to this criticism and this was dealt with by the Member at reasons [70]–[74].

   [154] Reasons in Clifford No 3, [62]–[69].

   [155] In particular see reasons in Clifford No 3, [65], [67].

8. In the dispositive section of the Member’s decision, the Member dealt with Dr Helprin’s opinion and Mr Prezant’s calculations, in the following manner:

   “Dr Helprin formed this opinion partly on the basis of the numerous scientific and epidemiological studies to which he referred in his reports. Subsequently, he had access to the report of Mr Prezant which suggested the deceased was exposed to a large measure of pollutants, particularly PM2.5, on the day of his death.”[156] (emphasis added)

   “The modelling by Mr Prezant for the substantially increased presence of TRAP on urban highways as opposed to nearby monitoring stations was based on a study in the United Kingdom. The modelling for the 10 fold increase in pollution on major highways was based on a study carried out in Los Angeles. Again, there are obvious difficulties in the transposition of the results to Sydney. It is by no means clear whether a similar study in Sydney would produce the same outcome to that reached in the Los Angeles study[157]. Quite apart from the evidence of Mr Strautins, which is often confusing and unsupported by references to the scientific evidence on which he relies, there must be a very substantial margin of error in Mr Prezant’s quantification of the deceased’s exposure to PM2.5 on the day of his death.”[158] (emphasis added)

   [156] Reasons in Clifford No 3, [109].

   [157] The study by Kang et al refers to a Melbourne Study which may have replicated the findings of foreign studies.

   [158] Reasons in Clifford No 3, [117].

9. Ultimately, at reasons [125]–[126], the Member concluded that Dr Helprin’s opinion was of less weight and that if there was no proper foundation for that opinion, the Member could not draw any lay inferences regarding the asserted connection between pollution and the deceased’s heart attack.

10. Unlike the situation in Dranichnikov, the second argument of the first appellant’s expert case, namely that based upon Mr Prezant’s calculations, was in fact dealt with by the Member. At reasons [117], the Member clearly considered that there had to be “a very substantial margin of error in Mr Prezant’s quantification of the deceased’s exposure to PM2.5 on the day of his death”. This was a submission advanced by the first appellant and dealt with in terms by the Member. No error of the Dranichnikov type has been established.

11. This appeal ground however is also advanced on the alternate basis as referred to in Wang. As I have highlighted at [222] above in the passage from [63] of Wang, what is necessary is for the Member to engage with the nature and materiality of the argument in the context of the issues in proceedings. In these proceedings, the principal issue revolved around assessing for the purposes of s 9A of the 1987 Act, the increased risk of cardiac arrest associated with exposure to traffic related pollution. The first appellant’s case was predicated upon Dr Helprin’s opinion, which had been based not only upon his own expertise but also scientific studies and Mr Prezant’s calculations of what he estimated the deceased’s exposure to PM2.5 was on the day of his death. The first appellant perhaps places Mr Prezant’s evidence too highly. In the first appellant’s submissions at [88] the following is stated:

    “As alluded to above, it had been submitted to the Member that based upon Dr Helprin’s response to question 7 of his report dated 17 January 2021, the evidence in relation to injury/causation was not solely predicated upon scientific literature, but was also based upon the actual exposure as evident from Mr Prezant’s assessment.” (emphasis added)

12. I have closely read Mr Prezant’s evidence with respect to his calculations of likely or possible exposure of the deceased to PM2.5. In particular, in Mr Prezant’s report of 28 July 2020,[159] Mr Prezant explained the methodology he employed in estimating the deceased’s exposure to PM2.5. Clearly, the calculations undertaken by Mr Prezant, doing the best he could, were based upon a number of estimates and assumptions which he clearly identifies in this report.

    [159] Mr Prezant’s report dated 28 July 2020, pp 6–11, [23]–[39], AALD, 28 July 2020.

13. Contrary to the first appellant’s submission at [88], which I have set out at [228] above, I would not categorise Mr Prezant’s evidence as establishing “the actual exposure” that the deceased suffered on 22 January 2016. At best, Mr Prezant’s evidence represents his best estimate of the deceased’s likely exposure to PM2.5 on the date of his death. I do not read Mr Prezant’s opinion as positing an “actual exposure”.

14. The Member dealt with his doubts about Mr Prezant’s estimations at reasons [117]. In the Dranichnikov sense, I accept the respondent’s submission that there is no established fact (meaning “actual exposure” being proven) and as a result the first appellant’s submission cannot be made good.[160]

    [160] See Dranichnikov, [24].

15. I also consider that the Member has dealt with the materiality of this submission. Whilst this was not dealt with at length, that is not the Member’s duty or obligation. Clearly the Member was not satisfied as to the provenance of Mr Prezant’s calculations as presenting a satisfactory basis to substantiate Dr Helprin’s ultimate opinion. Reading the decision as a whole, the Member went through not only the international scientific studies, but also considered Mr Prezant’s calculations before reaching his ultimate view with respect to Dr Helprin’s opinion.

16. Contrary to how the first appellant has advanced this appeal ground, the submission articulated by the first appellant was dealt with by the Member in terms. The error in the Dranichnikov sense does not arise. Secondly, the Member did deal with the materiality of the submission (Wang).

17. No error as asserted under this ground has been established. Ground Five is dismissed.

Second appellant’s appeal

1. The second appellant adopts and relies upon the grounds advanced by the first appellant. In addition to those grounds, the second appellant relies upon the following grounds.

As to Ground One: Failing to provide lawful reasons

1. The second appellant asserts that there is uncertainty as to whether the Member found that the deceased had suffered an injury, notwithstanding what appears at reasons [97]. The second appellant asserts that due to the paucity of the reasons, he does not know whether the application failed due to s 4 or s 9A of the 1987 Act. Further, the second appellant states that in so far as the Member’s dealing with s 9A is concerned, the reasons supplied do not comply with the minimum required by law.[161]

   [161] Second appellant’s appeal submissions, 2 June 2022, [34].

2. The second appellant alleges that the Member applied the wrong test, presumably to the construction of s 9A.[162] In the alternative, the second appellant alleges that the test applied by the Member was not explained.

   [162] Second appellant’s appeal submissions, 2 June 2022, [36].

3. The respondent contends that the Member found injury, submitting:

   “Concerning the question of whether the Member found ‘injury’ the position is untenable. The Member has addressed the issue and made the finding at paragraphs 96 and 97 of the Decision.”[163]

   [163] Respondent’s submissions in opposition to the second appellant’s appeal, [10.2].

4. The respondent also refers to a number of paragraphs where the Member dealt with s 9A in terms, contrary to the second appellant’s assertion.[164]

Consideration

[164] Respondent’s submissions in opposition to the second appellant’s appeal, [10.3].

1. I do not accept that there is any uncertainty or doubt about the Member’s finding that an injury occurred to the deceased in the course of his employment.

2. At reasons, [91], the Member deals with the characterisation of the deceased’s heart attack as being either an injury or a disease as being of more than academic interest. The Member quite correctly states as follows:

   “If the deceased died of an injury, it is necessary for the [appellants] to prove that [the deceased’s] employment was a substantial contributing factor to the injury in accordance with s 9A of the 1987 Act before compensation is payable. On the other hand, if the heart attack is characterised as the aggravation of a disease, it is necessary for the [appellants] to prove that the deceased’s employment was the main contributing factor to the aggravation etc of the disease.”

3. The Member then goes on at reasons [92] to describe his task pursuant to s 9B of the 1987 Act. Consequently, one can follow the structure of the decision from the posing of these questions and the Member’s review of cases, some involving heart attacks, in order to characterise the event as either the terminal part of an underlying disease process or an injury. The Member then reaches his ultimate finding that the ventricular fibrillation suffered by the deceased was an injury for the purposes of s 4 of the 1987 Act, and that is what he found at reasons [97]. There is no doubt that this was the finding made, because in the next paragraph, namely reasons [98], the Member proceeds to consider “whether the employment was a substantial contributing factor to the injury”, consistent with the path he detailed at reasons [91]. It is trite to say that the decision must be read as a whole.[165]

   [165] Beale.

4. Contrary to the second appellant’s submission, it is clear that injury pursuant to s 4(a) was found. What is also clear from a consideration of the decision after this finding was made at reasons [97] is that the Member was turning his attention to whether or not s 9A had been established. In terms of how the Member dealt with s 9A, the second appellant submits that the reasons do not comply with the minimum required by law and that the Member “ought to have set out the relevant legislation, together with the case law, and carefully applied it to the facts of the case.”[166]

   [166] Second appellant’s appeal submissions, 2 June 2022, [35].

5. I have dealt with the Member’s obligation to give reasons with respect to the first appeal point pursued by the first appellant. The Member dealt with the six factors in s 9A(2) at reasons [128]. I would note that no issue was taken with the findings themselves, that is whether they are correct or not, rather the complaint seems to be that the language of s 9A(2) ought to have been used in terms. With respect, this is not the Member’s obligation in terms of giving reasons. How the Member dealt with the factors in s 9A(2) was brief and succinct and met the Member’s obligations to provide reasons as provided for by s 294(2) of the 1998 Act, r 78 of the 2021 Rules and the description of this obligation that I have described above arising from cases such as Soulemezis and Bevan.

6. I do not accept the submission that the Member’s reasons do not comply with the minimum required by law.

7. The final argument advanced by the second appellant in this ground is that the Member either applied the wrong test, or in the alternative, “that the Member must have applied a test to s 9A that was not explained”.[167] The first appellant also states that the Member’s reliance upon Badawi at reasons [98] should be seen as obiter remarks in that decision.

   [167] Second appellant’s appeal submissions, 2 June 2022, [37].

8. Badawi considered the terms of s 9A. In Badawi beneath the heading “Substantial contributing factor” the Court of Appeal said as follows:

   “Causation is a fact-laden conclusion which the courts have been told must be based on common sense: March v Stramare (E & MH) Pty Limited [1991] HCA 12; 171 CLR 506; and Nunan. It is not possible and indeed would be incorrect, therefore, to lay down a principle which can be applied unbendingly to all cases. Nonetheless, we consider the following observations should be made.”[168]

   [168] Badawi, [81].

9. The Court of Appeal then proceeds to make various observations about the word “substantial” stating:

   “It is a word of ordinary English meaning. It is a word of evaluative concept.”[169]

   [169] Badawi, [82].

10. Ultimately the Court of Appeal said:

    “The ‘proper link’ in the legislative context was a causal connection expressed by the words ‘a substantial contributing factor’, meaning one that was real and of substance.”[170]

    [170] Badawi, [82].

11. However I would say that whilst the Member has not used the precise words “real and of substance”, the net effect of his findings on causation would reveal that the Member was not satisfied that causation was established.

1. It was the second appellant’s case that the ventricular fibrillation was induced or triggered by the deceased’s exposure to TRAP on one day alone, that is 22 January 2016. For the reasons I have outlined above in relation to the first appellant’s appeal grounds, the Member was not satisfied with respect to the expert opinion going to the question of causation. The Member stated, “I have concluded that there is an insufficient basis for Dr Helprin’s opinion of a nexus between pollution and death”.[171]

   [171] Reasons in Clifford No 3, [126].

2. This opinion was based upon the Member’s dissatisfaction with the appellants’ expert evidence. A fair reading of the Member’s reasons would conclude that the Member was not satisfied that the connection between the deceased’s exposure to pollution and his death was real and of substance.

3. This appeal ground has not been established. To the contrary, consistent with Badawi, the Member has performed a detailed evaluation of the expert evidence and was not satisfied that causation for s 9A purposes had been established. This ground is dismissed.

As to Ground Two: Failing to apply the correct legal test concerning s 9A

1. The second appellant asserts that the remarks at reasons [98] and [99] pose the incorrect test. The second appellant states that the commonsense test has been doubted and the Member’s duty was to interrogate the statute when dealing with s 9A.[172]

   [172] Second appellant’s appeal submissions, 2 June 2022, [46]–[47].

2. The second appellant asserts that rather than having to satisfy the “commonsense” test of causation, the appellants only had to establish that the causal connection was real and of substance.[173] Finally, the second appellant states that the Member’s findings with respect to s 9A(2) at reasons [128] were not satisfactory. I would remark that I have already dealt with this submission with respect to the first appellant’s Ground One, where I found this complaint with respect to reasons [128] to be without merit.

   [173] Second appellant’s appeal submissions, 2 June 2022, [49].

3. In response, the respondent states that the Member properly applied s 9A (at reasons [126]–[129]) and that the second appellant’s ground “does not give a proper account of the Member’s determination as a whole”.[174]

Consideration

[174] Respondent’s submissions in opposition to the second appellant’s appeal, [10.8].

1. With respect to the second appellant’s criticisms of the Member’s approach at reasons [98], I have dealt with that when considering the second appellant’s first appeal ground. I am not persuaded that error has been established on the part of the Member with respect to those remarks.

2. The next argument pursued by the second appellant takes issue with the commonsense test. As I have set out at [247] above, from Badawi [81]: “Causation is a fact-laden conclusion which the courts have been told must be based on common sense”. This is consistent with the longstanding approach in Kooragang Cement Pty Ltd v Bates[175] and the remarks of Kirby P as follows:

   “The result of the cases is that each case where causation is in issue in a workers' compensation claim, must be determined on its own facts. Whether death or incapacity results from a relevant work injury is a question of fact. The importation of notions of proximate cause by the use of the phrase ‘results from’, is not now accepted. By the same token, the mere proof that certain events occurred which predisposed a worker to subsequent injury or death, will not, of itself, be sufficient to establish that such incapacity or death ‘results from’ a work injury. What is required is a commonsense evaluation of the causal chain.”[176] (emphasis added)

   [175] (1994) 35 NSWLR 452 (Kooragang).

   [176] Kooragang, 810.

3. In terms of the Member’s consideration of the appellants’ expert evidence, reading the decision as a whole shows that the Member was performing precisely the common sense evaluative task which is mandated by the appellate cases I have referred to. It is not a mechanical approach as asserted by the second appellant in this ground. The Member has dealt with the elements of s 9A(2) and then, consistent with Badawi, undertook the process of evaluating the expert evidence on the question of causation.

4. The second appellant asserts the appellants do not know why they lost the application. I think it is clear from a reading of the decision that the salient findings of the Member were as follows:

   (a) Injury in the course of employment for the purposes of s 4 was established.

   (b) The Member then proceeded, having found injury, to address s 9A of the 1987 Act as to causation. The Member dealt specifically with the terms of s 9A(2). The Member then found that causation was not established for the reasons I have described earlier in this decision.

5. In my observation, the Member has found that s 9A causation was not established and that was the reason why the appellants failed in their application.

6. This ground has not been established and is as a consequence dismissed.

Third appellant’s appeal

1. The third appellant relied upon and adopted the appeal points advanced by the first and second appellants. Given that the first and second appellants’ appeal grounds have all been dismissed, as a consequence the third appellant’s appeal is also dismissed.

DECISION

1. The third appellant’s time to appeal the Member’s decision of 6 May 2022 is extended to 8 June 2022.

2. The Member’s Certificate of Determination dated 6 May 2022 is confirmed.

Judge Phillips
President

22 March 2023