Evers v Racecar Preparation and Management Pty Ltd

[2013] VCC 517

IN THE COUNTY COURT OF VICTORIA Revised
(Not) Restricted
Suitable for Publication

AT MELBOURNE

CIVIL DIVISION
DAMAGES AND COMPENSATION LIST

Case No. CI-12-05648

KEITH LEONARD EVERS	Plaintiff
v
RACECAR PREPARATION AND MANAGEMENT PTY LTD	Defendant

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JUDGE:	HIS HONOUR JUDGE BOWMAN
WHERE HELD:	Melbourne
DATE OF HEARING:	16, 17, 18 and 19 April 2013
DATE OF JUDGMENT:	26 June 2013
CASE MAY BE CITED AS:	Evers v Racecar Preparation and Management Pty Ltd
MEDIUM NEUTRAL CITATION:	[2013] VCC 517

REASONS FOR JUDGMENT
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Catchwords: Accident Compensation Act 1985 – s86 – claim for payment of statutory benefits – the plaintiff at the relevant time a motor racing mechanic – allegation that plaintiff’s exposure to benzene led to development of a particular form of leukaemia known as acute promyelocytic leukaemia – expert evidence – whether burden of proof discharged.

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APPEARANCES:	Counsel	Solicitors
For the Plaintiff	Mr C Blanden SC with Mr M Clarke	Maurice Blackburn Lawyers
For the Defendant	Mr T Casey QC with Mr M Richards	Minter Ellison

HIS HONOUR:

General background

1       This matter comes before me by way of a Writ and Statement of Claim issued on behalf of the plaintiff in which he seeks a determination that he is entitled to compensation in accordance with the provisions of the Accident Compensation Act 1985 (hereinafter referred to as “the Act”), and, in particular, to weekly payments of compensation as for a person with no current work capacity, together with the payment of reasonable medical and like expenses. In essence, the plaintiff is alleging that the particular type of leukaemia from which he suffers arose out of or in the course of his employment with the defendant. He was so employed as a motor racing mechanic. It is alleged that his leukaemia occurred as a result of exposure to benzene contained in the fuel with which he was working whilst employed by the defendant.

2       The Defence filed on behalf of the defendant admits employment from approximately 19 February 2002 until 27 May 2003.  It admits that the plaintiff has been through the required system of claiming and conciliation.  There are various other matters which were not contested, and to which I shall turn shortly.  That the plaintiff suffered injury arising out of or in the course of his employment with the defendant is denied, as is the assertion that he suffered an injury or disease due to the nature of his employment with it.  Essentially matters relating to causation are denied, as are the those which, accordingly, relate to any entitlement to statutory benefits.

3       Mr C Blanden SC with Mr M Clarke of counsel appeared on behalf of the plaintiff.  Mr T Casey QC with Mr M Richards of counsel appeared on behalf of the defendant.  Oral evidence was received from the plaintiff; by video link from England from Dr Stephen Vaughan, a consultant physician, haematologist and oncologist, who has specialised in the management of cancer and haematological malignancies, such as leukaemia, and who gave evidence on behalf of the plaintiff; Dr Raymond Hocking, a specialist in occupational medicine and a Fellow of the Faculty of Occupational and Environmental Medicine, who also gave evidence on behalf of the plaintiff; Professor Andrew Spencer, a professor of haematology and the current head of the Malignant Haematology and Stem Cell Transplantation Service at the Alfred Hospital, who gave evidence on behalf of the defendant; and Professor Richard Fox, a specialist in medical oncology and malignant haematology, who was director of the Department of Clinical Haematology/Medical Oncology at the Royal Melbourne Hospital from 1985 to 2006, and who also gave evidence on behalf of the defendant.  The balance of the evidence was documentary in nature and was tendered by consent or without objection.  This included a lengthy extract of transcript from a hearing involving these same parties which was conducted before His Honour Judge Wischusen in early 2012 and which was dismissed by consent without adjudication on its merits.  This transcript embraced evidence given by the plaintiff and an expert witness called on his behalf, namely Mr Michael Kottek, whose evidence related, in essence, to such things as the absorption of benzene by reason of skin exposure and the benzene content found in fuels.  This transcript was tendered by consent and was a particularly useful way of abbreviating the amount of evidence required, particularly from the plaintiff.  In the present Judgment, references to the earlier transcript shall be prefixed by “T 2012”, whereas references to extracts from the transcript of the present case shall simply be “T”.

4       I shall also say at the outset that this matter, which involved a considerable amount of complicated and technical evidence, was presented in a particularly sensible and effective manner by counsel, and I thank all concerned for the exemplary way in which this case was contested. 

5       It was made clear at the outset by Mr Blanden that the action brought by the plaintiff is essentially pursuant to s86 of the Act, with particular emphasis on s86(1A).  Mr Casey agreed that the claim was essentially one pursuant to s86 of the Act.  He also confirmed at the outset that questions such as incapacity, the appropriateness of medical treatment and the like were not in issue and that the question that had to be determined was that of causation in the context of s86.  In other words, liability was in dispute, but no other issue need concern me.  Mr Casey emphasised that epidemiological matters would be important.  In addition, it should be said that the credit of the plaintiff was not in issue.  That certainly coincides with the impression which he made of being an accurate, credible witness.

The legislative provisions

6       Section 82(6) of the Act deals with injury occurring by way of gradual process over time due to the nature of employment.  Section 86(1) concerns the entitlement of a worker to compensation for a disease due to the nature of employment as if the disease were an injury arising out of or in the course of such employment.  I shall not set out either of those sections in full, as the dispute in this case centred almost entirely upon s86(1A), which qualifies s86(1).

7       Section 86(1A) reads as follows:

“For the purposes of sub-section (1), a disease suffered by a worker is to be regarded as due to the nature of employment if, and only if, the nature of the employment gave rise to a significantly greater risk of the worker contracting the disease than had the worker not been employed in employment of that nature.”

Factual background

8       Much of the factual background was not in dispute.

9       The plaintiff is aged 49 years, having been born on 12 January 1964.  He is a married man.  He was educated to Year 10 level, and then did a three year apprenticeship as a mechanic with International Harvester, ceasing there when it closed down.  He admits being exposed to things such as paint thinners, diesel fuels and the like whilst in that employment.  He then worked as a back hoe and front end loader operator, and again was exposed essentially to diesel fuels and the like, but, to employ his terminology, “nothing great”.  He was employed there from approximately 1983 to 1985.

10      At about that time he first became involved with motor racing.

11      The plaintiff was employed at Peter Macrow Motors for a period of approximately two years from 1986 or 1987.  The vehicles that he was there working on were Formula 2 racing cars.  The fuel upon which those cars ran was avgas, or aviation fuel, which contained benzene.  Small components of the cars were washed in avgas and the plaintiff was also exposed to it in relation to such activities as refuelling the cars.

12      After a couple of years the plaintiff ceased his involvement with the motor racing industry and then worked for approximately 12−18 months for his father, building houses at Venus Bay.  He was not aware of any exposure to petroleum products or chemicals during that time.  He then returned to work as a mechanic, working for an organisation called Metro Lube.  His occupation there was that of a mobile motor mechanic.  He would repair or service motor vehicles.  He was exposed to normal petrol from the pump, and the contents of some aerosol cans and the like.  He was approximately two years in that employment, and then started his own business in partnership, this business being called Auto Tech.  Whilst the business had a base workshop, it was essentially much the same sort of work as the plaintiff had done for Metro Lube, involving the general maintenance of cars carried out at people’s premises or in the base workshop.  He was involved in this business for some six years and his exposure was of the same limited amount as that at Metro Lube. 

13      In approximately 1997 the plaintiff went to the United States of America where he had some family, and there worked as a motor racing mechanic for a NASCAR team.  In that employment he was again exposed to normal unleaded racing fuel.  The plaintiff performed this work for approximately six months.

14      He then returned to Australia, where he worked for an organisation called Borland Racing Developments, which involved working with Formula Ford racing cars.  Again he was doing work similar to that which he had done with Peter Macrow Motors and in the United States.  Avgas was used, both as a fuel and as a cleaning component.  The plaintiff performed this work for approximately three years, initially on a part-time basis.

15      Following that, the plaintiff set up his own business preparing Formula Fords for racing.  This involved similar work and similar exposure to petroleum products and the like as that previously done by him in relation to racing cars.  In this self-employment, he supplemented his income by doing general servicing and mechanical work on ordinary road cars.  This business ceased in early 2002 when the factory was sold.

16      During that period, the plaintiff also purchased a V8 super car to run himself.  In essence, the plaintiff would look after this vehicle, but lease it out to a driver for the purposes of competing in races.  The car competed in approximately four events in the year that the plaintiff had it.  It ran on Shell Optimax, which was effectively unleaded super petrol.

17      When the factory was sold, the plaintiff then commenced employment with the defendant, which is also known as “OO Motor Sports”.  I shall simply refer to this entity as “the defendant”, which term also embraces OO Motor Sports.

18      The plaintiff commenced such employment on 19 February 2002, and was employed as a number one or lead mechanic.  There were three drivers in the team, and he was in charge of one particular car.  The work performed was evenly distributed between duties performed at a workshop in Dandenong and duties at various racetracks around the country, whether that be for racing or testing purposes.  Whilst the plaintiff had a five year contract to engage in this work, it would appear that it only lasted for some 18 months.

19      The plaintiff’s duties included the construction of the racing car and the assembling of it.  After a race, the car would be taken apart, checked and rebuilt if necessary.

20      Between races, work would often be done on the fuel pumps.  I gather the fuel tanks in a “super” car are vastly different from those in a normal car.  There are some five fuel pumps which are inside a rubber bladder which in turn has in it some porous foam.  After a race, whatever fuel remained in the bladder was pumped out and the quantity of it recorded, this being done in the workshop.  In order to extract and measure the amount of remaining fuel, the foam inserts would need to be removed.  The removal and replacement of these was difficult, and they had to be “scrunched up” as hard as possible in order to manoeuvre them.  It was also necessary to put certain wires in position.  In order to do this, the plaintiff would have his arm in what was described as the “hatch”, his arm being in it to shoulder level.  When the foam was being removed, it would be saturated with fuel.  The plaintiff’s head would be right above the fuel tank with his arm going down into it.  In the transcript of the earlier hearing which was placed in evidence, he stated that the opening of the tank would be just a few inches from his face.  Whilst he was doing this, there would be fumes emanating from the tank.  The process of removing the foam and pumps and replacing them could take up to four or five hours.  When the plaintiff commenced this work, there had been a problem with the fuel pumps, which caused him to replace them all.  This then required considerable testing, including the immersing of the fuel pumps in a container or fuel which was sitting on a bench.  Testing of this nature was quite regular.  The immersing of the pumps was in an open plastic container.  Suffice to say that this type of work involved considerable exposure to fuel.  Much of this evidence can be found at T 2012–28 and following pages.

21      The plaintiff also engaged in the checking of flow rates of the pumps, this involving the immersing of the pumps in a container of fuel and the timing thereof.  This work was done on a bench and using an open container.  When the plaintiff engaged in the removal of the foam and the work with the pumps, he was not wearing gloves.  The tests and checks in relation to fuel were done after every race, qualifying session and the like.  There was constant checking and pumping out of the fuel after every use of the vehicle.

22      The plaintiff was also responsible for the removal and reinstallation of various components, including engines and gearboxes.  This would involve looking inside and under the motor whilst it was running and the gears were being engaged.  There was extraction of some exhaust gases when a car was running in the workshop.  However, fuel and gas does come out of the pipes or trumpets on the side of the vehicle and into the atmosphere.  When the motors are not fully warmed up, raw fuel spits out of the trumpets.  To use the words of the plaintiff, he would have his head “buried in the engine bay” and then be lying underneath the motor to check for leaks – see T 2012-40.  The plaintiff also gave evidence in the earlier hearing that he was exposed to other fuels or chemicals which contained benzene.

23      In the 2002 season, he would have attended in his working capacity at 15 events, and there were additional test days held at Winton when the car would effectively be running from dawn until dusk.  In the 2002 season there were approximately six such days.  When the car was racing, this effectively involved a minimum of four consecutive days of work for setting up, qualifying and racing.  Some events involved at least one additional day.  For normal events, the work on the car would start on the Friday morning and continue through to the end of racing on Sunday afternoon or evening.

24      Apart from being a mechanic, on race weekends the plaintiff was also a member of the pit crew.  When refuelling was taking place at speed, there could be quite massive spillage and the plaintiff would have a rag in his pocket so that he could wipe up any excess fuel, as the car would not be allowed back on the track if fuel was dripping.  The plaintiff’s description of what would occur can be found at T 2012–44 and following.  Suffice to say that the plaintiff was in a position where he was close to both the refuelling procedure and particularly to the exhaust of the vehicle when it came in for a pit stop.  On race days the defendant would have three cars out on the track, but all serviced by the same crew of which the plaintiff was part.

25      The plaintiff described occasions when he was overcome by fumes – see T 2012–48.  He also stated that, on test days, “We’d go through probably five or six hundred litres of fuel in one day”.  Indeed, some of the duties which he performed involved effectively being in the boot in order to access the fuel system whilst it was still in the car.  The plaintiff would also come into contact with the fuel because there was always a certain amount that would lie in the bottom of the tank and which had not been removed by the access pipe.

26      The plaintiff’s evidence-in-chief in the earlier hearing in regard to his employment duties with the defendant concluded with statements by him that his hands and forearms would often come up in a red rash after handling the foam and the fuel, and that he often got small cuts on his fingers when dealing with some of the more intricate areas of the fuel pumps.  Gloves could not be worn in such a situation – see T 2012–58 and 59.

27      In 2003 a different company came in and effectively took over the contract for the support of the Ford team.  The plaintiff ceased working for the defendant on 27 May 2003. 

28      The plaintiff then commenced working with Toll Motor Sport, where he was chief mechanic.  Whilst this was a rung further up the ladder, the plaintiff still performed “hands on” work.  However, with Toll Motor Sport there was not as much trouble with fuel pumps as with the defendant.  The plaintiff could recall no major problems there – see T 2012–52.

29      In mid-2004 the plaintiff left Toll Motor Sport and commenced to work for WBS Motor Sport on the Gold Coast, having climbed another rung on the ladder to the position of team manager.  He was no longer “hands on”, being responsible for the administration and operational sides of the team.  He was with that employer until 2007 when the effective proprietor sold the assets of the team.  The plaintiff then worked for that person in a real estate position until late 2007.  He then obtained a position as workshop manager with a manufacturing company, effectively looking after earth moving equipment.  He was exposed only to diesel fuel.  He did this work for a couple of months before working as the harbour master at Hope Harbour Marina in Queensland.  There was a refuelling jetty, but the plaintiff did not engage in any active pumping of the fuel.  In 2008 he also had an administrative role looking after Indi cars when they came to the Gold Coast for a period of a few months, but again he was on the operational side and not working with the cars.

30      From November 2008 until July 2009 he worked as a team manager for an entity called Team Inter which was involved in V8 super cars, but again was more involved in logistics than “hands on” work.  He then purchased a vehicle which could carry cars and boats between Queensland, Sydney and Melbourne.  That business was doing well when the plaintiff was first diagnosed with leukaemia in March 2010.

31      The plaintiff then did not work until 4 April 2011.  He then did some diesel maintenance work on trucks and trailers, moving away from motor racing.  He obtained this work through an agency and ultimately obtained a position with a firm called RML Diesel Repairs on the Gold Coast. 

32      The plaintiff continued working as described above until he suffered a relapse in September 2012.  He has not worked since.

33      I have gone into the history of the plaintiff’s employment over the years in some detail, because this did receive some attention in cross-examination, and particularly that of Dr Hocking.  It is fair to say that the only employments in which the plaintiff was exposed to racing fuels were with Peter Macrow Motors, commencing in 1986 or 1987 and for a period of two years; in the United States for a period of six months or less; with Borland Racing Developments for a period of approximately three years, initially part-time, from 1996 until 1999; when conducting his own business preparing Formula Fords, this being essentially on a part-time basis from 1999 until early 2002; with the defendant for the period described; and with Toll Motor Sport for a period of one year prior to moving to the Gold Coast, this being in 2004.  Thereafter the plaintiff was in an administrative position or was engaged in work which did not expose him to motor racing fuel. 

34      Another aspect of the case which received perhaps more attention in the earlier hearing is the level of benzene in motor racing fuel.  On this occasion Mr Blanden opened that the benzene content of the fuel at all relevant times was in the order of three and a half to four percent and that such fuel was used by all the vehicles that the plaintiff worked on whilst with the defendant.  There was no great challenge to this proposition in the present case.  Indeed, the position of the defendant was summarised in his closing address by Mr Casey at T 217 and 218 as follows:

“Both our experts, Professor Fox and Professor Spencer will simply not accept that there is any connection between exposure to benzene and the disease which has been suffered by the plaintiff in this case.  So it is not really a question of whether there is some risk but it is really not significant or it is not great, they will not accept any connection.”

35      This, in essence, was the approach foreshadowed by him at the commencement of the case when he stated:

“It really comes down to a study of epidemiological matters…to be the subject of questioning and debate from the four experts.” – see T 12.

36      In any event, the report of Mr Kottek refers to the fact that mixtures containing above 0.1 per cent benzene have been classified as carcinogenic and it would appear that motor racing fuel contains a greater level of benzene than that.

The case on behalf of the plaintiff, including expert evidence

37      The plaintiff’s case could be summarised as follows.

(a)      The plaintiff’s evidence

38      Apart from the adoption of his evidence as recorded in the transcript of the earlier hearing, the plaintiff gave comparatively brief evidence in which he updated his situation.  Immediately prior to the relapse of his condition, he was looking after large machinery, essentially for mining operations, and was exposed to little or no benzene. 

39      In cross-examination, the plaintiff described his exposure to avgas when working with Peter Macrow Motors as “very mild” – see T 16.  He also thought that his exposure in the United States was very light, and his exposure with Borland Racing Developments was in the same category.  He described his use of avgas as a cleaning agent as being very intermittent and a light exposure.  He considered his exposure when preparing his own vehicles in the period 1999−2002 as being the same, and it would appear (his answer as recorded on the transcript was partially indistinct) that he was agreeing with the proposition that it was very minimal – see T 19.  Certainly he described the preparation of the super car which he had himself and which he leased out to a driver as involving minimal exposure.  He further agreed that in the sprint events, of which there had been some 13 in the 2002 season, a refuel during the race was not required.  He also pointed out that the vehicle would be filled a number of times in the factory and the fuel removed for the purposes of conveying it to the track.  These processes produced fumes – see T 23.  The plaintiff stated that there had been a lot of problems with the fuel pumps.  He also made it clear that, when undergoing the process of the removal and replacement of the fuel pumps, he would in fact be in the boot of the car.  To remove the pumps from the fuel tank could take up to four hours – see T 27.  Cleaning of parts using fuel was something that was done on a regular basis.  The cleaning of parts would take place on a daily basis.  In relation to being splashed with some fuel from the trumpets whilst the engine was heating up, the plaintiff said that this took some 15−20 minutes.  He also stated that, whilst in sprint events cars might not come in for refuelling, they did come in for wheel changes.  He would be exposed to exhaust vapours when that occurred.  In addition, he stated that, at the racetrack, he wore gloves and a helmet, but not a mask over his face. 

40      In re-examination he said that, in sprint races, the car had to be refuelled each time it went out during five sessions of practice and qualifying and then two or three races.  Thus, for each individual outing, the fuel tank had to be emptied and then refilled – see T 35.  Whilst the cleaning of parts with fuel was done regularly, it was not done every day.  The five blocks of foam to which reference has been made were quite large, being approximately a metre wide by half a metre deep.  They have to be scrunched up to be moved, and there was almost always some fuel on them when they were removed.

41      Apart from the documentary evidence tendered, oral evidence on behalf of the plaintiff was adduced from Dr Vaughan and Dr Hocking.  I shall deal with them in turn.

(b)      Dr Vaughan’s evidence

42      Dr Vaughan had provided two reports to the plaintiff’s solicitors, in addition to the oral evidence which he gave.  Dr Vaughan is a specialist consultant physician, haematologist and medical oncologist, and has been carrying on that specialist practice since 1982.  His daily work includes the management of cancer and haematological malignancies such as leukaemia.  He is a Fellow of the Royal Australian College of Physicians and of the Royal College of Pathologists Australia.  Apart from holding visiting appointments at various hospitals, he is Chair of the Cancer Institute at Epworth Healthcare, and this also involves haematology. 

43      The earlier report of Dr Vaughan is dated 29 August 2011.  It includes the fact that the plaintiff suffers from a sub-type of Acute Myeloid Leukaemia, which shall hereinafter be referred to as “AML”.  The sub-type from which the plaintiff suffers is Acute Promyelocytic Leukaemia, which is referred to in some of the documents as “APML” but which was essentially referred to in questions and submissions as “APL”.  Hereinafter it shall be referred to as “APL”.  I would add that there is no dispute as to these matters, and it is agreed that the plaintiff is suffering from APL.

44      Another matter referred to in the earlier report of Dr Vaughan and concerning which there is no dispute is that APL involves a carcinogenic chromosome translocation identified as a 15;17 translocation.  Without going into some of the very technical details concerning this, it is sufficient to say that this translocation, referred to as “t15;17”, is the means of identifying APL as a specific sub-type of AML.  It is a peculiarity of APL and identification of it permits experts to isolate and diagnose APL.  I gather that t15;17 has become virtually a shorthand way of referring to APL.  I might add that none of this, including the plaintiff’s diagnosis, is contentious. 

45      Returning to the evidence of Dr Vaughan, in his report of 29 August 2011 he adopted the history obtained by Dr Hocking, with whose report of 30 January 2011 Dr Vaughan had been provided.  That history is not entirely accurate, as it refers to the plaintiff as working full-time with V8 super cars between 2000 and 2009, and I would refer to the history of employment which I have set out above.  The history obtained by Dr Hocking would suggest that the extensive contact with racing fuels described occurred throughout that period.  Again, I would refer to the history given in evidence and which has been set out above.  Whether that inaccuracy has any bearing on the overall decision to be made is another matter.  What is clear is that Dr Hocking’s report contains a reasonably comprehensive and accurate account of the work performed by the plaintiff for the defendant.  Dr Hocking, together with the plaintiff, also visited a workshop, inspected a V8 super car with the plaintiff, caused the plaintiff to simulate some of the tasks which he carried out and took photographs.  Details of this were supplied to Dr Vaughan.  In short, Dr Hocking’s report of 30 January 2011 includes a detailed account, with photographs, of some of the tasks carried out by the plaintiff when employed by the defendant.  This account does not seem to me to be inaccurate.

46      Dr Vaughan also had available to him the report of Professor Fox, examining on behalf of the defendant, this report being dated 2 November 2010. 

47      The conclusion of Dr Vaughan in his report of 29 August 2011 was that benzene is a recognised cause of AML, of which APL is a sub-type, and that further exposure was likely to increase the chance of the plaintiff’s leukaemia returning, as there was a reasonable probability it was involved in its initial development.  Dr Vaughan also observed that it had been known for a long time that benzene was a carcinogen involved in the causation of AML, of which APL is a sub-type.  He stated that, in this particular case, the duration of exposure was lengthy and consistent with the known latency of benzene exposure causing leukaemia. 

48      Dr Vaughan provided a second report dated 25 March 2013.  On this occasion he had provided to him a large number of reports, monographs, studies and transcripts.  In this later report he again referred to his expertise in the diagnosis and management of haematological disorders, including AML and APL.  He repeated his opinion that benzene exposure has a causal role in AML and all sub-types, including APL.  He emphasised the importance of looking at benzene exposure in the particular case, as opposed to in the petroleum industry.  He also expressed the view, later to be repeated in his oral evidence, that a review of all papers and a balancing of the various conclusions are required in order to come to a definitive conclusion about the role of benzene or any other carcinogenic causation of disease.  He concluded that benzene is a recognised carcinogen capable of causing APL.  It can be absorbed into the body in various ways, and, in the present case, by skin absorption and inhalation.  He was of the view that epidemiological studies show that there is an increased risk of APL in workers exposed to benzene as a component fuel in such workers’ course of employment.  He was also of the view that the plaintiff’s exposure to benzene in the course of his employment with race car preparation and management was a contributing factor in relation to his APL.

49      Dr Vaughan gave lengthy oral evidence.  He expressed the opinion that, based on the description of the work activities of the plaintiff which he had been given, per cutaneous exposure would seem to have been heavier than oral or inhalation exposure.  In addition, based upon the details of exposure which were contained in Dr Hocking’s report, he formed the view that the plaintiff’s exposure to benzene had been very significant.

50      In relation to the role of benzene as a carcinogen in the causation of AML, Dr Vaughan stated that it had been first been recorded as a carcinogen in 1928 and that there had been a multitude of studies since, these most recently being condensed in a 2012 monograph of the International Agency for Research on Cancer (“the IARC”).  I might say that this particular monograph received considerable attention during the conduct of this case.  It was tendered and I regard it as a significant piece of evidence.

51      Dr Vaughan also referred to a paper by Otto Wong and others, which paper I shall henceforth refer to simply as “Wong”.  Dr Vaughan referred to the assumption contained in Wong that APL is more common in benzene exposed individuals than is the general type of AML – see T 44.  Dr Vaughan was also at pains to emphasise a distinction between cause and mechanism, and it is to be remembered that, pursuant to s86(1A) of the Act, it is the concept of the nature of the employment giving rise to a significantly greater risk of contracting disease, rather than causation, that is to be considered. 

52      In examination-in-chief, Dr Vaughan essentially adopted the views which he had previously expressed in his reports concerning exposure to benzene and its probable role in the development of APL.

53      Dr Vaughan also stressed the importance of the recent IARC monograph, as well as stating that the best, most recent and largest epidemiological study suggests that a relationship exists between benzene exposure and APL.  He was of the view that the exposure to benzene, to which the plaintiff was subject, might lead to the development of the condition from which he suffers – see T 48.  He regarded benzene exposure as having a causal role in AML and all its sub-types, including APL.  He again emphasised the importance of the IARC monograph.

54      In cross-examination, Dr Vaughan agreed that the cytogenetic description of t15;17 was the correct description for APL and applied to the plaintiff’s case.  Dr Vaughan also referred to latency as a factor, meaning the time which passed between exposure and onset of the disease and the assessment of the probability or improbability of a relationship between the two.  An example of this, according to Dr Vaughan, is that a latency period of less than 20 years for mesothelioma would mean that exposure to asbestos within that shorter timeframe would probably not be considered causative of the ultimate disease.  He also pointed out that exposure could be cumulative, and that there was an argument that, for example, the mid-point of the exposure period could be selected as being the starting date in assessing the latency period.  In broad terms, in relation to cancer causation, a latency period shorter than a year or two would make the causal factor unlikely – see T 62.  In other words, the degree of exposure to the alleged carcinogen from time to time might also need to be taken into account.  In individual cases, as opposed to epidemiological studies, the date of first exposure does not necessarily mark the commencement of the latency period.  In the present case, Dr Vaughan was of the opinion that, if the interval between exposure and onset of disease was more than 12 to 18 months (perhaps two years), this was over the threshold.

55      In the present case, the proportion of benzene in the product was low.  In relation to the period and frequency of exposure, Dr Vaughan relied on the reports of Dr Hocking and Mr Kottek.

56      Dr Vaughan pointed out the problems associated with studies that have been done where the sample base was too low – see T 67.  When cross-examined about the various studies, which apparently number in the hundreds, Dr Vaughan again emphasised that one has to look at the totality of the studies, again referring to the IARC monograph.  He considered Wong to be the only study sufficiently recent (2010) to deal with the modern classifications of leukaemia and sufficiently powered to answer any question.  Earlier negative studies, if underpowered, do not mean much.  However, he was also not persuaded that, in terms of causation, there was any great difference between APL and AML.

57      In relation to Wong, Dr Vaughan was of the view that the study, whilst the best available, was somewhat “under-powered” – that is, not having enough sample cases.  However, it is the best study available.  According to Wong, exposure to benzene is associated with a significant increase in the risk of AML.  The amount of the exposure to the alleged carcinogen, such as benzene, is important.  In relation to “exposure to petroleum fuels”, there is a distinction between someone filling up their car’s tank at a service station and someone working on the pumps at a refinery.  Dr Vaughan also stated that, whilst there may be little doubt that exposure to benzene above a certain level can result in an increased risk of AML, there is no reliable information about a very low level exposure.  It might be that only a tiny dose is required for a person with a predisposition.  Wong, like all studies, has to be looked at with a fair amount of caution.  Dr Vaughan stated that he had some experience dealing with the petroleum industry in an administrative capacity, and with benzene levels, and the studies do not provide enough information concerning this.  General terms, such as petroleum workers, are least useful.  The starting point is the particular chemical, and the next most useful item is a detailed job description and identification of what is occurring in the workplace – see T 91.  Dr Vaughan placed less reliance on learning concerning occupational exposures in groups, unless he had much more detailed knowledge about what the title of the group meant or what the group did, than he does on a specific statement where the exposure to a particular chemical, such as benzene, has actually been assessed – see T 92.

58      In Dr Vaughan’s opinion, Wong is not a perfect study, and the process of going through study by study is highly likely to be misleading.  The appropriate process is to look at the totality, rather than a “line by line” approach.  Wong specifically looked at benzene, a particular chemical, and drew some conclusions about a particular sub-type of leukaemia, namely APL.  Wong has its limitations, but is the best of the available information – see T 93.  Wong looked at benzene and its particular relationship with APL.  This “…demonstrated that it was probably increased and I think that negates the possibility that APML (APL) is some way different from AML in more general terms” – see T 94.  APL is usually diagnosed at a younger age than other such diseases and proportionally women have it more commonly.  Its demographics are “a bit different” in that the onset age is younger and the male/female ratio is slightly different, being more equal than in AML.  Dr Vaughan was reluctant to draw any particular inference from this in relation to causation.  He agreed that one feature of APL that was different was the 15 and 17 chromosome translocation – t15;17.  That is the definition of APL.  Dr Vaughan repeated that benzene has carcinogenic effects and he presumed that it was carcinogenic for all types of AML.  In terms of mechanism, APL does not differ from AML. 

59      In re-examination, Dr Vaughan confirmed that the starting point was that the IARC monograph stated that benzene was a carcinogen.  He again emphasised the distinction between mechanism and causation.  He concluded by agreeing that the specific exposure of an individual to a chemical is relevant to whether or not that exposure is sufficient to fit the sort of causative outline to which he had referred in his report.

60      I would say now that I found Dr Vaughan to be a particularly well-informed and impressive witness.  His approach of viewing the literature as a whole and having particular regard to the IARC monographs – and especially to the most recent one – seemed to me to make sense.

61      Whilst, sequentially, Dr Hocking was not the next expert to give evidence, as I am dealing with the plaintiff’s case I shall now discuss his evidence.

(c)      Dr Hocking’s evidence

62      Dr Hocking’s specialty is occupational and environmental medicine, and his qualifications in that regard are impressive.  However, as he admitted in cross-examination, he has not been directly involved in investigating cases of AML and had not previously encountered APL – see T 141.  He freely admitted that his knowledge in this regard has been acquired from the reading of literature, research reports and the like.  I accept that his speciality has brought him into contact with leukaemia generally, toxicology, skin absorption of various chemicals and the like.  I am bearing in mind the limitations which Mr Casey suggested should be adopted in relation to the evidence of Dr Hocking because of what has just been stated, but would add that I found his evidence to be helpful.  It may be that a considerable part of his knowledge arises from research which he has done or, to use Mr Casey’s argument, information which is obtained from the internet and which is universally available.  The emphasis which Dr Hocking placed upon the IARC monographs seem to me to be appropriate and his explanation in relation to them, and in relation to the various studies and articles generally, was helpful. 

63      Turning to the evidence, written and oral, of Dr Hocking, it was to the effect that the plaintiff’s exposure to benzene in the course of his work would have been a significant contributing factor to his AML (of which APL is a sub-type) – see his report of 30 January 2011.  As part of the work done by him in relation to the preparation of this report, Dr Hocking took a reasonably comprehensive occupational history (parts of which were attacked by Mr Casey).  In particular, he took details of the work performed by the plaintiff with racing cars.  His research seems to have included the reconstructing by the plaintiff of various tasks which he performed, including the pouring of petrol into the petrol tank in the boot of such a car and the positioning of his body whilst so doing.  His report of 30 January 2011 includes a large amount of technical detail, much of which has been obtained from articles and via the internet.

64      His conclusion in that report, in addition to what has been stated above, includes observations that benzene has been internationally recognised as a cause of AML by the IARC since 1982.  He placed emphasis upon absorption of benzene by inhalation and skin absorption.

65      Dr Hocking provided a second report, this being dated 9 January 2012.  He did this without again seeing the plaintiff or reconstructing events causing exposure, but rather commented upon reports of Dr Vaughan and Professor Fox.  Essentially Dr Hocking agreed with certain remarks of Dr Vaughan concerning the sub-type relationship between APL and AML and felt that, accordingly, the epidemiological data regarding AML was also applicable to APL.  He disagreed with comments made by Professor Fox in his reports of 2 November 2010 and 3 December 2011.  In particular, Dr Hocking was critical of the absence of detail obtained by Professor Fox in relation to the particular tasks carried out by the plaintiff with car racing fuels.  He pointed out that he had accompanied the plaintiff to his place of work and photographed certain work practices, whereas Professor Fox had not done this.  Dr Hocking also emphasised the absence of reference in the reports of Professor Fox to the monographs of the IARC.  He disagreed with Professor Fox, and considered that the epidemiological evidence was strong in relation to an increased risk of APL among persons exposed to benzene.  I shall not go into the technicalities of these arguments. 

66      Dr Hocking reported again on 3 November 2012, not having seen the plaintiff again but having been asked to consider a substantial amount of material.  Dr Hocking again emphasised that the work performed by the plaintiff, being a motor racing mechanic, was atypical of work done by mechanics generally and was, in his opinion, associated with work practices which would lead to much greater inhalation and skin absorption of benzene.  Again, the report is quite technical, but items of interest include some of the problems which Dr Hocking perceived with Wong.  Nevertheless, Dr Hocking considered Wong to be supportive of the relationship between benzene exposure and APL.  Also, he considered the issue of the latency period to be consistent with the plaintiff’s case.

67      Importantly, Dr Hocking discussed the most recent IARC monograph, pointing in particular to the fact that the monograph reviewed the biochemical pathways whereby benzene can be carcinogenic.  He included a quotation from the monograph to the effect that benzene metabolites can produce multiple genotoxic effects resulting in chromosomal changes in humans, and those changes may include the t15;17 translocation such as that found in the plaintiff.  Dr Hocking also commented on the report of Professor Fox of 23 January 2012, having remarked on previous reports.  His criticism of that report is lengthy, but a major limitation highlighted by Dr Hocking was that Professor Fox had not obtained an adequate occupational history concerning the plaintiff’s unusual work practices and this, in the opinion of Dr Hocking, meant that Professor Fox’s reports were largely based on generalisations from the literature being applied to the plaintiff rather than looking at the specifics of the plaintiff’s exposures in assessing how they relate to the literature.

68      Dr Hocking had other criticisms of the reports of Professor Fox, returning to the reference to the most recent IARC monograph and its recognition that chromosomal changes in association with benzene may include t15;17 translocation.

69      In his report, Dr Hocking also made the point that the IARC review referred to benzene as a cause of AML, and APL is a sub-type of AML.  There is nothing in the statement contained in the IARC monograph that suggested APL is excluded from the statement concerning AML.  Therefore, in the opinion of Dr Hocking, statements by the IARC regarding AML also apply to APL unless it is specifically excluded.

70      Given the frequent references to the IARC monographs, and the 2012 one in particular, perhaps I should point out that the IARC effectively runs a rolling or ongoing review of literature and studies relating to forms of cancer, then summarises these.  It provides an overview and states some conclusions.

71      As stated, Dr Hocking also gave oral evidence.  At T 134 and following, Dr Hocking stated that further material had been provided to him since his report of 3 November 2012 in order that he could comment on this.  Such material, if anything, reinforced the view that he had previously expressed.  The material included another report from Professor Fox and a report from Professor Spencer.  In his oral evidence Dr Hocking again placed emphasis on the most recent IARC monograph.  Dr Hocking felt that this document was very supportive of the proposition that benzene had a direct relationship in causing the chromosome or abnormality t15;17, which existed in the case of the plaintiff.  He again pointed out that, in the concluding paragraph of the monograph in which an overall evaluation is made, no exceptions are stated to exist to the proposition that chromosomal abnormalities, including t15;17, have been found in the lymphocytes of workers exposed to benzene.  He did not feel that Wong was a definitive study, but concluded his evidence-in-chief by stating that, having again reviewed the IARC monograph, if anything, that further substantiated his view that there is a considerable likelihood that the plaintiff’s work practices and exposure to benzene in the fuels led to the development of the APL. 

72      Dr Hocking was cross-examined at length and in detail.  In relation to his expertise, Dr Hocking said that he had a wide understanding of toxicology and particularly in relation to workplace exposure to toxic substances and the absorption methods of same.  He has been involved in the study of the relationship between leukaemia and the positioning of television towers, but he had not previously been directly involved in investigating cases of AML in the workplace, and had not previously come across APL – see T 141.  He had obtained the knowledge required to express the views contained in his reports from extensive reading of the literature and of the research.  Dr Hocking again emphasised the importance of history-taking, stating that being involved in occupational medicine meant that he was taking very thorough histories.  I might say that it was quite apparent that Dr Hocking placed very considerable significance upon the IARC monograph.

73      Dr Hocking agreed that he did not have the expertise that, for example, Professor Spencer possessed in relation to haematology, but had a general working knowledge of it.  He again referred back to the IARC document.  He again emphasised the importance of the IARC statement about the relationship between the particular chromosomal abnormality suffered by the plaintiff and benzene – see T 153.  In addition, Dr Hocking again emphasised the importance of the particular details of the plaintiff’s exposures, including immersing his hands in the fuel, placing his head close to a funnel with the fuel in it and like matters.

74      Dr Hocking was also cross-examined concerning the latency period.  He agreed that the latency period in the case of the plaintiff was considerably longer than the 10 years which he had originally thought it was.  However, he did not feel that, between 1985 and 2000, the plaintiff was having ongoing and appreciable exposure to fuels.  Dr Hocking also stated that the mechanisms whereby benzene causes leukaemia were not fully understood, but there are indications of how it may have its causative effect.  He felt that the IARC monograph gave reasonably good evidence that the chromosomal abnormalities involved in the present situation may in some cases be due to benzene. 

75      In re-examination he referred to the existence of a type of domino effect – see T 164.  Dr Hocking also stated that, at the time of earlier IARC monographs dating back some 30 years, it was unlikely that the t15;17 translocation would have been recognised.  In relation to latency, Dr Hocking said that the situation became complicated where there are variations in a job and variations in exposures.  He concluded by again emphasising the unusual nature of the plaintiff’s work practices. 

76      In his closing address Mr Casey was somewhat critical of Dr Hocking’s expertise and as to whether it enabled him to express the views which he did, in essence saying that he had done no more than obtain certain information either from books or the internet, and that was something which anyone could do.  To me, that criticism is a little unfair.  Dr Hocking may not be a haematologist who has actually looked after or professionally consulted with patients suffering from AML or the even rarer condition of APL.  However, he is an occupational physician familiar in the broader sense with exposure to toxins in the workplace.  He has done very considerable research in relation to the problems associated with this particular case.  He is far better equipped to understand and assess the material contained in the research papers than a lay person would be.  Whilst he may not previously have encountered APL, his evidence, based on the technical material to which he has had access, was helpful.  The shortcomings which he saw in Wong, and with which other witnesses essentially agreed, seem to me to be logical.  The same could be said for the importance which he attached to the particular duties performed by this plaintiff and the exposure involved accordingly, and for the importance which he attributed to the 2012 IARC monograph.  I am certainly not of the view that his evidence should simply be swept aside.

The expert evidence on behalf of the defendant

77      Professor Andrew Spencer has various degrees and is a Fellow of the Royal College of Pathologists of Australasia.  Currently, he is the Head of the Malignant Haematology & Stem Cell Transplantation Service at the Alfred Hospital, a Professor of Haematology at Monash University, Head of the Myeloma Research Group at the Australian Centre for Blood Diseases and is the immediate past President of the Haematology Society of Australia & New Zealand.  He provided a report dated 29 March 2013 to the defendant’s solicitors, in addition to giving oral evidence.  His report is based upon various documents provided to him, including reports of Professor Fox, Dr Vaughan, Dr Hocking, Mr Kottek and Wong.  In formulating the opinions, he had reference to some six publications, essentially epidemiological in nature and relating to APL.  His conclusions were that the plaintiff’s employment with the defendant was not a significant contributing factor to the subsequent development of APL, which would have evolved irrespective of that period of employment.  He also expressed the opinion that the plaintiff’s condition was not due to the nature of his employment, including potential exposure to benzene.  He agreed with the views of Professor Fox.  He expressed the opinion that Dr Vaughan had failed to provide an answer to the question as to whether benzene was a recognised cause of APL, also stating it was erroneous to claim that prior benzene exposure must have contributed to the recurrence of the disease.  He disagreed with what had been said by Dr Hocking to the effect that, because APL is a sub-type of AML, it is reasonable to conclude that agents that cause AML would also cause APL.  This, according to Professor Spencer, was illogical and an inappropriate simplification without scientific basis.  In relation to Mr Kottek, Professor Spencer expressed the opinion in his report that the views of Mr Kottek seemed to be based upon Wong which was flawed.  Professor Spencer set out his reasons as to why this was so. 

78      In his oral evidence, Professor Spencer described the development of knowledge over the years in relation to AML and its sub-types.  He also referred to the t15;17 translocation which is the specific genetic abnormality in question.  He stated that APL was treated differently to other forms of leukaemia – see T 107.  Professor Spencer was also of the view that what had occurred in the present case was not the acquisition by the plaintiff of another leukaemia, but the re-occurrence of the original which had never been fully eradicated. 

79      Professor Spencer also expressed the opinion that there was a paucity of evidence linking APL with environmental exposures, and that the demographics would support the notion that it is not really known why people contract APL.  He was not aware of any particular risk factor, such as those within a family, which operate in relation to APL.  It was not known why the t15;17 translocations occur when they do or, to an extent, why they do.  Professor Spencer said that medical science did not know of environmental factors which promote a translocation and the commencement of the disease – see T 111.  The literature establishes that APL is highly distinctive compared to other forms of AML.  He also referred to the paucity of literature that specifically looks at risk factors for APL in terms of environmental exposure, saying that there were no properly, statistically powered and coherent publications which have addressed the question.  He did not regard Wong as advancing medical science in relation to the particular disease of APL.  There were problems with the patient sample which was analysed, particularly in relation to the average age.  For a study or paper to be sufficiently powered, enough people with the particular disease must be considered.  There would also have to be sufficient controls.  The figures in Wong did not demonstrate a “glaring association” in the sense of anything of biological significance – see T 115.

80      A study conducted in Italy concerning the use of benzene in glue used for the repair of shoes revealed “an association”, but the interpretation of that is uncertain.  However, Professor Spencer agreed with what had been stated by Dr Vaughan that benzene exposure could be said to have increased the risk of AML.  He did not agree with the further proposition that this included all the sub-types, including APL – see T 117. 

81      Professor Spencer was of the view that it was not scientifically valid to draw the conclusion that studies indicating an increase in risk of the contraction of AML by reason of exposure to benzene meant that there was an increase of suffering APL by reason of such exposure.  In relation to latency and dosage, Professor Spencer said that it was a very poorly understood area.

82      In cross-examination, Professor Spencer stated that the conclusion which he had reached was based on epidemiological data and his understanding of the disease itself.  He did not disagree with the proposition that the IARC might have stated that benzene was a Class 1 carcinogen – see T 120.  He did not take issue with the proposition that exposure to benzene above a certain level can result in an increased risk of AML, nor with the finding of Wong that there was little doubt in this regard.  It is correct to say that the point of distinction between his opinion and that of Dr Vaughan was that, because there was no paper that said specifically that benzene exposure can cause APL, Professor Spencer was of the opinion that it was not scientifically valid so to conclude.  He also referred to the characteristics of AML which arise from known carcinogenic exposure and the fact that they do not resemble APL.  In addition, he mentioned that APL occurs in a distinctive younger population of patients.  He again emphasised the rarity of APL.  He agreed that the association in a particular case would be based on evidence of exposure, dosage, length of exposure, latency and other factors relating to the disease itself.  Everything would be taken into account in a clinical assessment that may be a broader assessment than one simply based on various papers – see T 123.

83      In re-examination, Professor Spencer stated that he had not been shown any clinical assessment in the present case which would support a connection between APL and exposure to benzene.  Speaking anecdotally, he said that he had never seen an APL patient who had been in the petrochemical industry with a job that related to such exposure.  He emphasised that this was not a scientific finding, but was purely his own experience.  There are certain sub-types of AML where it is known that they have been driven by a previous exposure because they harbour certain genetic abnormalities which are not consistent with the APL genetic abnormality.  Professor Spencer agreed that the issue in the present case of whether there was an increased risk of developing APL from exposure to benzene could not be answered in the normal clinical way in which doctors try and see what has caused a disease. 

84      The other expert witness called by the defendant was Professor Richard Fox, who, as stated, had also provided reports.  Professor Fox has a PhD in Medicine and a Fellowship of the Royal Australian College of Physicians.  His special field of practice has been medical oncology and malignant haematology.  He has looked after patients with leukaemia in various forms and was director of the Department of Clinical Haematology/Medical Oncology at the Royal Melbourne Hospital from 1985 until 2006.  Over those years, he saw something in the order of 10 persons per year who suffered from AML, but APL was much rarer.

85      I will briefly summarise the numerous reports of Professor Fox.  His earliest report is of 2 November 2010.  It would appear that he had not seen the plaintiff prior to providing this report, but had access to various documents.  In addition, he carried out computer searches.  Professor Fox commented that various forms of AML develop after very heavy benzene exposure, but also referred to what is seen today in service stations, car refuelling and the like.  He stated that there was no evidence that APL with its specific chromosome changes is caused by benzene exposure in the modern workplace.  He stated that data did not show an increased risk for AML in relation to the modern petroleum industry, but Professor Fox’s ability to report further seems to have been inhibited by a lack of appropriate information.

86      Dr Fox reported again on 3 December 2011.  On this occasion he not only had materials that were available to him, but saw and examined the plaintiff.  Professor Fox observed that the benzene content of the petrol to which the plaintiff was exposed was the same as that used in regular commercial petrol in Australia.

87      Professor Fox also went into a certain amount of technical detail.  He was critical of the opinions reached by Dr Vaughan and Dr Hocking.  Professor Fox was also critical of Wong as the foundation for an opinion.  He referred to a number of papers which he considered to be of possible relevance, although I note that none of these were specifically concerned with APL, save for a paper by Mele and Colleagues which was a study of some 38 cases of shoemakers using benzene-related glues.  In that regard, the studies showed a link to AML.  However, Professor Fox commented that the concentration of benzene was believed to be very high.  He also referred to a paper by Douer which, in 2003, stated that as at that point of time no environmental and/or occupational risk factors had been found for APL. 

88      In any event, the conclusion of Professor Fox was that the plaintiff’s work was not related to the development of his APL.  He also observed that it was not possible to suggest a latency period that would be relevant.  He concluded by stating that APL usually occurs without any known precipitating factors.

89      Professor Fox reported again on 23 January 2012.  On this occasion he commented in considerable detail upon the reports of Dr Hocking and Mr Kottek.  Again, the discussion is highly technical.  Various papers, some of them now well in excess of 10 years old, are discussed.  Interestingly, Professor Fox commented that the IARC does not make any comment on APL.  Whether this observation is meant to include reference to the most recent IARC monograph is not clear, although the timing of events might suggest that the report of Professor Fox may have pre-dated the circulation of that monograph.

90      In relation to the report of Mr Kottek, Professor Fox, in essence, placed emphasis upon that part of Mr Kottek’s report which appeared to be reliant upon Wong.  He pointed out that APL is different from AML, even if Wong appears to add some support to the hypothesis that benzene plays a role in the aetiology of AML with its specific t8;21 translocations.

91      Another report from Professor Fox was tendered, this being undated, but apparently following receipt of a letter from the defendant’s solicitors of 20 March 2013.  This letter contains a commentary on the report of Dr Hocking of 3 November 2012, also referring to a report of Mr Kottek, although, as far as I can tell, that is the same report upon which Professor Fox earlier commented (indeed, only one report of Mr Kottek has been put in evidence and there was no suggestion that another existed).  Professor Fox referred to the observations of Dr Hocking concerning the plaintiff’s unusual work practices, but questioned how unusual they in fact were.  The report also contains further discussion concerning Wong.  Professor Fox was of the opinion that the results in Wong contradict the views of Dr Hocking, rather than supporting them.  There is then some discussion concerning the IARC monograph of 2012.  Professor Fox was of the view that the monograph in fact does not support the position of Dr Hocking.  He also disputed some of the criticisms made of his earlier reporting by Dr Hocking. 

92      Finally, Professor Fox provided another report to the defendant’s solicitors, this being dated 12 April 2013.  It deals with the difference between AML and APL, pointing out that APL is characterised by translocation between chromosomes 15 and 17.  He also referred to the fact that APL has a higher female/male ratio than AML, and the patients are younger.  He referred to the higher incidence of AML amongst smokers, but these chromosomal changes were those of t8;21 translocation and not t15;17.

93      The oral evidence of Professor Fox could be summarised as follows.  Professor Fox again referred to factors which distinguish APL from AML are that the mean age of occurrence is somewhat younger, that there is somewhat more predominance of females, and that it is more common in people of Latin origin.  However, the cytological appearance of the cell is quite different.  The distinctive translocation of chromosomes 15 and 17 was again noted.  In relation to the evidence of Dr Vaughan and Dr Hocking concerning studies which show that there is an increased risk of contracting AML by exposure to benzene products, and this being useful in making a judgment as to whether benzene exposure might promote the contraction of APL, Professor Fox stated that that might be correct in theory, but that there was nothing to say that APL was included in that group of people which had the increased risk of development of leukaemia.  In fact, he said some studies, such as those in relation to cigarette smoking, would seem to demonstrate the opposite.  He repeated what he had stated in one of his reports, namely that Wong could show no relationship of the development of leukaemia or APL to petrol exposure.  He agreed that studies published 20 or 30 years ago did not make the distinction between the umbrella of AML and its various sub-groups.  In addition, more recent studies had been concentrating more on certain cancer chemotherapies which could cause a secondary leukaemia.  However, there were no epidemiological large scale reports of which Professor Fox was aware that promoted the idea that benzene or petrol may be a cause of APL – see T 176 and 177.

94      In relation to latency, Professor Fox stated that in science the latency period was measured from a starting pointing when someone was working with a product, how long they were working with it and with what sort of exposure, to the end point of the disease in question being diagnosed.  I might say that it seems to me that, by including reference to duration and the sort of exposure, Professor Fox may have been moving from the position of first exposure marking the commencement of the latency period (save in situations where only minimal exposure is required – for example, asbestos and mesothelioma) to a position possibly akin to that of Dr Vaughan.  However, he did seem then to qualify this by stating that the starting point in a situation such as the present would be the first exposure to the petrol in question.  However, he also seems to me to have then placed provisos on that relatively simple proposition, referring to the heaviness of exposure – see T 179.  In answer to a question as to whether there was a relationship between benzene exposure and APL, he was again critical of Dr Vaughan for expressing the view that the studies have shown that there can be such a relationship.

95      Professor Fox also stated that, based on Wong, there is a suggestion that, if persons have had a relatively more recent exposure to benzene, there is an increased risk of APL.  He emphasised that this was exposure to benzene and not to petroleum, and that if people had had a longer latency period (essentially in excess of 10 years), they did not have an increased of development of APL. 

96      Professor Fox was also taken in some detail to the recent monograph of the IARC.  He was taken to passages which he stated did not support the thesis put forward that exposure to benzene can cause APL.  He agreed that the monograph stated that benzene can cause AML and also suggested a link with other forms of leukaemia.  However, Professor Fox stated that there was a lot of other evidence that goes against that statement, which is a generic one which does not include the issues of the sub-types of acute leukaemia.

97      In cross-examination, Professor Fox agreed that the monograph was an important document which states unequivocally that benzene is a carcinogen.  That had been stated not only in the most recent monograph but in an earlier one.  His explanation for not including reference to it in his original reports was that “Probably that I just missed it” – see T 193.  He also stated that he was not quite sure what difference it would have made had he referred to it in those early reports.  His attention was taken to two earlier IARC monographs of 1982 and 1987 which referred to the carcinogenicity of benzene and that it was classified as a Class 1 carcinogen.  He was also taken to the passage in the 2012 monograph in which it was said that benzene causes AML, he agreeing that APL was a sub-type of AML.  He also agreed that a Class 1 carcinogen was the highest evaluation of carcinogenicity which the IARC reaches when doing a monograph – see T 196.  Ultimately, and after some persistence by Mr Blanden, Professor Fox agreed that the reason why the IARC concluded that benzene was carcinogenic was because of a genotoxic effect from exposure to it, this meaning an alteration of the normal genotoxic state in order to have a mechanism for the causation of the disease.  He further agreed, when pressed, that the IARC effectively found that benzene was carcinogenic because it had in some way a genotoxic effect on the body.  He agreed that the numerous papers referred to in the monograph had their limitations.  He would not agree that the best large scale analysis done in relation to benzene and its carcinogenic effect was the IARC monograph.  Basically he agreed with a statement from the monograph that the chromosome aberrations and gene mutations detected in therapy-related and de novo AML are identical, this meaning that therapy-related and de novo AML are considered identical diseases – see T 198.  He agreed that the monograph did not seek to distinguish the carcinogenity of benzene in relation to AML generally as compared to its sub-types – see T 200.

98      It was put to Professor Fox that, in essence, the precise nature of exposure is a relevant issue in determining whether such exposure is likely to have given rise to an effect and that he had not obtained this.  Ultimately, again when pressed, he agreed that he had no specific information distinguishing between motor racing mechanics and regular car mechanics.  He assumed that the plaintiff’s work would be similar in ways to other car mechanics “under certain circumstances”.  He agreed that benzene could act either subcutaneously, via skin contact, or via inhalation of fumes.  He accepted that the plaintiff had heavy exposure to petrol containing benzene, distinguishing that from benzene itself.  He accepted that benzene was carcinogenic and that it leads to the production of certain types of leukaemia.  He agreed that benzene was described by the IARC as influencing the commencement of non-specified AML leukaemia, being the broad category under which the leukaemia of the plaintiff fits – see T 206.  However, he would not accept that exposure to benzene may have had an effect on the production of the plaintiff’s AML (or APL) condition because that it is hard to find evidence of leukaemia after petrol exposure as opposed to benzene exposure. 

99      Professor Fox stated that no one knows exactly why, in APL, the t15;17 chromosomal translocation takes place.  He agreed that the IARC could have excluded APL from its conclusion that benzene causes AML, but that it did not, adding “I don’t know what you could make about that” – see T 209.

100     In re-examination, Professor Fox stated that the relevant tables shown in the monograph demonstrating genetic pathways clearly, without saying it, exclude APL.  He also stated that a reading of the transcript of the evidence given by the plaintiff in the earlier case did not cause him to qualify the conclusions to which he had come.  He also stated that the distinction between benzene and petrol was important because of the concentration level factor.

Other expert evidence

101     Other material from experts placed in evidence was that of Mr Kottek and of Dr Michelle Bryson.  That of Dr Bryson, a haematologist at the Gold Coast Hospital and a treater of the plaintiff, deals with the fact that the plaintiff’s APL had relapsed and refers to the treatment in that regard.  It also deals with capacity.  In other words, the report of Dr Bryson focuses upon issues not in contention. 

102     I have previously referred on a number of occasions to Mr Kottek.  In this hearing not a great deal was said concerning his evidence, most aspects of which did not appear to be contentious.  A small number did provoke some argument.  Mr Kottek, who is an occupational and environmental health consultant, reported to the plaintiff’s solicitors on 16 January 2012.  In that report he referred to the fact that benzene had been recognised as a Category 1 carcinogen and that this classification applied to mixtures containing above 0.1 per cent of benzene.  He was of the view that it was reasonable to assume that the plaintiff frequently handled fuels containing around four per cent benzene.  He also stated that for a worker in the plaintiff’s circumstances, inhalation and skin absorption are the relevant modes of uptake of benzene.  He stated that there are a number of studies indicating that workers, including mechanics, handling petrol can experience elevated exposure to benzene.  He expressed the opinion that the plaintiff could have experienced significant exposure to benzene vapour.  In addition, Mr Kottek mentioned Wong and the “somewhat confusing result” obtained.  Mr Kottek had access to material provided by Dr Hocking, and stated that Dr Hocking’s reliance on APL being a sub-type of AML seemed reasonable.

103     Mr Kottek gave evidence and was cross-examined in the hearing before His Honour Judge Wischusen and, as stated earlier, portions of the transcript of that hearing were placed in evidence before me.  These included the evidence of Mr Kottek. 

104     In evidence-in-chief, material was put to Mr Kottek suggesting that the precise percentage of benzene for Shell Optimax fuel in 2002 and 2003 was 3.3 per cent, a proposition which he thought was quite plausible.  Whether the percentage was 3.3 or 4 did not alter his conclusion.  He reiterated his opinion in relation to both inhalation and skin exposure to benzene.  He stated that there was some discussion in the literature that cuts and abrasions will lead to increased uptake through the skin, it having been put to him that the plaintiff gave evidence that at times he cut himself and had abrasions to his hands and forearms whilst working inside petrol tanks.

105     A detailed description of the duties engaged by the plaintiff when employed by the defendant was put to Mr Kottek.  On the basis of it, he thought that the level of airborne benzene to which the plaintiff would have been exposed would have exceeded the Australian Standard, at least in part.  He concluded that the type of exposure to which the plaintiff was subject would have led to an increased risk of disease. 

106     In cross-examination, Mr Kottek agreed that APL was a sub-type of AML, but was distinct, and agreed that he was not a haematologist and did not profess any particular expertise in the science of leukaemias.  Much of the early cross-examination of Mr Kottek centred upon distinguishing features of APL, an area in which he had no specialised knowledge.   He was also taken to various studies, including Wong.  In relation to his agreeing with Dr Hocking concerning APL being a sub-type of AML, and the conclusions reached by him seeming to be reasonable, Mr Kottek said that there would be a need for caution.  He also confirmed that the older studies generally dealt simply with AML and had not considered the different sub-types.  In relation to Wong, essentially he agreed that it did not tell one a great deal. 

107     In cross-examination, there was also reference (by counsel not involved in the present case) to a study called Hotz, but that study was not put in evidence before me and I do not think the references to it in the transcript take matters further or need to be considered.

108     In re-examination, Mr Kottek was asked whether, if a mechanic had greater than usual exposure to petrol containing benzene, either by way of inhalation or skin absorption, that would increase the degree of risk, he thought that that was an assumption that one would make, although also referring to epidemiological studies.  Unfortunately, part of his answer is shown as being “indistinct”. 

109     As stated, whilst the evidence of Mr Kottek by way of his report and his earlier testimony was before me, it was not something that received a great deal of attention in the conduct of his case. 

110     I have spent a substantial amount of time summarising what seem to me to be the more important aspects of the evidence of the experts because counsels’ closing addresses, in turn summarising their respective cases, were to a very considerable extent based upon the evidence of those experts.  Hopefully, the above discussion will enable the following summary of counsels’ submissions to be briefer than would otherwise have been the case and to be more intelligible. 

The cases put by the parties – final addresses

(a)      The case on behalf of the defendant

111     The submissions on behalf of the defendant could be summarised as follows. 

112     Pursuant to s86(1A), the plaintiff must establish that the nature of the employment gave rise to a significantly greater risk of the worker contracting the disease.  The word “significant” means more than de minimis and has been interpreted as meaning “of considerable amount or effect”.  Reference is made to the decision of Popovski v Ericsson Australia Pty Ltd [1998] VSC 61.

113     However, in the present case, this distinction  between “risk” and “significantly greater risk” may not make any real difference.  Professor Fox and Professor Spencer simply do not accept that there was any connection between exposure to benzene and the disease suffered by the plaintiff.  The plaintiff’s experts say that there is such a connection and, in an elliptical way, that connection exists in the present case. 

114     Mr Casey then dealt with the characteristics of APL, much of which has been set out above.  The views of Professor Spencer in particular were advanced by Mr Casey, he referring to that witness as being very highly qualified and giving his evidence in a dispassionate way, which was to be highly commended.  His experience should be noted.  APL has the distinctive t15;17 translocation of chromosomes and is treated differently from other forms of leukaemia.  Professor Spencer’s opinion was clear that the plaintiff’s condition was not due to the nature of his employment, including potential exposure to benzene.  Professor Spencer stated that it was not known to medical science why the translocations occur when they do.  He also stated that it is not known to medical science that there are any environmental factors which promote the translocation.

115     The argument advanced by Dr Vaughan and Dr Hocking that, if there is a connection between exposure to benzene and the umbrella disease of AML that is sufficient to satisfy the court, requires a giant leap of faith.  It would be treating the wide range of leukaemic cancer diseases as having the same susceptibility to environmental influences.  As stated by Professor Spencer, medical science has not advanced far enough to say what is the cause of this particular type of cancer.  If that is accepted, then the plaintiff’s case should fail.

116     It is emphasised that APL is a stand-alone disease with stand-alone features requiring its own stand-alone treatment.  It is not possible to say that this applies to other diseases which fall under the heading of AML. 

117     Dr Hocking’s evidence does not assist.  His only knowledge is recently acquired by means of looking things up on the internet and finding certain articles.  Further, whilst he emphasised the importance of obtaining a thorough history, in fact the history that he obtained was in part based upon incorrect facts.  He took an occupational history of 10 years’ exposure to petrol from working with V8 racing cars up to the time of diagnosis in 2010.  He did not take a thorough, reliable, detailed history. 

118     Dr Vaughan was at first promoting Wong as being relevant.  However, in cross-examination he started to go into reverse and become critical of Wong, saying that it was underpowered and did not really prove an increased risk by reason of exposure to petroleum products.  Professor Spencer and Professor Fox were critical of Wong, as was Dr Hocking.  The defendant submits that Wong adds no information, or brings no assistance, to the case. 

119     In relation to the logic of the plaintiff’s argument, it was put to Dr Vaughan that, if exposure to benzene affects all sub-groups of AML, is it not unusual that chromosomic changes are not found in other areas?  Why, in this particular case, is it restricted to t15;17?  The reasoning of Dr Vaughan seems to be that because this particular disease is one of the diseases which falls under the general heading of AML, benzene increases the risk of contracting that particular disease simply because it is such a sub-type.  Dr Vaughan’s logic is effectively that, when people or studies refer to substances that increase the risk of AML, after that can be added in brackets (and all its sub-types).  This should not be accepted, bearing in mind what Professors Spencer and Fox have said.

120     In relation to the IARC monograph, what Dr Hocking said in relation to the reference to t15;17 was never put to either Dr Vaughan or Professor Spencer.  However, we do have Professor Fox’s view that the passages in question are referring to specific findings made following treatment such as chemotherapy.  The 2012 monograph virtually ignores APL.  It is submitted that Dr Hocking, who thinks it is very important, has misinterpreted the passages in the monograph. 

121     Dr Hocking conceded that, under the heading “Evaluation” in the monograph, there is no reference to APL.  However, he says that the Evaluation must be read as referring to AML and all of its sub-types.  Professor Fox says that it is not to be read in that way.  Further, the reference to t15;17 is in the context of secondary leukaemia after anti-cancer drug therapy. 

122     In summary, Professor Fox gave evidence that the thesis that was being put forward that exposure to benzene can cause APL was not supported by the relevant passages in the monograph.  The Evaluation tells us that benzene can cause AML and suggests a link with other forms of leukaemia, but it was Professor Fox’s view that there is a lot of other evidence that goes against that, and what is said is a generic statement which does not address the issues of the sub-types. 

123     The evidence and interpretation of Professor Fox, who is an expert, should be preferred to a misinterpretation by a non-expert.

124     In relation to the latency period, in the scientific and epidemiological world the commencing date is that of the first known exposure and the concluding date is that of diagnosis.  If that be so, the latency period in the present case is 24 years and not 10 years.  As previously stated, the normal latency period for APL is considerably shorter than 24 years.

125     In summary, the evidence of Professors Spencer and Fox should be accepted, and that of Drs Hocking and Vaughan rejected.

(b)      The case on behalf of the plaintiff

126     The submissions on behalf of the plaintiff could be summarised as follows.

127     The plaintiff essentially agrees with what has been said about the word “significantly” and also refers to the observations of Ashley J in Popovski.  Essentially what is said is that the plaintiff will need to show something more than de minimis, but after that it depends upon the facts of the situation as found.  

128     Reference is made to the decision of His Honour Judge Wischusen in Spina v Galaxy Paints [2008] VCC 1173. In particular, reference is made to the various authorities cited at paragraphs 73 and following of that decision. Reliance is placed upon the decision of Accident Compensation Commission v Botezatu [1993] 1 VR 304 and what was stated by Marks J at 305. Marks J referred to a consideration of the employment and the risk to which the worker was exposed by its nature, “…that is in virtue of its tendencies, incidents or characteristics” – that quote being extracted from the Judgment of Dixon CJ in Commonwealth v Bourne (1961) 104 CLR 32. It was also made clear in Botezatu that the particular circumstances of the particular worker may be examined – that is, the conclusion may be based on a finding of correspondence between the environment in which the worker actually worked and the environment attributed by the witnesses to the particular industry in which the relevant risk was said to exist.  As was stated by His Honour Judge Wischusen, as shown by Botezatu, it is the environment in which the risk exists, rather than the classification of the people in that environment, that is to be examined. 

129     The evidence relied on by the defendant in the present case relates more to actual causation of APL as a result of exposure to benzene.  However, as established by case law, the plaintiff does not have to prove actual causation.  He has to prove that there is an increased risk associated with the exposure that he was subject to in the course of his employment.  The evidence in this case establishes that increased risk.

130     The plaintiff relies upon the evidence of Dr Vaughan.  The starting point is that benzene is a Class 1 carcinogen.  It is said to be so by the IARC, it having reviewed a multitude of papers on the topic, and all medical experts in the present case agreed in relation to this.  It seems beyond contention that benzene causes leukaemia and particular AML.  The uncontradicted evidence is that the plaintiff has been exposed to benzene in a moderate to heavy fashion.  Professor Fox said that the washing of engine parts in a fluid containing benzene was of itself heavy exposure.  The conclusion is that the plaintiff’s exposure to benzene was in the range of moderate to heavy over the couple of years of his employment with this defendant.  If the argument stopped at that point, and it was assumed that the plaintiff had AML as opposed to APL, it would be very easy to reach the conclusion that he was exposed to an increased risk over the period of his employment.  The contrary would effectively be unarguable.

131     In the present case, there is no dispute but that the plaintiff’s condition is APL.  It is agreed by all the experts that APL is a sub-type of AML.  It is agreed by everyone that it is particularly identified by the genetic marker t15;17, a translocation of chromosomes.  Dr Vaughan referred to the fact that the World Health Organisation had given to the IARC the task of researching the relevant literature on occupational carcinogens and coming to a consensus view about the role of various substances, such as benzene, in the causation of disease by reviewing all of that relevant literature.  He described what the monograph said and how it related to the plaintiff’s diagnosis, and he certainly placed reliance on the fact that APL was by definition a sub-type of AML. 

132     As set out in the monograph, benzene can cause cancer by multiple mechanisms.  The specific genetic abnormality can indicate a diagnosis of APL, a specific treatment and a mechanism, but not necessarily the cause.  Dr Vaughan also stated that the description of exposure given to Dr Hocking was the sort of exposure that might lead to the type of complication from which the plaintiff has suffered.  Smoking may also have contributed.  Dr  Vaughan’s final view was that benzene exposure has a causal role in the development of AML and all its sub-types, including APL.

133     The various studies have been criticised by the experts.  That is why the IARC monograph has particular importance, because, as stated by Dr Vaughan, it is the latest, biggest and best compilation and assessment of all those papers.  It is an overall assessment and has particular relevance and importance in the present case.

134     Dr Vaughan gave evidence in relation to the argument that APL is different from AML, although it is clearly defined as a sub-type.  He gave evidence that Wong demonstrated that APL probably increased in the context of benzene exposure and this negated the possibility that APL is in some way different from AML in general terms.  In making that statement, Dr Vaughan said that he was relying upon all the literature, and also saying that the particular argument that somehow APL is not AML is not supported by the best available epidemiology.  He emphasised the distinction between a mechanism and a cause, using smoking and lung cancer as an example.  In terms of causation, APL is not different.  The mechanism may be. 

135     Reference is made to the IARC monograph.  The monograph is the primary document, even though Professor Fox did not refer to it in any of his reports.  In his oral evidence, Professor Fox tried to confine the reference to t15;17 in the monograph to situations where people had received treatment such as chemotherapy.  However, in the monograph it is also stated that therapy-related and de novo AML are considered identical diseases.

136     Professor Spencer and Professor Fox have really directed their arguments to ultimate or legal causation.  That is not what the plaintiff is arguing.  The plaintiff is arguing that his exposure to benzene increased his risk of contracting APL.  That is the effect of Dr Vaughan’s evidence.  In APL, genotoxic changes occur, and that is exactly what the monograph says happens in the development of APL.  The plaintiff in the present case was placed at an increased risk of contracting APL. 

137     In relation to latency, that also is an issue involved in causation as opposed to increased risk.  In any event, latency should not be taken as commencing literally from the first date of exposure if the rate of exposure over the period is altered.  In the present case, the evidence establishes that the plaintiff’s exposure before the relevant time, or at least until approximately a year before the relevant time, was light.  That is consistent with the plaintiff’s evidence and the history obtained by Dr Hocking.  It was not until the employment with the defendant commenced that the exposure became moderate to heavy.  The latency period should be weighted accordingly.  It would then fit approximately with the 10 year latency period which has been discussed.

Ruling

138     I would like to make two general observations at the outset.  Firstly, no argument was advanced along the lines that s86(1A), which was introduced by Act Number 80 of 2010 and which seems to have had a commencement date of 20 October of that year, did not apply because the employment in question clearly pre-dated it.  I was told at the outset that s86(1A) did apply – see T 4, 5 and 9.  Closing addresses proceeded on the basis that it did, and this was again specifically stated – see, for example, T 216 and T 241.  Accordingly, in the circumstances I am not required to deal with any arguments concerning retrospectivity.

139     Secondly, the expert evidence, and particularly that of Dr Vaughan and Professor Spencer, was impressive.  When there are very well-presented cases involving competing views from well-qualified experts, it might be thought that it is difficult or impossible to chose between them.  Of course, if that were the situation, and no choice could be made between them, the plaintiff would fail to discharge the burden of proof which he carries.  However, that is not the situation here.

140     In my opinion, the plaintiff has discharged the burden of proof.  I am satisfied that the disease suffered by him (APL) is due to the nature of the employment in which he was engaged and that the nature of that employment gave rise to a significantly greater risk of him contracting the disease than had he not been employed in employment of that nature.  I have come to that conclusion for the following reasons, which are not listed in order of importance or significance.

(a)I am satisfied that the plaintiff did have moderate to heavy exposure to benzene during the course of his employment with the defendant.  I accept his evidence in that regard, along with the evidence of Mr Kottek and of Dr Hocking.  I accept that the fuel to which he was exposed contained the level of benzene described by witnesses such as Mr Kottek and that the plaintiff’s exposure to it was both by way of inhalation, sometimes in very cramped quarters such as a car boot, and subcutaneously as a result of using the fuel as a cleaning product, suffering minor cuts and abrasions whilst so doing.  There is no argument but that benzene has been classified as a Class 1 carcinogen.

(b)The employment in which the plaintiff was so exposed was that of a motor racing mechanic.  With the defendant, he was specifically so employed.  Whilst earlier in his career he at times performed work as what could be described as a general mechanic dealing with ordinary vehicles, at times mixing this with working with racing cars, there is no doubt but that his employment with the defendant was specifically that of a motor racing mechanic, and indeed a lead mechanic.  This directly involved him with the exposure to which I have referred.

(c)There is also no doubt but that the form of leukaemia from which the plaintiff suffers is APL.  There is equally no dispute but that APL is a sub-type of AML, or that APL is a disease within the meaning of the Act.

(d)I am also satisfied that I can look not only at the nature of employment as a motor racing mechanic generally, but also at the particular tasks performed by the plaintiff and the environment in which he actually worked – see the observations of Marks J in Botezatu, to which there has been earlier reference.  In any event, there is little in the evidence to suggest that the exposure to which the plaintiff was subjected differed from that to which motor racing mechanics generally might experience.  It might be that, as lead mechanic, he worked longer hours or was more frequently in confined spaces and the like.  In any event, I am taking into account both the environment in which the plaintiff actually worked and the nature of the employment in which he was engaged in a more general sense.

(e)The issue then becomes whether the nature of the plaintiff’s employment as a motor racing mechanic, involving as it did the exposure to benzene which has been described, gave rise to a significantly greater risk of him contracting the disease of APL than if he had not been employed as a motor racing mechanic.  On balance, I am of the opinion that he has established this.  I find as a matter of fact that the nature of the employment gave rise to a significantly greater risk of the plaintiff suffering the disease of APL.

(f)I am particularly persuaded in this regard by the evidence of Dr Vaughan generally and specifically in relation to the approach to be adopted.  That approach is not to engage in a word by word, line by line analysis of the many papers and studies done over the years, but to take an overall view of the literature.  The best vehicle for doing this is the most recent IARC monograph.

(g)It is to be remembered that the full name of the IARC is the International Agency for Research on Cancer, and that it operates under the umbrella of the World Health Organisation.  In his report of 25 March 2013, Dr Vaughan described the IARC as an internationally recognised agency that regularly collates and reviews all the relevant medical and scientific literature so as to make decisions about whether a particular substance causes a particular cancer.  In that same report, Dr Vaughan emphasised that, as evidenced by the IARC process, a review of all papers and balancing of the various conclusions is required in order to come to a definitive conclusion about the role of benzene or any other carcinogenic cause of disease.  Dr Hocking had a similar approach in relation to the importance of the IARC monographs, and particularly the most recent one.  I accept this.  I see no reason why the 2012 IARC monograph, based on an overview of the available papers, studies and information, should not be accepted as being an authoritative publication presenting important and persuasive conclusions and observations.  I can well understand why both Dr Vaughan and Dr Hocking have such regard for it.

(h)The 2012 IARC monograph is a very technical and complicated document.  However, there are some matters which can be elicited from it.  These include the following:

(i)Benzene is carcinogenic to humans (Class 1).

(ii)Benzene causes AML.

(iii)In multiple studies in different occupational populations in many countries over more than three decades, a variety of genotoxic changes, including chromosomal abnormalities, has been found in the lymphocytes of workers exposed to benzene.

That APL is a sub-type of AML and involves genotoxic changes, including chromosomal abnormalities, seems to be beyond dispute.

(i)        Accordingly, the above conclusions contained in the Evaluatioin of the IARC point strongly to a link between benzene, AML and diseases involving genotoxic changes, including chromosomal abnormalities.  A positive association has been observed between exposure to benzene and AML.  As pointed out in evidence, in the Evaluation there is no mention of sub-types of AML, including APL, being excluded from the conclusions which have been reached.  There is no suggestion that the genotoxic changes, including chromosomal abnormalities, which have been found in the lymphocytes of workers exposed to benzene, do not include the changes or chromosomal abnormalities which relate to APL.  I accept the argument essentially advanced by the plaintiff’s experts that one would have expected the IARC to have referred to exclusions in its Evaluation if such exclusions in fact existed.  The broad statement is that benzene causes AML.  In the following paragraphs there is nothing to suggest that a sub-type of AML, such as APL, should be excluded from that conclusion.  Indeed, the following paragraphs, with their references to genotoxic changes and chromosomal abnormalities, could be interpreted as suggesting the opposite.

(j)        There is no argument but that the chromosomal translocation t15;17 is the hallmark or signature of APL.  If there exists any doubt as to the conclusions reached in the Evaluation paragraphs of the monograph, it seems to me that such doubt (which I consider to be negligible) is removed by what is said earlier in the monograph.  Omitting some technical references, which do not seem to me to advance or clarify the situation, what is said at p282 of the IARC monograph is as follows:

“These findings demonstrate that benzene … can … probably cause leukaemias with chromosome translocations and inversions … including … t15;17.”

In other words, the IARC seems to me to have reached a conclusion based upon various findings that benzene can probably cause leukaemias, including APL, identified by its signature chromosome translocation.

(k)I am not persuaded by the argument of Professor Fox concerning an earlier reference in the monograph to translocations arising from therapy-related cases.  That seems to me to take matters no further.  On the same page of the IARC monograph, and indeed in the same column, it is said that recent research has shown that chromosome aberrations and gene mutations detected in therapy-related cases and AML are identical, although the frequencies at which they are observed in different sub-types may differ.  A conclusion is that therapy-related and de novo AML are considered identical diseases.  Given that APL is a type of AML, the argument that the t15;17 chromosomal translocations are, according to the IARC, found in therapy-related cases loses much of its impetus.  It seems to me to take nothing away from the conclusion reached by the IARC that benzene can probably cause leukaemias including those where the hallmark or signature is t15;17 – that is, APL.

(l)I might say that I am persuaded generally by the arguments of Dr Vaughan and Dr Hocking concerning benzene and its link with APL.  The IARC monograph, the importance and significance of which I have stressed, seems to me to underline, or provide the foundation for, the correctness of their conclusions.  I accept the conclusion of the IARC that there is sufficient evidence that benzene causes AML and that it probably causes leukaemias with chromosome translocations such as that found in APL.

(m)That being so, there appears to me to be ample foundation for my finding of fact that the nature of the plaintiff’s employment gave rise to a significantly greater risk of him contracting the disease from which he suffers had he not been employed in employment of that nature.  As earlier stated, the case was essentially argued on the basis of whether or not any link existed, and, as stated by Mr Casey, the importance of the word “significantly” effectively receded or disappeared.  Even leaving that to one side, it seems to me that if, as I find, in accordance with the IARC monograph, benzene is a probable cause of APL, the risk of contracting it was significantly greater for the plaintiff than had he not been employed in employment of that nature.  The facts that it is a very rare disease and that he worked in a comparatively unusual occupation probably underline this.  There is no argument but that very, very few people contract this disease.  I have found that the plaintiff, who worked in an unusual occupation, had moderate to heavy exposure to benzene.  I have also found that benzene is a probable cause of that rare disease.  It seems to me that this leads inevitably to the conclusion that his employment gave rise to a significantly greater risk of contracting that disease than had he been employed in employment of a different nature.  There was a significantly greater risk than had he been employed as, for example, a hairdresser, a barman or, essentially, in any employment where his exposure to benzene was not what it was as a motor racing mechanic.

(n)As stated, it was not argued that s86(1A) did not apply.  It was essentially agreed that it did.  I am not totally convinced of that.  There seems to me to be an argument that, given that it did not commence operation until 20 October 2010 and that there is nothing in the amending Act which impacts upon the possible retrospective operation of s49 (which introduced s86(1A)), s86(1A) does not apply to employment engaged in by workers prior to the commencement date.  If it does not, and therefore would not apply in relation to the present case, the burden upon the plaintiff would not have been as great.  That seems apparent, and there was reference during the conduct of the case as to how s86(1A) had “tightened up” the disease provisions.  It seems to me patent that, if s86(1A) of the Act has no application, the discharge of the burden of proof by the plaintiff is even more obvious.  The requirements in relation to “a significantly greater risk” would be removed.  However, as pointed out by Mr Casey, given the manner in which this case was contested, the concept of significantly greater risk probably made no real difference – see T 217.

Conclusion

141     The plaintiff is successful.  He has discharged the burden of proof.  I shall hear the parties as to any ancillary orders that are required.