Fisher v Nonconformist Pty Limited
[2022] NSWPIC 201
•6 May 2022
| CERTIFICATE OF DETERMINATION OF MEMBER | |
CITATION: | Fisher v Nonconformist Pty Limited & Ors [2022] NSWPIC 201 |
| APPLICANT: | Kerry Lillian May Fisher |
| FIRST RESPONDENT: | Nonconformist Pty Limited |
| SECOND RESPONDENT: | Mark Barry Clifford |
| THIRD RESPONDENT | Nicole Megan Clifford |
| MEMBER: | Paul Sweeney |
| DATE OF DECISION: | 6 May 2022 |
| CATCHWORDS: | WORKERS COMPENSATION - Worker with pre-existing ischaemic cardiomyopathy dies of cardiac arrythmia in the course of his employment as a courier; conflicting evidence as to whether traffic-related air pollution to which the worker was exposed whilst driving substantially contributed to his death for the purpose of section 9A Workers Compensation Act 1987; evidence established that the pollution increased the risk of cardiac injury and death; Held- Commission not satisfied that the evidence established that the deceased’s death was caused by traffic -related air pollution; award for the first respondent. |
| DETERMINATIONS MADE: | Award for the first respondent. |
STATEMENT OF REASONS
BACKGROUND
During his lifetime, Terry Clifford (the deceased) was the working director of Nonconformist Pty Limited (the first respondent), a company which provided courier services to Direct Courier (Aust) Services Pty Ltd.
On 22 January 2016, at about 3pm, the deceased was driving his courier van on Richardson Road, Camp Vale when the vehicle left the roadway and collided with a steel fence post and a tree. When police officers gained access to the vehicle they found the deceased upright in the driver’s seat without a pulse. He was not breathing.
An autopsy report for the coroner concluded that the direct cause of the deceased’s death was ischaemic heart disease. The antecedent cause of death was coronary artery atherosclerosis.
By these proceedings, the applicant claims the compensation provided for by s 25 of the Workers Compensation Act 1987 (the 1987 Act) when the death of a worker results from employment injury. She alleges that exposure to air pollution while driving his courier vehicle on 22 January 2016 either caused an injury to the deceased’s cardiovascular system or, alternatively, materially aggravated pre-existing cardiovascular disease.
The first respondent denies that the deceased suffered an injury pursuant to s 4(a) of the 1987 Act and that the deceased’s employment was a substantial contributing factor to that injury. It also denies that the deceased suffered an injury pursuant to s 4(b)(ii) of the 1987 Act and that the deceased’s employment was the main contributing factor to the aggravation etc. of that disease. Finally, the respondent disputes that the applicant has established for the purpose of s 9B of the 1987 Act that the nature of the deceased’s employment as a courier driver:
“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.”
PROCEDURE BEFORE THE COMMISSION
When the matter came on for arbitration hearing on 4 April 2022, Mr Adhikary of counsel, represented the applicant, Mr McMahon, of counsel, represented the first respondent,
Mr Parker, of counsel, represented the second respondent, and Mr Hickey, of counsel, represented the third respondent. The arbitration was heard over the telephone.As the workers compensation legislation does not permit the settlement of death claims on a compromise basis, the matter proceeded to a hearing without an attempt at conciliation. It was agreed that all the evidence admitted by Arbitrator Edwards at the arbitration hearing on 30 October 2020 would be evidence in these proceedings. It was also agreed that the transcript of the submissions of counsel at that arbitration hearing should be considered as submissions on the present hearing.
EVIDENCE
In addition to the documents tendered at the previous hearing, the following documents were tendered in evidence without objection:
(a) Applications to Admit Late Documents dated 15 September 2021, 3 February 2022 and 30 March 2022.
SUBMISSIONS
The submissions of counsel are recorded and it is, therefore, unnecessary to reiterate each of the arguments put at the two arbitration hearings. I note that in the previous Statement of Reasons the Arbitrator meticulously recorded each of the arguments put by counsel on the previous occasion and I propose to incorporate that summary in these reasons. I add the following compendious account of the arguments on 4 April 2022.
At the commencement of submissions, Mr Adhikary emphasised that he relied on the submissions he made on the previous occasions and also on the submissions made by
Mr Parker and Mr Hickey on that occasion.Mr Adhikary submitted that Dr Helprin had consistently stated in his written evidence that although the deceased was vulnerable by reason of his underlying coronary disease:
“The injury which ultimately led to the worker’s passing was a new injury and this new injury was an electrical injury as opposed to a vascular injury.”
Mr Adhikary then turned to the most recent report of Dr Helprin dated 17 January 2022, where the doctor stated that there had been “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”. The deceased worker was such a vulnerable patient.
Mr Adhikary referred to the “scientific material” summarised by Dr Helprin in his reports including, importantly an article from the Heart Foundation of Australia. It was submitted that the article reinforced Dr Helprin’s opinion that air pollution could lead to “abnormal heart rhythms”. The body of scientific knowledge relating to the nexus between air pollution and cardiac risk was no longer “negligible”. Dr Helprin was clearly of the opinion that:
“Exposure to small air pollution particles explains fatal ventricular fibrillation on a busy road.”
Further, Dr Helprin provided a reasoned explanation as to why Dr Herman’s opinion, the first respondent’s cardiologist was erroneous.
Mr Adhikary then traversed the opinion of Mr Prezant, the occupational hygienist, who calculated the deceased’s exposure to particulate matter of 2.5 microns on the day of his death as 10 times the ambient level measured by air pollution monitoring stations in the vicinity of the route which he travelled as a courier. That led to a conclusion that the worker on the day of his death had four times greater exposure to particulate of 2.5m than a person who was not driving. In addition to the 2.5m particulate the worker was also exposed to “ultrafine particulate matter”.
In respect of the evidence of Dr Herman, the respondent’s qualified cardiologist, Mr Adhikary submitted that he had omitted to refer to reports of the American Heart Association and others referred to in an article by Tane and others, which supported a causal connection between air pollution and cardiac injury. In rejecting the causal nexus between air pollution and the death of the deceased, Dr Herman was “simply discussing what happens in the general population” without considering the specific circumstances of this case. Dr Herman was “acting as an advocate”. He had ignored the most logical explanation of the deceased’s heart injury.
Mr Adhikary then addressed the evidence of Carl Strautins, the respondent’s occupational hygienist. As he had focused on the worker’s exposure to dust and issues relevant to the law of negligence, his opinion “completely misses the point”. Mr Prezant addresses these issues and “dismantles” Mr Strautins’ opinion.
In respect of s 9A, Mr Adhikary adopted a submission made by Mr Parker before
Arbitrator Edwards that non-work-related or underlying factors were “effectively irrelevant in this matter”. There was no other cause of the “aggravation injury” other than employment.Mr Parker submitted that the evidence of Mr Strautins should not be accepted. It was outside his specialty. It failed to acknowledge the connection between air pollution and cardiovascular injury, which all of the other experts in the case had acknowledged.
In respect of substantial contributing factor Mr Parker submitted that it was “almost inescapable” that the Personal Injury Commission (the Commission) would find a substantial contributing factor in this case. The deceased had been exposed to four times the level of air pollution at work than he had been exposed to at home. This emphasised the submission that Mr Parker had made at the earlier hearing where he said that “everybody considers that employment was a contributing factor”.
In his oral submissions on the previous occasion, Mr Parker also referred to a number of other “a causative factors” or aggravating factors including the sedentary nature of the year deceased’s employment and “stress”. Against that background of everyone accepting an “increased risk”. He argued that term against that background of an acceptance of an increased risk he had “that very event”.
Both counsel referred to the principle that the respondent takes a worker as he finds him.
Mr Hickey joined in the attack on Dr Herman. Aspects of his opinion were unsupported by reasons. They were bare ipse dixits. He had changed horses mid-stream. He had not referred to all of the scientific articles.
Mr McMahon also relied on his previous submissions. He argued that the applicant had failed to address through its evidence the undeniable fact that the worker was always at risk of ventricular fibrillation due to his pre-existing heart condition and “he did not need a trigger to invoke that arrythmia”. Dr Helprin does not consider that issue. Dr Herman had consistently stated that the deceased’s pre-existing condition could cause ventricular fibrillation without a triggering event and his opinion had not been responded to by the applicant.
In his oral submissions on the last occasion, he described Dr Herman’s opinion as “simple”. He identified the pre-existing risk heart disease as a known cause of ventricular fibrillation. “That was the cause”. He invoked the principle known as Occam’s razor. He submitted that the scientific articles on which the applicant’s case was built were from “all over the world” and did not address local circumstances.
Mr McMahon also addressed s 9B. He submitted that the applicant had not established that the deceased was at a “significantly greater risk” of suffering the injury than had he not been employed as a courier.
In response to my question as to what weight should be given to the autopsy report
Mr Adhikary stated that the purposes of the autopsy was merely to identify the cause of death. It did not raise issues of causation that are relevant here. He submitted that the pathology report was “deficient” for the purposes of the dispute between the parties at this arbitration.In reply to Mr McMahon’s submission, Mr Adhikary submitted that in the respondent’s defence to the s 9B issue wrongly confined the analysis of the risk in the deceased’s work to one day. It also took a global approach. It was impermissible to compare the deceased with other drivers or other employees who were not exposed to the same level of air pollution to which it had been proven the deceased was exposed on the day of his injury. Further, contrary to the submissions of Mr McMahon, Dr Helprin had accepted that the worker had an underlying coronary disease which made him “more susceptible to harm”.
Before attempting to resolve the issues in dispute, it is first necessary to compendiously set out the respective medical cases. What follows is not intended to be a comprehensive recital of all of the medical evidence. Rather, I set out the salient points so that the parties can understand the way in which the Commission has resolved the dispute.
Dr Garry Helprin
By his initial report of 5 December 2019, Dr Helprin considered that the autopsy report disclosed that the deceased suffered from an old myocardial infarction and narrowing of the coronary arteries. He expressed the opinion, however, that the direct cause of the deceased’s death was ventricular fibrillation and cardiac arrest. That was a “new injury” superimposed on the deceased’s pre-existing coronary artery disease. Dr Helprin referred to a number of studies which reported an association between air pollution and ventricular arrythmia.
A study by Ljunman et. al. “Rapid effects of air pollution on ventricular arrhythmias” in European Heart Journal 2008 volume 29 reported that moderate increases in air pollution appeared to be associated with ventricular arrythmias in patients with implantable cardiovascular defibrillators (ICD) after two hours. It recommended that future studies including a large number of events were required to confirm the findings.
An article entitled Effects of Carbon Monoxide Inhalation on Ventricular Fibrillation by De Bias et. al. in Archives of Environmental Health volume 31 was a study involving animals which concluded that a “vulnerable heart with previous myocardial infarction is more susceptible to ventricular fibrillation”.
A study entitled Association of Short-Term Ambient Air Pollution Concentrations and Ventricular Arrythmias published by Rich et. al. in the American Journal of Epidemiology demonstrated “an increased risk of ventricular arrythmias on exposure to air pollution”.
A study entitled Association of Air Pollution with Increased Incidence of Ventricular Tachyarrhythmias Recorded by Implantable Cardioverter Defibrillators: Vulnerable Patients to Air Pollution by Kim et. al. in the International Journal of Cardiology, volume 240 (2017) records that an “association between air pollution and ventricular tachyarrhythmias were observed in metropolitan areas of an east Asian country”.
An article entitled Ambient Air Pollution and Out of Hospital Cardiac Arrest by Kang et. al. in International Journal of Cardiology volume 203 (2016) also demonstrated an association between air pollution and out of hospital cardiac arrests within one to two days of exposure which had a dose dependent relationship.
A study entitled A Systematic Review of Air Pollution and Incidence of Out of Hospital Cardiac Arrest by Teng et. al. published in the Journal of Epidemiology and Community Health volume 68 number 1 January 2014 states that “larger studies have suggested an increased risk of out of hospital cardiac arrests with air pollution exposure”.
A study entitled The Impact of Short Term Exposure to Air Pollutants on the Onset of Out of Hospital Cardiac Arrest. A systematic review and meta-analysis published by Zhao et. al. in International Journal of Cardiology volume 226 (2017) concluded that:
“The current evidence confirmed the association between short-term exposure to (pollutants) and a higher risk of out of hospital cardiac arrests.”
Dr Helprin concluded his report thus:
“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.”
By a further report of 17 February 2020, Dr Helprin responded to several enquiries by the applicant’s solicitor. He stated that the ventricular fibrillation which caused the death of the deceased was a separate injury. While the damaged heart muscle and severely narrowed left anterior descending artery found on autopsy was pre-existing, ventricular fibrillation was an electrical disturbance of the heart i.e. it is an electrical injury as opposed to a vascular injury. He reiterated that it was:
“most likely that exposure to ambient pollution triggered the electrical disturbance and this otherwise would not have occurred i.e. had it not been for the ambient pollution, ventricular fibrillation would not have occurred.”
By a further report dated 17 January 2021, Dr Helprin considered the reports of Mr Prezant and Dr Herman and a number of scientific articles including a public health policy recommendation from the National Heart Foundation of Australia.
Dr Helprin reviewed an article entitled Air Pollution and Cardiac Arrhythmias: A Comprehensive Review by Shahrbaf et. al. in Current Problems in Cardiology volume 46 (March 2021) which reported that particulate matter especially PM 2.5 (particular matter 2.5 microns or less) has a “strong association” with cardiac arrhythmia among all air pollutants.
The Shahbraf article stated:
““Short-term and long-term exposure to the air pollutants can interact with the 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.”
An article entitled Cardiovascular Dangers of Air Pollution by Agarwal in the Journal of Clinical Cardiology Interventions April 15, 2021. Dr Helprin notes that it includes the following remark:
“Ventricular arrhythmic activity related to air pollution has been described even in healthy populations”.
He states that in studies of more than 5,000 individuals in Rome exposure to particulate matter and carbon monoxide “predicted sudden cardiac death” on the day of exposure.
An article entitled Exposure to Air Pollution and Particle Radioactivity with the Risk of Ventricular Arrhythmias published in Circulation 2020, volume 142 which studied 176 patients with dual chamber implanted defibrillators in Boston Massachusetts concluded that in the “high risk population, intermediate (21-day) particulate matter 2.5 exposure was associated with higher odds of a ventricular arrhythmia event onset among patients with known cardiac disease independent of particle radioactivity”.
An article entitled Air Pollution, Climate and Cardiac Arrest by Chatterjee in the journal Heart August 2020, volume 106 “evaluated up to a 3-day time lag effect between environmental exposure and subsequent out of hospital cardiac arrest risk”.
Finally, Dr Helprin refers to the Heart Foundation recommendation in an article entitled Environment, Climate Change and Heart Health which warns that:
“If you have a heart condition, it’s especially important to avoid spending a lot of time in places that have high air pollution levels, such as busy roads or near factories.”
After reviewing these articles, Dr Helprin concludes:
“I feel that this association is no longer mere hypothesis but established scientific fact. In the articles that I have quoted it has described air pollution as a modifiable risk factor. In other words, if we can reduce air pollution we will reduce cardiac deaths.”
Dr Helprin also says that:
“Dr Herman doesn’t produce a scientific discussion of ambient air pollution in studies of conventional risk factors.”
He continues:
“Mr Clifford’s risk factors would not explain sudden death from ventricular arrhythmias and only explain the prior myocardial infarction which we agree was not work-related. Exposure to small air pollution particles explains fatal ventricular fibrillation on a busy road (identified by the National Health Foundation as a major risk).
I certainly don’t agree that the body of data indicating association between exposure to air pollution and cardiac events is negligible. It is obvious from the studies I have quoted that there is now an extensive scientific body of knowledge on this subject which cannot be reasonably categorised as “negligible” as indicated by Dr Herman. Shahrbaf reviews no further than 121 scientific studies – hardly negligible.
Certainly Dr Herman is unable to explain the timing of Mr Clifford’s death while at work on a busy road.”
Dr Helprin notes that the timing and circumstances of Mr Clifford’s death was “unusual”. He did not die in the early hours of the morning which is common in ischaemic heart disease. It therefore requires “an explanation”. The exposure to environmental pollution is “definitely a trigger and explains why the death did not occur, e.g. during sleep or the early hours of the morning. The environmental exposure to toxins provides the most logical and likely explanation for the death which did not occur during sleep or early hours of the morning but occurred in the working environment on the road”.
Bradley Prezant
Mr Prezant holds a Master of Science in Public Health with a background in Occupational Hygiene and Epidemiology. He states that he is qualified to address the issue of exposure to various chemical and physical agents in air pollution.
Mr Prezant says that he agrees with Dr Helprin’s opinion that there is a causal relationship between ambient air pollution and sudden cardiac death such as ventricular fibrillation. He continues:
“I believe that the literature addressing this issue, particularly as pertains to PM 2.5 particulate matter and ultra-fine particulate matter (UFP) demonstrates a significant association with sudden cardiac events.”
He quotes extensively from the Review of Evidence on Health Aspects of Air Pollution – REBIHAAP Project Technical Report, 2013 in support of his opinion. Included among the quotations is the following:
“The evidence for short-term effects of PM2.5 and PM10 on mortality, morbidity and physiological end-points has also significantly increased since 2005 (Brook et al., 2010; Rückerl et al., 2011). Several new multicity studies have confirmed the previously reported small increases (0.4–1% per 10 µg/m3 ) in daily mortality associated with PM2.5 (and PM10) (Katsouyanni et al., 2009; Zanobetti et al., 2009; Ostro et al., 2006). Estimates of effects for daily mortality were similar in the United States and Europe, but somewhat larger in Canada (Katsouyanni et al., 2009). Most of the European studies are based on PM10, such as the Italian EPIAIR study (Colais et al., 2012). A recent study from Stockholm reported associations of daily mortality with both PM2.5 and the coarse fraction of PM10 (Meister, Johansson & Forsberg, 2012). A study in Barcelona also found a significant association between daily mortality and PM2.5, which was further shown to differ for particles from different sources (Ostro et al., 2011). New evidence of effects on hospital admissions was based on PM10 in Europe (Brook et al., 2010). A large study in the United States reported significant associations with hospital admissions for a variety of cardiovascular diseases, including ischaemic heart disease, cerebrovascular disease and heart failure (Dominici et al., 2006). For a comprehensive review, we refer to previous reviews (Brook et al., 2010; EPA, 2009; Rückerl et al., 2011).”
The reference to PM 10 is to larger particulate matter fund in pollution, including traffic pollution. Which the studies suggest is harmful to health but not as conducive to cardiovascular problems as the smaller PM.5 particulate matter.
Mr Pezant reconstructs the deceased’s likely exposure to pollution if he had remained at home on the day of his death and compares it with his actual exposure as a courier driver on that day. For this purpose, he addresses the level of exposure to PM 2.5 along freeways. He assumes that the motor vehicle-pollutant concentrations are many times higher on roadways than ambient concentrations. He chose to “model the exposure to PM 2.5 along freeways at 10 x the ambient levels” measured by air pollution monitoring stations.
His modelling for freeways or major highways was based on research by Fruin, S., Westerdahl, D., Sax, T., Sioutas, C., & Fine, P. M. (2008) in an article entitled Measurements and predictors of on-road ultrafine particle concentrations and associated pollutants in Los Angeles. Atmospheric Environment, 42(2). It concluded that air pollution on major highways in Los Angeles was 10 times that of that recorded by air quality monitoring stations.
Mr Prezant relied on another study by Goel and Kumar in 2015, which found a peak concentration of pollutant particles at traffic lights, to conclude that exposure to PM 2.5. on urban roads was seven times that found at the nearest monitoring station.
Mr Prezant presented his modelling in the form of a table which I attempt to reproduce below.
Location Exposure Factor Inside Reference Vehicle Exposure Factor Within vehicles 0.5-0.8x Hudda,2013 Rural roads lx 0.8x Assume no traffic Urban roads 7x 5.6x Goel, 2015 Major Highways 10x 8.0x Fruit, 2008 Secondary 7x 5.6x Rough estimate based on Highways reduced truck density compared with major highways
Mr Prezant estimated that exposure to PM 2.5 at the deceased’s residence during the period 6pm to 6am:
“absent indoor activities that would increase this value beyond what would be expected from outdoor air infiltration would be approximately 80 to 90% of this value, which is 5.6 UG/M3.”
Mr Prezant stated the deceased’s PM 2.5 exposure for the entire time from 5.59am, when he left home, until his death at 3pm, was an average of 25.7 UG/M3 (microns per cubic metre). He continued:
“Thus, I calculate that Mr Clifford by virtue of his employment as a courier driver had approximate 4 x greater exposure on the day of his death than a person not driving a vehicle.”
Mr Prezant also observes that utilising PM 2.5 data rather than ultra-fine particles may underestimate the level of exposure to dangerous particulate matter associated with roadways and, consequently underestimate the degree of risk experienced by the deceased.
On the basis of his assumptions, Mr Prezant offered the following conclusion:
“The levels of exposure to which Mr Clifford was exposed are consistent with those levels of exposure that the scientific literature has associated with increased risk of sudden coronary events. Multiple studies as cited above have demonstrated this association both with fatal coronary events and non-fatal coronary events, as well as the biological basis for such effects.”
Mr Prezant also expressed the opinion that courier drivers experience a greater exposure to.
“traffic-related air pollution compared with other occupations. The epidemiological studies have found an association between truck driving and the risk of heart attack although these studies are not considered to be strong evidence by reason of other risk factors in addition to the inhalation of fine particulate.”
Carl Strautins
By a report dated 11 September 2020 Mr Strautins, an occupational hygienist, reviewed the documentary evidence in the matter including the report of Mr Prezant.
Mr Strautins was specifically asked to address workplace exposure standards in Australia. He refers to SafeWork Australia’s “Workplace Exposure Standards for Airborne Contaminants” which sets out workplace exposure standards (WES) for airborne contaminants. He states there are no prescriptive requirements in this document for general non-toxic particulate matter and it is considered “a nuisance dust” or dust otherwise classified. He also refers to SafeWork Australia’s “Guidance on the Interpretation of Workplace Exposure Standards for Airborne Contaminants”.
Section 5 of that document states:
“Where no specific exposure standard has been assigned and the substance is both of inherently low toxicity and free from toxic impurities, exposure to dust should be maintained below 10mg/m3, measured as inhalable dust (8-hour TWA).”
He expresses the opinion that Mr Prezant’s modelling suggests an exposure to respirable dust on a time weighted basis of “about 2 orders of magnitude less” than that which is considered reasonably safe to prevent chronic obstructive pulmonary disease by the Australian Institute of Occupational Health.
Mr Strautins also refers to the Guidelines of the Assessment and Management of Absolute Cardiovascular Disease Risks published by the Stroke Foundation and endorsed by the Royal Australian College of General Practitioners (RACGP) and notes that particulate matter is not presented there as a “risk factor”. He, therefore, expresses the opinion that there is:
“no indication of workplace exposure to particulate matter that is substantial and there would be no intervention that would make any meaningful difference to the outcome of a cardiac event when considering established risk factors.”
Mr Strautins states that he believes that Mr Prezant has attempted to provide the best estimate of the deceased’s exposure to particulate matter on the day of his death. However, there is “a high degree of uncertainty in this because it is unknown or has not been evaluated”. He also states that the uncertainty is “magnified” as the exposure has not been meaningfully compared to that which an ordinary worker would be exposed.
Contrary to the opinion of Mr Prezant, Mr Strautins does not believe that the exposure to respirable dust of a courier driver “would not be considered so different to the ambient levels of air pollution that would make any meaningful difference in the risk”.
In respect of the articles on which Mr Prezant relies, Mr Strautins says that they identify an increase in risk that is relevant to the burden of global health in respect of air pollution. These studies luck specificity and applicability and may include “spectrum bias compared with those in the workforce”.
Bradley Prezant 4 October 2020
By his supplementary report Mr Prezant argues that Mr Strautins was incorrect in his categorisation of PM 2.5 as “nuisance dust or dust not otherwise classified”. He refers to the guidance on the Interpretation of Workplace Exposure Standards for Airborne Contaminants April 2013 and the Position Paper by the Australian Institute of Occupational Hygienists. The former states that:
“The exposure standard for dust not otherwise classified should not be applied where the particulate material contains other substances which may be toxic or cause physiological impairment at lower concentrations.”
The latter document states:
“Where no specific exposure standards has been assigned and the substance is both inherently of low toxicity and free from toxic impurities, exposure to dust should be maintained below 10mg/m3, measured as inhalable dust (8-hour TWA).”
Mr Prezant states that PM 2.5 adjacent to highways “does not meet the definition of nuisance dust or dust not otherwise classified, either in letter, or intent”. He argues that the toxic impact of PM 2.5 is greater than other forms of dust. The particles produced by condensation of diesel exhaust, below 2.5 microns in diameter, have vastly greater surface area and greater biological significance than dust produced by grinding. PM 2.5 primarily deposits in the lower lung whereas large particles are deposited in the airways of the head, prior to the larynx. The toxic impact of the particle is “different in the lower lung”.
Mr Prezant was asked to comment on Mr Strautins “focusing solely on PM 2.5 exposure, rather than the effect of road and traffic air pollution as a whole”. He responded that much of the epidemiological research on traffic-related air pollution has focused on the “aggregate effect of all of these components rather than assessing each individually and summing effects”. He criticises Mr Strautins for only considering the PM 2.5 component and ignoring other important contributors to TRAP[1] toxicity such as CO, NOx[2] and ozone “each of which has been documented to be of health significance”. He states that TRAP has “unique toxicity” that goes beyond what PM 2.5 describes.
[1] Traffic-related air pollution
[2] Nitrogen oxides
In respect of Mr Strautins’ invocation of various standards and guidelines, Mr Prezant argued that none of the standards or guidelines are applicable to the present matter. He stated that:
“The cited regulations above are generic documents related to work, health and safety and/or sampling for airborne particulate.”
He continues:
“The absence of a specific workplace exposure standard (WES) for a substance, such as TRAP, does not automatically mean that one can apply the nuisance standard. There are many examples of chemicals, minerals or biological substances that do not have a WES. If the substance “is both of inherently low toxicity and free from toxic impurities” then that might be appropriate. Clearly that is not the case with TRAP.”
In response to Mr Strautins’ assertion that the dust to which the deceased was exposed would not be measurably statistically or meaningfully different to that of the general working population, Mr Prezant argued that employments do not place,
“members of the general working population along a highway, with elevated toxic air contaminants present in breathing air. It does for courier drivers, truck drivers, toll operators (if any exist, I think not at this point), and maybe some other occupations such a bus drivers. For many of these occupations epidemiological studies such as the ones quoted below have shown elevations in cardiovascular end points.”
Carl Strautins dated 23 October 2020
In response to Mr Prezant’s second report Mr Strautins opined that Mr Prezant had not considered risk factors other than particle size and toxicity which “are more relevant to the cause of the cardiac event”. Thus his link was “tenuous” and “speculative”.
Studies commenting on air pollution in other cities did not address “individual circumstances”. It is inappropriate to use this information “in isolation” to infer that the deceased suffered a cardiac event because of exposure to particulates as a courier driver. He states that the “attributable risk” due to particulate matter in this case is “so low that it does not warrant further consideration”. The attributable risk involves a comparison of all the relevant risks: not just TRAP.
Mr Strautins states that assuming an increase of 20 ug/m3 calculated in accordance with
Mr Prezant’s methodology, multi- city studies suggest an average increase in risk of 0.66% for such an increase in. He states that such an increase:“cannot be said to be the main contributing factor when compared with Australian cardiovascular risk charts (assuming non-smoking male aged 64 with systolic blood pressure of about 164 [last medical with GP] and HDL ratio of 4 (best case scenario) as previously cited in my original report.”
He continues:
“the attributable fraction due to blood pressure, age, smoking status, gender and cholesterol is at least 97% where Mr Clifford was at significant risk regardless of workplace exposure.”
Dr Mark Herman
Dr Mark Herman, a cardiologist, reviewed the papers in this matter at the request of the first respondent’s solicitor and provided an initial report of 4 March 2019. He noted that the deceased had a history of hypercholesterolemia, hypertension, impaired fasting glucose, and depression. He stated:
“All of these conditions are strongly associated with cardiovascular risk and pre-existent in a gentleman who was found to have significant coronary artery disease at autopsy and importantly, an old anterior and septal myocardial infarction in association with left ventricular hypertrophy. He was furthermore found to have significant disease in his left anterior descending artery and right coronary arteries.”
Dr Herman hypothesised that an episode of chest pain reported by the deceased in March 2012 may have been due to coronary ischaemia although he had no formal cardiac investigations at that time.
Dr Herman noted the observations of the deceased made between 60 and 90 seconds after the accident. He concluded that the deceased experienced a sudden cardiac event before his accident which was probably due to ventricular fibrillation in a person with a prior anterior myocardial infarction and probable ischaemic cardiomyopathy.
Dr Herman observed that in the setting of an ischaemic cardiomyopathy “the annual mortality rates range from 5-10%, half of which are sudden and due to cardiac arrhythmia”. He was of the view that the deceased’s occupation did not “contribute in any way towards his pre-existing coronary heart disease nor the provocation of an ischaemic event which provoked the fatal arrhythmia on 22 January 2016”.
By a supplementary report, dated 16 April 2020, Dr Herman considered the opinion of
Dr Helprin and some of the studies referred to in his report. He expressed the opinion that it was unlikely that the deceased would have experienced similar levels of air pollution as those presented in the literature. He considered the impact of the air pollution on the cardiovascular system “remains unclear”. He thought, however, that the relative risk was “weak” compared to conventional risk factors. He also expressed the opinion that quinine, which was found in the deceased’s blood was “more likely” to provoke cardiac arrhythmia then “environmental exposure to toxins (even at high levels)”.He reiterated his opinion that term the deceased was the permanently at a substantial risk of the sudden cardiac arrest (and arrhythmic death) whether or not he had environmental exposure to toxins”. This risk was “very high” and did not require a specific trigger to initiate the event.
By a supplementary report, dated 9 October 2020, Dr Herman reiterated that employment was not the main contributing factor to the deceased’s injury. He stated that he had “multiple traditional cardiac risk factors including a previous myocardial infarction and evidence of ischaemic cardiomyopathy “which is a high risk situation for sudden arrhythmic cardiac death”.
In response to the opinion of Mr Prezant, he states that even if it was proven that the deceased had a high exposure to air pollution “the risk in the overall clinical scenario is negligible”.
By a further supplementary report of 23 March 2022, Dr Herman reiterated that the mortality rate with ischaemic cardiomyopathy is in the order of 5-10% and “worse than most cancers”. He stated:
“Whilst environmental exposure to toxins is increasingly recognised as a potential risk factor for an arrhythmia, the vast majority of sudden death (associated with ischaemic cardiomyopathy) occurs in the absence of any known environmental triggers. Millions of people with ischaemic cardiomyopathies drive each day and it’s ludicrous to suggest that they refrain from driving due to the risk of exposure to environmental toxins.
I therefore feel that employment was not the main contributing factor to the deceased’s injury/ventricular fibrillation.”
Dr Herman then referred to recent evidence and said that he did believe that air pollution may have been a contributing factor “but do not feel this is substantial”. He continued:
“Whilst short and long-term exposure to air pollutants can interact with cardiac rhythms through various mechanisms, this is a strong association rather than definite proof and, in my opinion, further studies are required before making any definitive statements in that regard. Whilst the link with air pollution and cardiac arrhythmia is increasingly being recognised, in light of my statements addressed in question 1 above I do not believe this is substantial in Mr Clifford’s particular circumstances. He was always at a very high risk of cardiac arrhythmia given his ischaemic cardiomyopathy. He did not need a trigger to invoke the arrhythmia.”
In respect of the issues arising under s 9B of the 1987 Act, Dr Herman said:
“Whilst I agree that the deceased’s employment possibly created a greater risk of him suffering a cardiac arrhythmia, I am not convinced that the risk was significantly greater than in any other person with an ischaemic cardiomyopathy at his age and with the additional cardiac risk factors.”
DISCUSSION AND FINDINGS
There is no doubt about the hours that the deceased worked or the route that he drove on the day of his death. He left his home in Woy Woy shortly before 6 AM and drove to Sydney Airport, and on to Banksmeadow. He then drove west to Luddenham. From there, he commenced to drive north to Medowie but died shortly before he reached that destination.
Similarly, there is no doubt that he died of what is commonly described as a heart attack in the course of his employment as a courier on the afternoon of 22 January 2016. Both cardiologists who have provided reports in the case agree that the most likely cause of death was a cardiac arrhythmia, ventricular fibrillation. However, they differ as to the cause or causes of the arrhythmia.
The case is pleaded as one of personal injury in accordance with s 4(a) of the 1987 Act or, alternatively, a disease which has been aggravated in the course of the employment and to which the employment was the main contributing factor to the aggravation in accordance with s 4(b)(ii). The characterisation of the deceased’s heart attack as an injury or disease is of more than academic interest. If the deceased died of an injury, it is necessary for the applicant to prove that his 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 applicant to prove that the deceased’s employment was the main contributing factor to the aggravation etc of the disease.
In either event, the applicant must also prove in accordance with s 9B of the 1987 Act that the “nature of the employment concerned 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”.
Prior to the decision of the High Court in Zickar v MGH Plastic Industries Pty Ltd (1996) 187 CLR 310 (Zickar), ventricular fibrillation occurring against the background of proven ischaemic heart disease death would almost certainly have been characterised as the terminal part of an underlying progressive disease process. Zickar cast aside the legal theory that led to this conclusion and left open the possibility that the terminal event might be an injury simpliciter.
In Kennedy Cleaning v Petkoska [2000] HCA 45, Gleeson CJ and Kirby J, on considering the case law before and after Zickar, said this:
“All of those cases require that consideration be given to the precise evidence, on a fact by fact basis concerning the nature and incidence of the physiological change accepted at trial. If this evidence amounts, relevantly, to something that can be described as a sudden and ascertainable or dramatic physiological change or disturbance of the normal physiological state, it may qualify for characterisation as an “injury” in the primary sense of that word. If such an injury happens within the protected period of employment, it is ordinarily compensable without proof of a specific causal connection with the worker’s employment [41]. 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 unnecessary to proceed to the alternative and additional basis whereby, in such cases, compensation may also be recovered for the disease process if the statutory pre-conditions are met [42].”
This passage was quoted with approval by the plurality in Military Rehabilitation and Compensation Commission v May [2016] HCA 19 (11 May 2016) at [45]. The plurality also stated that physiological change or “disturbance of the normal physiological state” may be internal or external of the body of the employee. While suddenness of physiological change is not an essential ingredient, an injury may be “sudden and ascertainable” or “dramatic” or the worker’s condition might simply be a “disturbance of the normal physiological state”.
Arguably, ventricular fibrillation has sudden, dramatic and terminal consequences. It results in the failure of the heart and then the brain. While most of the previous case law concerned with the distinction between injury and disease addressed myocardial infarction and what are commonly referred to as strokes (the different characterisation of aneurysm and haemorrhage), a consideration of the dramatic pathological changes following the ventricular arrhythmia in this case seems to suggest the likelihood that the deceased suffered a personal injury. Certainly, that is the opinion of Dr Helprin.
As the condition of the ventricular fibrillation is “sudden and ascertainable and “distinct from the underlying pathology”, I propose to find that it is an “injury” which arose in the course of the deceased’s employment.
If that is right, it remains to consider whether the employment was a substantial contributing factor to the injury. That requires the applicant to prove a connection between the injury and the deceased’s employment that is “not less stringent” than the test of “arising out of” the employment: Badawi v Nexon Asia Pacific Pty Ltd trading as Commander Australia Pty Limited [2009] NSWCA 324 (8 October 2009). It also involves an evaluation of the matters set out in s 9A(2).
As s 9A involves a test of causation, it is necessary to consider whether the deceased’s employment substantially contributed to the ventricular fibrillation that resulted in his death. Presumably, the test of causation invokes the common sense test in accordance with the reasoning in Zinc Corporation Ltd & Anor v Scarce (1995) 12 NSWCCR 566. That leads to a consideration of the proof necessary to establish causation in a case such as this.
The headnote to the decision of the Court of Appeal in Seltsam Pty Limited v McGuiness [2000] NSWCA (7 March 2000) (Seltsam), includes the following under the heading “Causation: General”:
“1. Epidemiological evidence that exposure to a substance is a possible cause of an injury may be used to establish that exposure is the legal cause of the injury.
2. The balance of probabilities test is not satisfied by evidence which fails to do more than establish a possibility: St George Club Ltd v. Hines [1961-62] 35 ALJR 106; Tubemakers of Australia Ltd v. Fernandez (1976) 50 ALJR 720; Fernandez v. Tubemakers of Australia Ltd (1975) 2 NSWLR 190.
3. Causation is not established by showing that a defendant’s act or omission increased the risk of injury to a plaintiff when the risk had not eventuated: Chappel v. Hart (1998) 195 CLR 232; Naxakis v. Western General Hospital (1979) 73 ALJR 782; McGhee v. National Coal Board (1972) UKHL 7 considered.
4. 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.”
In his submissions at the previous arbitration hearing, Mr Parker also referred to EMI Australia Ltd v Bes [1972] NSW LR 238 and Tudor Capital Australia Proprietary Limited vChristiansen [2017] NSWCA 260 (Tudor Capital) and Department of Corrective Services v Clifton [2006] NSWWCCPD 310 (16 November 2006) relevant to the s 9A issue.
A logical starting point for an enquiry as to whether there is a causal connection as envisaged by s 9A between the deceased’s employment and his heart attack is the autopsy report for the coroner which certified that the direct cause of the deceased’s death on 22 January 2016 was ischaemic heart disease and the antecedent cause was coronary artery atherosclerosis. Under the heading “Pathology Summary”, the report records:
“1. Ischaemic heart disease as evidenced by:
(a) enlarged heart (590 grams);
(b) old myocardial infarction in the anterior free wall and septum;
(c)greater than 75% atherosclerotic narrowing in the left anterior descending and right coronary arteries;
(d) 50% atherosclerotic narrowing in the left circumflex coronary artery.”
Under the heading “Comments”, the following appears:
“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 atherosclerosis in all the main arteries. The extent of the 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.”
When Dr Herman first reviewed the papers in the matter, on 4 March 2019, he concluded that the deceased was at a substantial risk of a sudden arrhythmic cardiac death because of his ischaemic cardiomyopathy. He expressed the opinion that this is what occurred. The deceased’s employment did not contribute in any way towards the:
“ischaemic event which provoked the fatal arrhythmia on 22 January 2016”
This report was prepared well before Dr Helprin proposed that exposure to traffic related pollution caused or contributed to the deceased’s death and it is improbable that this hypothesis was in the forefront of Dr Herman’s mind. Nonetheless, he provided an unqualified opinion as to the cause of death which is consistent with the comment of the pathologist that the deceased died from ischaemic heart disease and the extent of the disease was such that “sudden death would have occurred at any point in time”.
While various attacks have been made on Dr Herman’s opinion, he has remained of the opinion that the deceased was at very high risk of death by coronary artery disease, although he does consider that “air pollution may have been a contributing factor but do not feel this is substantial”.
He explains this position by stating that the link between exposure to pollutants and cardiac arrhythmia “is a strong association rather than definite proof’. At the conclusion of his final report, he reiterates that he is not convinced that in this case the increased risk resulting from pollution is “significantly greater than in any other person with ischaemic cardiomyopathy at his age and with the additional cardiac risk factors”.
The language of the cardiologists is not always entirely consistent. Risk and cause is sometimes conflated. Dr Helprin is of the opinion that the exposure to traffic pollution increased the risk of cardiac arrhythmia and heart failure. Plainly, however, he is also of the opinion that the increased risk caused the injury. He refers on several occasions to air pollutants being the “trigger” of the deceased’s cardiac arrhythmia. Thus, in his opinion the risk of injury “came home” to use the language of McHugh J in Chappel and the numerous cases which have recited it.
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 PM 2.5, on the day of his death. He also thought it relevant that the deceased died while he was driving, in the midst of exposure to the pollution, rather than at another time. Further, he argued that Mr Clifford’s conventional cardiovascular risk factors would not explain sudden death from ventricular arrhythmias. It only explained the prior myocardial infarction found on autopsy.
I accept that the evidence establishes that there is an increased risk of cardiac arrest associated with traffic -related air pollution. Many studies have reached this conclusion. It seems likely that the risk is greater for individuals with existing heart conditions. Thus, the warning from the Heart Foundation that those with existing heart conditions should “avoid busy roads and factories”. There is no doubt that the deceased fell within the category of an individual with an existing heart condition. Contrary to the opinion of Dr Herman, the evidence establishes these matters as a fact as opposed to a hypothesis.
However it is difficult to understand Dr Helprin’s contention that “Mr Clifford’s risk factors would not explain sudden death from ventricular arrhythmias and only explain the prior myocardial infarction”. In his analysis, the deceased’s ischaemic cardiomyopathy created a vulnerability. But it could not and did not cause the ventricular arrhythmias. They were triggered by pollution. The assertion that ventricular arrythmia and death cannot be caused by ischaemic cardiomyopathy is difficult to reconcile with the other evidence in the case.
Dr Herman reasoned that there was a causal relationship between the deceased’s ischaemic cardiomyopathy and the onset of ventricular fibrillation before the issue of the traffic pollution was raised. His opinion is consistent with the comments of the pathologist and, while it cannot be determinative, appears consistent with common sense.
Contrary to Dr Helprin’s opinion, I accept Dr Herman’s reasoning that at the time of his death that the deceased was at significant risk of death from his ischaemic cardiomyopathy. That was the cause of death determined at autopsy. The likelihood of arrythmia and death from exposure to air pollution in his work as a courier must be considered against that background.
However, it is difficult on the evidence to reach definite conclusions as to the magnitude of the risk created by the TRAP to which the deceased was exposed on the day of his death. Many of the scientific studies on which Mr Prezant and Dr Helprin rely have limitations. Many of them relate to Europe and Asia.
The World Health Organisation document, REBIHAAP Project Technical Report, which
I have referred to above, does consider articles from all over the world. The report contains numerous references to “black carbon” found in air pollution. In a passage quoted by
Mr Prezant, the following appears:“Diesel engine exhaust is rich in PM, mostly below 2.5 μm. A large database describes all sorts of adverse health effects due to exposure to diesel engine exhaust. Exposure to diesel engine exhaust in healthy volunteers causes inflammation of the airways (Behndig et al., 2006) and reduces vascular function (Mills et al., 2005). In patients with heart problems (stable myocardial infarction), diesel engine exhaust causes myocardial ischaemia and reduces the clot resolving function (endogenous fibrinolytic capacity) (Mills et al., 2007).”
Obviously some care needs to be taken in the transposition of the studies referred to in this document to Australia given its different geography, population, and uptake of diesel vehicles which the review describes as being particularly rich in particular it 2.5um. It is not readily apparent how this can be done.
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[3]. 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 PM 2.5 on the day of his death.[3] The study by Kang et al refers to a Melbourne Study which may have replicated the findings of foreign studies
This compounds the difficulty of establishing the magnitude of the increased risk of cardiac arrhythmia experienced by a driver on NSW roads who also has the traditional cardiovascular risk factors such as the deceased. It follows that is also difficult to establish in the increased risk of death from cardiac arrhythmia in these drivers. Dr Helprin does not attempt to quantify the increased risk, possibly because he thought that the only possible cause of the ventricular fibrillation that led to the deceased’s death was substantial exposure to PM2.5.
The REBIHAAP Project Technical Report states that several new multicity studies have confirmed the previously reported small increases (0.4–1% per 10 µg/m3) in daily mortality associated with PM2.5 (and PM10). Certainly, these figures suggest a real risk of death from increased exposure to particulate matter. Again, however, it is difficult to extrapolate from these figures the increased likelihood of death by reason of short-term exposure to pollution in those with significant pre-existing ischaemic cardiomyopathy.
The study by Kang et al, which was conducted in Seoul, South Korea concluded that ambient levels of PM 2.5 were significantly associated with increased risk of out of hospital cardiac (OHCA) within 1 to 2 days of exposure to TRAP. It also indicated that there was a dose-response relationship, and that subjects with conventional cardiovascular risk factors were more susceptible to harm. An elevation in PM 2.5 by 10 UG/M3 increased the risk of OHCA by 1.3%.
The study stated that OHCA is a cause of cardiovascular mortality. It also stated that:
“Conventional cardiovascular risk factors, including coronary heart disease, explain the majority of the risk for sudden cardiac arrest. However, many patients with coronary heart disease are not even aware that they have the disease until the development of the of cardiac arrest. In addition, the occurrence of cardiac arrest is not random but triggered by short-term factors. Circadian and seasonal variations in cardiac arrest occurrence rates have been reported. Only recently has ambient air pollution gained attention as a possible short-term trigger” (footnotes omitted)
The authors acknowledged a number of limitations including the lack of detailed information on the aetiology of the cardiac arrests in the study, the unavailability of firm clinical variables including body weight, smoking status, and the absence of a record of underlying disease in a proportion of cases. Nonetheless, there is no reason to doubt the conclusion that OHCA can be triggered by TRAP and that, in some cases of individuals with underlying cardiovascular disease, it is triggered by TRAP. The difficulty is determining whether an at risk individual died as a result of the underlying conventional cardiovascular risks or as a result of the interaction of TRAP with those risks. This is not adequately addressed in the evidence.
In my opinion, the epidemiological surveys and scientific studies adduced in evidence do not provide any clear answer to this difficulty. They do not permit any firm conclusion to be drawn that the risk of death from TRAP was equivalent to, or a significant fraction of, the risk of death from the conventional cardiovascular risk factors described in the autopsy report. The evidence only touches on the question but does not engage with it. While it is possible that the deceased may have died as a result of exposure to air pollution on the day of his death, is not probable. It is more likely, as Dr Herman contends that the traditional cardiovascular risk factors explain his death.
In Seltsam, Spigelman CJ said this at [137]:
“In Australian Law, the test of actual persuasion does not require epidemiological studies to reach the level of a Relative Risk of 2.0, even where that is the only evidence available to a court stop nevertheless, the closer the ratio approaches 2.0, the greater the significance that can be attached to the studies for the purposes of drawing an inference of causation in an individual case. The “strands in the cable” must be capable of bearing the weight of the ultimate inference”
Of course, this is not a case where the epidemiological studies are the only evidence of causal nexus between TRAP and of the death of the deceased. However, the opinion of
Dr Helprin is plainly underpinned by these studies. If they are not capable of proving causation in an individual case, the doctor’s opinion is of considerably less weight.Mr Parker submitted it was open to the Commission to draw a lay inference, in the same way that Dr Helprin had drawn a medical conclusion, from the circumstances of the death of the deceased while exposed to high levels of TRAP in the course of his duties. However, this is not a case in which common experience can provide an answer to the dispute as to whether TRAP triggered the applicant’s death. I have concluded that there is an insufficient basis for Dr Helprin’s opinion of a nexus between pollution and death. If there is no proper foundation for medical opinion, it is unlikely that there is a proper basis to draw a lay inference of a connection.
127.Mr Parker also submitted that the evidence established that the risk of injury of death triggered by TRAP “came home”. I have reached a contrary conclusion. In my opinion the evidence does not permit a determination that it was the risk of injury created by traffic -related air pollution that caused the applicant’s death. Dr Herman thought that that the additional risk created by TRAP was negligible. But it is not necessary to accept that to find against the applicant. Plainly, the deceased had advanced ischaemic cardiomyopathy which was capable of causing a fatal cardiac arrhythmia at any time. The evidence of the extent of the additional risk to the deceased caused by traffic pollution is vague and unsatisfactory.
To turn briefly to s 9A (2) while the time and place of injury, and that the nature of the work performed by the deceased weigh in favour of a causal connection, the deceased the state of health though prior to his death and the likelihood of him suffering a cardiac event at about the same stage of his life weigh against a connection. The other factors are largely immaterial.
A consideration of these factors does not alter my opinion that the applicant has not proven a causal connection between the deceased’s employment on 22 January 2016 and his death.
I make an award for the first respondent.
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