Plaintiff v Defendant

3 Over time, the plaintiff developed asthma and a psychological reaction to that condition. He ceased work in 2006 and has not worked since. He issued proceedings initially in the County Court in March 2008. These proceedings were alleging that he suffered personal injury arising from the negligence of the employer. These proceedings were transferred to the Supreme Court in 2009 and have become No 9226 of 2009. I shall refer to these proceedings as "the asthma case".

4 In early 2008, the plaintiff was diagnosed as suffering from a single plasmacytoma. Plasmacytoma is a plasma cell malignancy. The mass was located adjacent to the plaintiff's only kidney (the left one). Treatment has been complicated by this locus and so far the plaintiff has refused surgery. Radiotherapy has been thought to be inappropriate because of the proximity of the tumour mass to the kidney.

5 By August 2009 the plaintiff's cancer had developed to multiple myeloma, as a consequence of the dissemination of plasmacytomas.

6 In No 9113 of 2009 ("the cancer case") the plaintiff initiated another proceeding alleging that the exposure to the previously mentioned solvents throughout the course of his employment with the defendant caused the plaintiff's plasmacytoma and now multiple myeloma.

7 Both cases, therefore, allege an identical exposure in the context of the plaintiff performing his normal duties at work. In the asthma case the defendant admits negligence[1], admits causation (insofar as occupational asthma and psychiatric reaction are concerned) and makes submissions on the assessment of damages. In the cancer case the defendant effectively admits the faults that gave rise to the 'asthma case' negligence but says

(a) that plasmacytoma was not a foreseeable risk in the circumstances[2] and

(b) that the plaintiff has failed to prove that the exposure was a cause of his plasmacytoma/multiple myeloma.[3]

As the case for the plaintiff developed, it became clear that it was the exposure to the solvent, benzene, that the plaintiff relied upon in order to establish a causal link to his cancer. It also became clear that this causation issue was the predominant issue in the case.

8 The plaintiff was given leave by an Associate Justice of this Court to bring the cancer case as permitted by s 135BA of the Accident Compensation Act 1985 (Vic). The question of whether the plaintiff had suffered a serious injury within the meaning of s 134AB(38) was left to be determined at trial. The plaintiff's plasmacytoma/multiple myeloma is obviously a serious injury within that meaning and the defendant did not contend otherwise. Insofar as it is necessary, I find that his cancer case injuries are serious from both a pain and suffering and a pecuniary loss perspective. With the consent of the parties I considered it appropriate to determine the issue of the relationship between the plaintiff's work and the illness within the context of the trial proceedings, rather than in the context of s 134AB(38) proceedings.

9 The plaintiff was employed by Palmone Shoes Pty Ltd on 6 November 2002. Up until that time he had been in reasonable health. He had lost a kidney in 1995, apparently as a result of kidney stones. Although he had smoked moderately in the past, he had no prior symptoms of asthma or shortness of breath. He was born in Syria and qualified as a mechanical engineer in that country but had been unable to pursue that vocation in Australia.

10 He had worked at other shoe factories before working for the defendant. The plaintiff gave evidence (which I accept) that the had never been involved in operations in those previous jobs that exposed him in any meaningful way to glue fumes. At Palmone his duties were as follows:

• He would remove a batch of leather uppers from an oven. There would usually be 10 pairs in a batch.[4]

• Sometimes he would have to beat out wrinkles in the hot leather upper with a hammer[5]

• He would then roughen the bottom of the upper to prepare it for gluing.[6] This process would take 10 to 15 minutes.[7] Leather and dust particles floated around.

• He would then commence the gluing process by applying the appropriate glue to the upper. In the case of an upper to receive a rubber sole, he would apply PA5000 over the entire bottom area of the upper.[8] In the case of an upper to receive a leather sole he would apply black neoprene adhesive to the upper.

• He would then hold the upper upside down and at about collarbone/shoulder level about 20-30 centimetres from his mouth and nose.[9]

• The PA5000 was applied with a brush. The black neoprene was applied with a gun.

• Twenty uppers were treated this way in succession.

• The soles would then have glue applied - PA5000 for rubber soles applied by brush; black neoprene for leather soles applied by gun.[10]

• Before the rubber soles were glued, they were washed with Halo Primer.[11] This was applied with a brush.

• When glue was applied to the soles, the plaintiff held them in the same position as he held the uppers when applying glue to them.

• Rubber soles and leather soles each constituted about 50% of the batches.[12]

• The uppers were then attached to the soles, heated and pressed.[13]

• The process was then repeated over an eight hour day.

• He performed these duties from November 2002 to February 2006.

It is unnecessary to go into any further detail about the gluing processes[14] for present purposes. I accept that for approximately 30 to 40 minutes of every hour over an 8 hour working day, the plaintiff was involved in the gluing process with either the uppers or soles in his 'breathing space' between 20 to 30 cm from his mouth and nose.[15]

11 I accept the plaintiff's evidence that despite repeated requests, he was not supplied with any breathing safety apparatus by the Palmones who were apparently hostile to his complaints about the level of glue fumes.

12 The plaintiff alleges that the defendant, as the plaintiff's employer, owed a common law duty to ensure the safety of the plaintiff by providing a safe plant and equipment, a safe workplace and a safe system of work. In breach of that duty the plaintiff alleges in substance that the defendant:

(a) Exposed the plaintiff to hazardous substances including solvents containing benzene.

(b) Failed to reduce or eliminate that exposure, in particular by failing to provide adequate ventilation, an extraction system or protective masks.

(c) Failed to train the plaintiff or act on his repeated complaints.

(d) Required the plaintiff to perform his work where he was exposed to levels of benzene for periods of time well in excess of the 2003 Safe Work Australia national standard.[16]

(e) Breached the Occupational Health and Safety (Hazardous Substances) Regulations 1999.[17]

13 The plaintiff's evidence as to his working conditions was uncontradicted and it is a simple exercise to find that the defendant breached the relevant statutory duties and common law duties.[18]

14 As I perceive it, the issues in this case are not whether the defendant breached these duties but

(a) whether the consequence of the development of plasma cytoma/multiple myeloma was a foreseeable consequence of the actual level of exposure to benzene that the plaintiff encountered; and

(b) whether the actual exposure to benzene caused or materially contributed to the plasmacytoma/multiple myeloma.

15 Before reviewing the evidence, I propose to analyse briefly the relevant authorities. As I have said, the plaintiff's position is that the exposure to benzene at his work with the defendant was a cause of the development of plasmacytoma/multiple myeloma and the evidence is sufficient to satisfy the court of that proposition on the balance of probabilities.

16 In recent years, Australian courts have considered how causation principles apply to circumstances where it is alleged that an exposure to a particular substance increases the risk of a person suffering a particular injury, illness or disease and the person subsequently contracts that disease. In Bennett v Ministry of Community Welfare [1992] HCA 27; (1992) 176 CLR 408 at 420-421 Gaudron J said

...generally speaking, if an injury occurs within an area of foreseeable risk, then, in the absence of evidence that the breach had no effect, or that the injury would have occurred even if the duty had been performed, it will be taken that the breach of the common law duty caused or materially contributed to the injury. (citations omitted)

17 In Naxakis v Western General Hospital (1999) 197 CLR at 278-279 Gaudron J returned to the issue

There is, in my view, a tendency to exaggerate the difficulties associated with proof of causation even in medical negligence cases. For the purposes of allocation of legal responsibility, "[i]f a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contributed to that injury occurring." And in that situation, the trier of fact - in this case, a jury - is entitled to conclude that the act or omission caused the injury in question unless the defendant establishes that the conduct had no effect at all, or that the risk would have eventuated and resulted in the damage in question in any event.[19] (citations omitted)

18 I consider that what Gaudron J is describing in this passage is a process of reasoning by which, in an appropriate case, a plaintiff may prove on the balance of probabilities that the wrongdoing caused or materially contributed to an injury. In Freidin v St Laurent [2007] VSCA 16, Chernov J said of this passage

I take Her Honour to have been saying no more than that if the jury were satisfied that the defendant's wrongful conduct resulted in an increased risk of injury to the plaintiff and that risk occurred, ordinarily they were entitled (but not required) to infer from these circumstances that the wrongdoing materially contributed to the injury and was causative of it unless the defendant persuaded them that the conduct had no effect at all or that it would have happened in any event.[20]

19 In Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262 Spigelman CJ considered that the Naxakis test was inappropriate to the circumstances of that case. In Seltsam the plaintiff had inhaled asbestos dust and fibre and had subsequently developed renal cell carcinoma. The seminal issue was whether that exposure actually did increase the risk of that consequence. The plaintiff's case[21] in Seltsam demonstrated no more than a possibility of an increased risk. It followed therefore that the plaintiff had not demonstrated as a matter of probability an increased risk and thus a Naxakis type inference could not be drawn (predicated as it was on a factual basis of increased risk).

20 There is a clear issue in this case of whether the plaintiff's exposure to benzene did increase his risk of developing plasmacytoma/multiple myeloma at all or in any meaningful way. Before the plaintiff could contend for the Naxakis inference, I would need to be satisfied that there was in fact this increase in risk.

21 The plaintiff's case is that I ought to conclude on balance, that his exposure to benzene in the workplace between November 2002 and February 2006 materially contributed to or was a cause of him developing a plasmacytoma and subsequently multiple myeloma. The plaintiff says I can conclude this directly from the evidence or "if necessary" the plaintiff relies on the degree of proof described by Chernov JA in Freiden v St Laurent [2007] VSCA 16 at paragraph 15.

22 I take Mr Adams to be saying that the plaintiff relies on direct evidence of causation but alternatively on the Bennett/Naxakis process of reasoning.

23 The evidence in the case in relation to benzene exposure tended to merge issues of epidemiologically observed increase in risk in the abstract, actual increase in risk in this particular case, and direct evidence of causation (which was inevitably based on the former two issues in any event). With the exception of evidence concerning the actual levels of benzene exposure at the defendant's premises, I consider it is artificial to try to break up the evidence of epidemiological risk, actual risk in this case and actual causation into categories. I propose to examine the evidence on a witness by witness basis and, because of the complexity of it, it will be necessary to do so reasonably comprehensively.

24 I believe it is appropriate to consider the evidence with the following issues in mind:

(1) What was the actual level of benzene exposure that the plaintiff was subject to at relevant times at his workplace.

(2) Whether the plaintiff has demonstrated that exposure to benzene increases the risk of development of plasmacytoma to a significant degree.

(3) Whether the plaintiff has demonstrated that his actual exposure to benzene in the workplace increased his risk of his developing plasmacytoma to a significant degree.

(4) Whether the plaintiff has demonstrated that his exposure to benzene in his employment was a cause or material contributing factor to his development of plasmacytoma.

25 As mentioned above the plaintiff initially suffered a single plasmacytoma proximate to his left kidney, but this has since disseminated to various sites resulting in the diagnosis of multiple myeloma. All of the epidemiological studies relied upon by the various expert witnesses dealt with the development of multiple myeloma, as opposed to a single plasmacytoma. I do not regard this as a significant distinction; I note it was not the subject of a developed submission by the defendant and indeed Professor Fox, called for the defendant, accepted in evidence-in-chief that they were virtually the same disease[22] and if there is a cause, it is likely to be the same cause.[23]

26 Before any evaluation can be made of the risk issues, it is necessary to determine as best as can be done the actual level of the plaintiff's exposure to benzene.

27 PA5000 Adhesive is manufactured by Barham Pty Ltd. The Material Safety Data Sheet[24] generated by the manufacturer in accordance with National Occupational Health and Safety Commission criteria demonstrates that the ingredients of PA5000 are

Confusingly the proportions of the whole are expressed as follows:

• MEK 60-100%;
• P/U 10-30%;
• A/ct 10-30%; and
• Toluene 10-30%.

NE 1821 Black Neoprene is also manufactured by Barham Pty Ltd. The Material Safety Data Sheet[25] demonstrates that the ingredients and corresponding proportions of Black Neoprene are

• Non-hazardous Ingredients 10- > The Neoprene adhesive had 80ppm and the other adhesive had 40ppm benzene. These are very tiny amounts...

Also the minute benzene concentrations of the products must be compared with the very high levels of toluene, up to 30% (30,000ppm). A significant benzene exposure would require an enormous toluene exposure...[30]

30 Late in the trial Mr Adams, who appeared with Mr Grabau for the plaintiff informed the Court of the following

It is conceded by the plaintiff that last week Mr Pinda at the plaintiff's request conducted a test on the glues and found no benzene. An important part of that concession is there is controversy as to the testing process and that is a concession that both sides wish to have added to that concession.

There is no evidence of the manner of testing, or the nature of the controversy that attached to that testing, or whether the substances tested were identical in every respect to those used by the defendant. In the circumstances, I do not propose to act upon this concession and it forms no part of my ultimate conclusion on the actual benzene exposure suffered by the plaintiff.

31 It is one thing to point to the amount of benzene in the glues, it is another to assess the actual benzene exposure that the plaintiff was subjected to. Benzene is a hydrocarbon like other solvents in the glues. When the glues were applied to the shoes they gave off strong fumes. The plaintiff described them as follows:

I smell them. It's the most dangerous time when you start to brush the shoes and soles with glue. Here start the fume, disappear and vapour in the air. Here it is most critical for me because when I stay long I start feeling difficulty to breathe, cough, wheeze.[31]

So it's a very volatile mix of vapours coming off[32]and in light of the fact that the nose has to be bought up close for inspection I can conclude that the vapours would be in the breathing zone of the operator...

33 Mr Pinda did not seek to conduct or have conducted any simulated tests in order measure the level of solvents and more specifically the level of benzene that was "flashing off" into the breathing space of an operator performing the plaintiff's duties.

34 Dr Helen Sutcliffe, an occupational physician, prepared a report for the plaintiff's solicitors.[33] She was provided with the Material Safety Data Sheets for PA5000 Adhesive, NE1821 Black Neoprene and Halo Primer. She took a history from the plaintiff of strong fume inhalation, similar to the plaintiff's evidence at trial. In relation to the level of the plaintiff's exposure, she described it in these terms

...in the case of the plaintiff there has been excessive exposure of hazardous substances of solvents and glues during his employment at Palmone Shoes.[34]

Assessing the MSDS, and the exposure history indicted that the plaintiff was exposed to significant very high levels of volatile solvents (including some heated solvents and glues) including Methyl Ethyl Ketone, Acetate, Toluene, Light Aliphatic Petroleum Solvent, together with n-Hexane, Polyurethane and Trichlorocyanuric Acid. There is likely to be contamination with benzene in the preparation of Methyl Ethyl Ketone, Acetate, Toluene and Light Aliphatic Petroleum Solvent."[35]

35 In evidence-in-chief Dr Sutcliffe expanded on her opinion as to levels of exposure

• Assessing the exposure to solvents was very important in determining the relationship of occupation to cancer.[36]

• She could assess exposure from her experience as an occupational physician and by listening to the history given by the affected person.[37]

• Her opinion was that the plaintiff was exposed to excessive quantities of benzene "in the absence of testing".[38]

• Her estimate is that the plaintiff was exposed to benzene in the breathing zone in the range of "three or four, maybe five parts per million."[39] She believed that the Australian standard for ambient air concentration for benzene was one part per million.[40]

• She said that measuring exposure to solvents can be done either

(a) by using volatile organic measure badges pinned to a persons lapel in the breathing zone which will catch volatile hydrocarbons in the breathing space; or

(b) by collecting air from the breathing space removing it to a laboratory and "measuring on a chromatograph what amount of volatile substances are present"[41]

Dr Sutcliffe did not carry out or commission tests to endeavour to ascertain the likely level of benzene exposure in the plaintiff's working environment.

36 It is necessary to observe that the Australian Standard for benzene exposure of one part per million (ppm) is expressed as an eight hour time weighted average(twa).[42] Prior to 2003 the standard was 2.5ppm/twa. The effect of the twa is that if, for instance, a person was exposed to .5ppm for 16hrs or 2ppm for 4hrs per day on a twa, the exposure would be the same at 1ppm/twa. In other words, if a person is exposed to an average of 1ppm of benzene over an 8 hour day his exposure can be expressed as 1ppm/twa.

37 In December 2007, the defendant's solicitors Minter Ellison commissioned an "Occupational Hygiene Contaminant Testing" at the defendant's premises. The tests were conducted by Mr Paul Addison, a partner of Noel Arnold & Associates, occupational hygienists. Mr Addison has been a director of Noel Arnold & Associates since 1989. He has practised in the field since 1987[43] and has a Bachelor of Science, a diploma of occupational hygiene and memberships of professional bodies.

38 On December 13 2007[44] Mr Addison conducted a range of tests at the defendant's premises. His report was tendered as part of his evidence.[45] The tests included simulation (by Frank Palmone,on behalf of the defendant) of the plaintiff's shoemaking duties over a period of nearly 4 ½ hours during which Frank Palmone glued for 2¾ hours. The object of the testing was to "reflect the typical exposures associated with the batch production processes."[46]

39 When the tests were conducted the glues used were PA5000 Adhesive, Black and White Neoprene[47] and Halo Primer. The methodology of the taking of the samples is set out in full on Page 4 of Exhibit D3.

40 The collection devices used to measure the airborne contaminants were "passive organic vapour monitors", "sorbent tubes" and "sampling pumps."[48] All devices collected material from the breathing zone.[49] The breathing zone is the area up to 30 centimetres from the nose of the operator[50]

41 Long and short term sampling was undertaken.[51] The samples were analysed by two independent laboratories and the results set out in Table 3 on Page 7 of Exhibit D5. Tests were conducted over a range of activities carried out by various employees and the samples were screened for a range of solvents. The only directly relevant result is that for "Frank Palmone, morning/gluing 61595 104-246 minutes". It was in this test that the shoemaking duties of the plaintiff were simulated by Mr Palmone. Of the 4 hours and 26 minutes spent working, 2 hours and 45 minutes were spent gluing. The proportion of work time spent actually gluing is roughly the same as the plaintiff's estimate. Reported in mg/m3[52] and as a twa the relevant results were reported as follows:

42 These results were converted into a parts per million expression by Mr Addison so that some comparison could be made with the Australian standard.[53] Expressed as ppm and as work shift twa exposures, the results were as follows:

43 The defendant argues that none of them are above the Australian standard. Specifically, the defendant points to the benzene result which is 0.4ppm, 60% below the Australian standard for twa exposure and approximately 10% of the exposure estimated by Dr Sutcliffe. It follows, so the defendant argues, that the plaintiff's exposure to benzene was modest and not of the order that realistically could cause any carcinogenic effects.

44 In written submissions, the plaintiff argues that the Arnold "test is highly suspect. We know that 20 'orders' per day equals not least 160'items' per day. The plaintiff said 200. Why would the proprietor work for four hours creating a level of intensity, in term of toxicity, which was against his view, just to satisfy the Insurer."

45 Other witnesses called for the plaintiff considered his exposure to benzene or solvents generally as "excessive" without conducting any scientific testing. Mr Pinda considered that the plaintiff's exposure to solvents was "excessive"[54], but confined this opinion to solvents generally and was unable to express an opinion as to benzene specifically.[55]

46 Professor Winder is a professor of toxicology and professional health at the University of New South Wales. His report was tendered, subject to objection by Mr Gorton and became Exhibit P13.

47 Professor Winder considered the plaintiff's exposure to hazardous chemicals to be at "unacceptable levels"[56], including his exposure to "adhesives, solvents and chlorine containing compounds...". I note that under the conclusions heading in his report he does not offer any opinion as to whether the exposure to benzene itself (as opposed to the more general term "hazardous chemicals") is at "unacceptable levels."

In cross-examination, Professor Winder accepted that exposure to solvents generally such as to cause asthma, did not permit the conclusion that there had been any particular level of exposure to benzene.[57]

48 The defendant sought to develop the hypothesis that had there been an exposure to benzene of any significant amount, given the small quantities of benzene in the overall mix of hazardous substances, then the exposure to the other solvents including Toluene would be very much greater. If this were the case, one (so the argument went) would expect to see powerful narcotic effects from the exposure to those other solvents. In the absence of these powerful narcotic effects, it was put that the conclusion was readily open that the exposure to the chemical fumes was not as great as the plaintiff's witnesses asserted and therefore the exposure to benzene was insignificant. This hypothesis was advanced by Dr Crank,[58] consultant in chemistry and toxicology.

49 The plaintiff gave evidence that he suffered from headaches (a known narcotic effect of heavy exposure to toluene)[59] "all the time" which occurred "when he woke up" [60] and "when he left work".[61] The plaintiff, it was put, did not suffer from any of the other known narcotic effects of heavy exposure to toluene (nausea, dizziness and weakness)[62], nor did he suffer from effects of heavy exposure to n-hexane (peripheral neuritis - tingling of the extremities). An examination of the treating general practitioner's notes do not demonstrate any complaints of these symptoms.

50 I do not believe that this hypothesis advances the defendant's position to any degree. The plaintiff certainly complained of one "narcotic" symptom, headaches, albeit occurring at a time different to what would normally be expected.[63] The other symptoms, I accept, occur in greater or lesser degrees, if at all, depending on the susceptibility of the particular person to such effects.[64] I believe it would be speculative to base any, even tentative, conclusions on this hypothesis.

51 Ultimately, I am not satisfied that the plaintiff's exposure to benzene was at the levels argued by the plaintiff. The only proper scientific testing of the actual exposure was conducted by Mr Addison, who impressed me as a conscientious and impartial witness. Mr Addison conducted the tests, described by Dr Sutcliffe as the "correct" ones to undertake, if tests be undertaken.

52 Mr Adams and Mr Grabau criticised the testing in their submissions. They cited Dr Sutcliffe's criticism of the testing - this was based on Dr Sutcliffe's assertion that the photographs of the testing demonstrated that the shoe being glued was further from the breathing zone than as described in evidence by the plaintiff. An examination of the photographs[65] suggests that the shoe component being glued was within 20 to 30 centimetres of the badge like "passive organic vapour monitor", visible in those photographs. The "sorbent tubes" and "sampling pump" are not visible in the photographs, but both in examination-in-chief and in cross-examination Mr Addison stated that these devices were within the "breathing zone";[66] that is, within 30 centimetres of the nose, "somewhere on the lower lapel".

53 I accept the proposition that no amount of simulation testing can ever duplicate the precise quantities and mixtures of solvents that the plaintiff was exposed to which, no doubt, themselves, varied on a day-to-day basis over more than three years.

54 Nevertheless, I am of the opinion that the Addison evidence provides the best evidence relating to the issue of the actual amount of benzene that was present in the breathing space of the plaintiff throughout the relevant period.

As I have observed, it is the only scientific testing of the exposure the plaintiff was subjected to. The evidence for the plaintiff was essentially an intuitive estimate by Dr Sutcliffe based on her experience and the history the plaintiff gave her.[67] She did not express her estimate of 3-5ppm as a time weighted average[68] but as an estimate of the exposure during the time the plaintiff was performing the gluing.[69]

55 Accordingly, I find, on a time weighted average, that the plaintiff's exposure to benzene was approximately 0.4 parts per million. I am not satisfied that it was much greater than this level and I find that it was not at the level of 1 part per million or more.

56 To put these findings into some perspective, all medical and toxicological experts in this case who offered opinions related to risk and/or causation, relied on epidemiological studies published in various journals. One meta-analysis[70] that did find a link between benzene exposure and multiple myeloma was that conducted by Peter Infante D.D.S, Dr P.H..[71] Infante considered a study by Fu et al[72] which considered the mortality rates among a cohort of shoe manufacturers in Florence and which also concluded that there was a relationship between benzene exposure and multiple myeloma. Benzene was used by the Florentine workers the subject of that study from the early 1950s. "They estimated that 70% of the glue consisted of benzene before 1960. By the end of 1963 however, a national law required that the benzene content of glues be limited to 2% ...".[73]

57 70 per cent benzene is 700,000 parts per million. Two per cent is 20,000 parts per million. The glue analysed by Intertek Probe[74] returned the following results:

By any measure, the quantity of benzene in the glues used at the defendant's factory was low.

58 I am not satisfied of the plaintiff's allegation that the quantity of benzene in the breathing space of the plaintiff was excessive. This is a finding limited to benzene only. I shall deal with the other solvents as part of the asthma case.

59 For the plaintiff, the following witnesses gave evidence relevant to this issue

Each witness relied, to a significant degree, on the published epidemiological studies and meta-analyses that have investigated any link between benzene exposure and multiple myeloma. All concluded, on the basis of the published studies, there was an increased risk of contracting multiple myeloma after exposure to benzene. None offered any opinion as to what level of exposure to benzene was necessary in order to establish the increased risk.

60 Dr Wassouf, the plaintiff's GP, initially in a report dated 15 August 2008[75], was not prepared to offer an expert opinion on the relationship between the plaintiff's condition and employment and recommended seeking the advice of an industrial oncologist. By 27 October 2008, he felt qualified to offer an opinion in these terms: "there is a strong association between the plaintiff's plasmacytoma to his employment as a shoemaker." In forming that opinion, he relied upon studies by Hux[76] Walrath, Sonoda, Linet, La Vecchia, Rinsky, Decoufle, Infante, Infante (a meta-analysis), Rajnarayan and Fu.[77] He accepted that the Hux report referred to "an increase in multiple myeloma among production workers [which] was found in the highest solvent exposure category...." He expressed no knowledge as to the latency periods for multiple myeloma

You have no basis for saying that it [the plasmacytoma] first developed after November 2002?

No[78]

Dr Wassouf said in evidence-in-chief that his conclusion that there was a strong association between the plasmacytoma and the plaintiff's employment, took into account:

(1) The epidemiological studies with statistically significant positive findings showing the increase of plasma cell neoplasm due to exposure to benzene and solvents as well as the carcinogenicity of leather dust compounds

(2) The well documented biological plausibility that benzene and solvents induce biological effects to B-Lymphocyte cells and plasma cells; and

(3) Most diseases which do not have an infectious cause can be caused by an external agent or environmental exposure.

In his evidence-in-chief he expressed his opinion on the cause of the plaintiff's cancer this way

Actually I have read several articles which support the connection between the disease and the type of work. This makes me inclined to the high probability.[79]

In cross-examination ,Dr Wassouf accepted that he had made no notes of the plaintiff ever complaining to him about headaches.[80] In one of his reports, Dr Wassouf described the plaintiff's condition as a blastocytoma. When asked, he stated that he did not know whether a blastocytoma was different to a plasmacytoma.[81] Mr Gorton asked him what steps he took between his report of 15 August 2008 (where he did not offer an expert opinion on causation) and 27 October 2008 (where he did). The following exchange occurred

What did you do between 15 August 2008 and 27 October 2008 to develop your qualification to comment on the relationship between work and his condition?---Just looking for researches and articles.

You enclosed with your report in August 2008 copies of literature connected with multiple myeloma and glue. Was that material provided to you by the plaintiff?---He gave me some sources, yes.

Did he give you the epidemiological papers that are referred to in your report of 27 October 2008?---He gave me some of them. I am not sure whether this was one of them.

Did you carry out any investigations yourself to see what other papers there were? --- What do you mean, sorry?---He gave you some papers? --- He gave me a lot of papers, yes.

Did you carry out any investigations to see what other papers there were? --- I looked at the internet and other text books.[82]....

In relation to the papers that are referred to in your report of 27 October 2008, are any of those papers papers that you found or are they all papers that were given to you by the plaintiff? --- Actually, I did not print what I have read about it on the internet so the only materials that I have got in hard copies is his materials.

The only papers that are referred to in your report are papers that were provided to you by the plaintiff, is that correct? --- Yes.

Did you in your researches find any of the papers which say there is no identified scientific proof of a relationship between exposure to benzene and multiple myeloma? --- Well, I was looking for the positive side effect and not the negative. I just stopped there.

You were writing a report which was designed to refer only to positive papers for a connection? --- Yes.

For the purpose of assisting the plaintiff in his claim? --- To support my opinion, actually, regarding this matter.

And in developing your expertise you ignored any report that didn't support the view you wanted to put forward? --- Yes, but the majority of support - - -

Do you agree with the proposition I put to you: you ignored any paper which did not agree with the position you wanted to put forward? --- I didn't ignore but I didn't give it probably the preference to believe in.

HIS HONOUR: Doctor, did you seek out any paper that spoke of there not being a scientific connection between exposure to benzene and the development of multiple myeloma? --- Specifically not.

Did you actually ever see a paper to that effect? --- Probably. I remember - I recall reading something about it, yes, but I didn't stress it.[83]

He was asked about the latency period that would normally be expected between the exposure to benzene and the development of the illness:

Do you agree there is a latency period between the date of first exposure to benzene and the development of multiple myeloma? --- I agree there is a latency, yes.

What is it? --- I can't tell. I'm not an expert in that area.[84]

Mr Gorton took the witness to the Sonoda study which Dr Wassouf had referred to and quoted in his report[85] as evidencing the proposition of an eight-fold increase in risk of multiple myeloma after occupational exposure to chemical products including organic solvents or petroleum.

I want you to look at the bottom portion of the page, below that line 379 and the right-hand column. It says there and do you agree with this or can you comment on it

"It is well-known that the bone marrow is damaged by chronic exposure to benzene". You were relying on that in expressing the view that you did, were you? --- It's one of the facts, yes.

"Benzene is included in petroleum and is discharged into the environment as engine exhaust. Were you including that as a risk for the development of multiple myeloma as engine exhaust in the environment? --- I can't go into such detail. This is beyond my ability to go through all of this. My aim is to support my opinion that there is a connection between multiple myeloma and benzene inhalation. That's all I can do.

Did you report and consider the part of this paper where it says: "On the other hand, petroleum benzene and organic solvents did not show significant increased risk in our meta-analysis?" --- Yes. However, if you continue on: "Similar results have been reported in some cohort studies. In the present study occupational exposure to organic solvents or petroleum significantly increases the risk for multiple myeloma but exposure to car fumes during driving had no association."[86]

I consider that Dr Wassouf's research and acquired knowledge (by 27 October 2008) was insufficient to allow me to accord his opinion any real weight. I make no criticism of the plaintiff for supplying Dr Wassouf with the material he subsequently reproduced in his report. The plaintiff has a vital interest in his treatment and these proceedings. I do consider, however, that Dr Wassouf's opinion is eroded to a very substantial degree by his effective failure to research "the negative side" after researching "the positive side." He "just stopped there."[87]

61 Associate Professor Max Wolf is the plaintiff's treating haematologist and oncologist. The plaintiff's plasmacytoma was diagnosed in February 2008. Treatment has been complicated by the unsuitability of radiotherapy due to the proximity of the tumour to the plaintiff's remaining kidney and the plaintiff's refusal to accept surgery. Associate Professor Wolf's opinion on the risk is expressed in his report of 24 October 2008.

There is a high level of evidence supporting the relationship between benzene exposure and multiple myeloma. Although the research is hindered by the small number of case studies, several published cohort studies support the association. Therefore, there is scientific evidence to support the plaintiff's claim of occupational exposure as a cause of his plasmacytoma.

In his report of 8 August 2009[88]he cited Decoufle, Donoda (sic), Berlin, La Vecchia and Walrath

In summary I have to state that, although the cause of multiple myeloma in each individual patient is not known, there is extensive literature that supports the association between chemical and benzene exposure and the development of the disease.

In his evidence, he said that from the five papers he referred to, the incidence of multiple myeloma in people exposed to benzene was between two and four times that of the standard incidence in the population.[89]

He explained the significance of meta-analyses: "A meta-analysis is like a review of all the published studies. So to increase the power of a finding they combine all published studies and sometimes they go into unpublished studies as well and look at the findings and combine all the studies together..."[90]

He then referred to the Infante meta-analysis[91] which found an 'average risk of development of myeloma [from benzene exposure] of just over 2."[92]

If the exposure was heavy [he then set out the plaintiff's working hours and proximity to glue] is it relevant...the relationship of the exposure to the multiple myeloma, the intensity and duration of the exposure?---I think it is relevant, although I don't know what exposure you need - what duration of exposure you need to cause the necessary mutation in the gene. I think on first principles the answer is yes to that question.[93]

In cross-examination, Associate Professor Wolf accepted that there were other studies which offered a tenable medical view that there was no relationship between benzene exposure and the development of multiple myeloma:[94]

There's conflicting studies I said that, and its not a scientifically proven fact.

He said that benzene is a bone marrow toxin and it is biologically plausible that it could produce multiple myeloma.[95]

The balance of the literature indicates there is approximately a doubling of the risk of myeloma in people exposed to benzene.[96]

We are all exposed to benzene all the time, aren't we, due to petrol extracts and cigarette smoke around the air and other things? --- Yes.

So the degree of exposure to benzene must be relevant to determining the change in relative risk. That's right, isn't it? --- I would say so, yes.

In the studies that have been performed and the meta-analyses that have been conducted there is no reliable evidence as to the degree of exposure, is there? --- No.

But the studies which show a relationship between benzene and multiple myeloma, generally speaking, relate to people who are exposed in the periods between, say, 1940 and 1980. Is that a fair statement? --- It's a fair statement. Quite a number of years earlier, yes.

In that period of time pure benzene was commonly used as a solvent, wasn't it? Are you able to say anything about that? --- I don't know.

You don't know either about the amount of benzene that was included in any solvents? --- No.

So that you are not able to make - I say this with no disrespect but you are not able to make any comment about the extent of exposure that has been used in the studies that say there is a relative risk increase? --- No, I'm not. I don't claim expertise in that area. [97]

Associate Professor Wolf was asked about the latency period for multiple myeloma after exposure to benzene. After a series of questions about this aspect, the following exchange occurred:

There is a broad area in between. Are you able to say, on balance, that is whether it's more probable than not, whether or not this tumour came into existence after November 2002 or before it, or just can't you say? --- I find that too difficult to - I understand what you are saying about speculation and dogma but I find it too difficult to say. I am not able to answer, to say. To the question did this tumour commence existence after 2002, the answer is, "I can't really say", and equally, did this tumour come into existence before 2002, the answer is the same...[98]

Associate Professor Wolf was asked by me how his views about the latency period could sit with the view that, on balance, the tumour was related to the plaintiff's employment, confined as it was, from 2002 onwards.

How does that opinion sit with your inability to express an opinion as to when this tumour might have commenced existence? Do you follow? I am having difficulty lining one up with the other? --- Well, can I interrupt? Sure. Please. I want you to? --- I mean, clearly if the exposure due to his employment caused the tumour it would have had to come on after 2002, whenever he commenced work. I said in answer to the question could it have been there prior to 2002, I have to say well, it could have. On balance, what's more likely - it's nearly six years between the time he started work and the time it was diagnosed.[99]

A little later on I asked the witness the following questions and received the following answers

Perhaps I will put it this way and you tell me what comments you have or answers you have to this. Knowing what you know about the plaintiff's exposure and the time over which that exposure occurred are you able to say one or other of the following:

(a) that it was a cause of the cancer, that is the exposure was a cause of the cancer;

(b) that it was probably a cause;

(c) that it was possibly a cause; or

(d) that it was not a cause? Are you able to say which one of those alternatives, if any, is the attractive one? --- My strongest - I would be dogmatic or definite that (c) is correct.

That it was possibly a cause? --- Yes. Would I be as - I mean, the facts that we know are that he has multiple myeloma and that he was exposed to benzene. I don't think that's disputed. The question is was that the cause?

Not the cause, a cause? --- Sorry, a cause. The evidence that I have presented is that exposure to benzene, sure with a latency period, with a prolonged exposure has been associated - increases the risk by twofold, maybe up to fourfold. Therefore I have to say that it's possibly a cause - it is probably a cause. It would be better if you gave me something between (b) and (c); (c) plus.

Really it comes back to a question of statistics, doesn't it? --- Yes.

If you are at risk for something to occur, double the risk that otherwise you would normally be at, and it does occur and in the absence of any other obvious precipitating factor does that make the exposure possible or probable? It's a statistical question, I guess, and you seem to be - - -? --- Well, you know, as we have seen, the data is that - as I said before, it increases it two to fourfold. Now, does that make it possible - I mean, if it was fiftyfold you could be feeling stronger. The answer would be (b) much more definitely.

MR GORTON: In the scenario that his Honour put to you he didn't raise with you directly - and we have already dealt with it - the size of the tumour and the rate of growth, nor the uncertainty as to the quantum degree of exposure to benzene, nor the fact that while employment started in November 2002 the tumour wouldn't have developed until some time after that, if exposure to that benzene was affecting it. Those factors would lead you to go to (c) minus, wouldn't they, rather than (c) plus? --- I will stay with (c).

Give away the (c) plus? --- Well, yes, a difficult question."[100]

Could I be permitted to ask the same question again almost?

When his Honour was talking about probabilities he was talking about what's more likely than not which is the civil standard. The civil standard is likened to putting both things, both competing ideas into the scale, one on one side and one on the other and it's sufficient for someone in a civil case to express an opinion on the balance of probabilities, that is what's more likely than not and his Honour posed the question that (b) was probable. I would just like to ask that question again. Can you express an opinion as to causation in terms of what is more likely than not? In other words, are you able to tip your own decision-making or opinion-making scales? --- Well, as I said a few times already, we have got the statistics and there is a statistically increased incidence of myeloma. I wanted to give it a score of (c) plus, now I've been - the word is not "persuaded" but advised maybe I should drop it down, but I am happy to stick to what I said before, that it's at least possible and maybe a bit stronger than this, that there was a contributing factor the benzene exposure to the development of the myeloma.[101]

I regarded Associate Professor Wolf as an impartial and impressive witness. In the passage cited above he wrestled with a difficult question and, at times, his opinion was expressed unclearly. I did not understand him to be saying the plaintiff's exposure to benzene was probably a cause of his multiple myeloma; rather I understood him to be saying that it was at least possible that it had that effect. ".....maybe

a bit stronger than this" seems to me to be saying it was "possibly probable". Ultimately, I consider Associate Professor Wolf was offering the opinion that it was highly possible that the plaintiff's exposure to benzene was a cause of his plasmacytoma/multiple myeloma.

I consider that ultimately Associate Professor Wolf's opinion was:

(a) That generally, exposure to benzene increased the risk of the development of multiple myeloma

(b) That he did not possess the expertise to say what levels of exposure to benzene were required before the risk increased.

(c) Given the uncertainty about the age of the tumour and the levels of the plaintiff's actual exposure, he believed it was highly possible that it was related to the plaintiff's employment from November 2002, onwards but was not prepared to say that it was probable.

62 Dr Sutcliffe prepared a report for the plaintiff's solicitors on 9 August 2008. I have referred to parts of this report earlier. She saw the plaintiff once on 8 August 2008. She did not approach the issue of increased risk directly, but merged it with her discussion on "whether the plaintiff developed the plasmacytoma as a result of his occupational exposure to hazardous substances at Palmone Shoes."[102]

It is clear that Mr Karam has developed plasmacytoma adjacent to his sole left kidney and that further treatment will be difficult and radiotherapy is not appropriate because of the proximity to the kidney. Surgical treatment is being considered.

The histology is reported to indicate a malignant infiltrate with immunohistochemical features favouring a plasma cell neoplasm.

The question now is essentially whether Mr Karam developed the plasmacytoma as a result of his occupational exposure to hazardous substances at Palmone Shoes.

I note that A/Prof Wallin concludes that there is no occupational relatedness.

In assessing the occupational relatedness several factors need to be taken into account.

Most research about work relatedness of cancers relies on epidemiological research which is limited in extent and outcomes by the rarity of plasmacytoma occurrence and so no useful epidemiological studies are available.

Even if the evidence is extrapolated to that concerning multiple myeloma (which can be an outcome of plasmacytoma, but not always) again the evidence is hindered by the relative low prevalence of the condition.

There have been many epidemiological studies directed to assessing the relationship to work exposure to benzene (contained in solvents and glues) to onset of multiple myeloma but again the evidence is hindered by size of the studies and the inaccuracy of levels of exposure to benzene in workers.

In addition the powerful petroleum industry lobby funds research related to petroleum based benzene exposure and the independence of this research is questioned.

The World Health Organisation (WHO) International Agency of Research into Cancer (IARC) is the peak international body which assesses work relatedness of cancers, by hazardous exposure and by industry.

IARC has classified boot and shoe manufacturing as a hazard for the development of occupational cancer in Category 1, indicating the strongest association of cancer with an occupation.

The use of solvents containing benzene have been found to be related to development of multiple myeloma in many studies, and in the most recent study, a multicentred case control study from Italy.

However there are older studies which indicate the opposite.

In assessing the connection between specific work and the onset of specific cancers the criteria of biological plausibility needs to be met, and I believe that there is sufficient evidence to indicate that this has been met for the relationship of solvents to development of multiple myeloma.

The assessment of the exposure is also very important in determining the relationship of occupation to development of cancer, and in the case of the plaintiff there certainly has been excessive exposure of hazardous substances of solvents and glues during his employment at Palmone Shoes.

Assessing the MSDS and the exposure history indicates that the plaintiff was exposed to significant very high levels of volatile solvents (including some heated solvents and glues) including methyl ethyl ketone, acetone, toluene, light aliphatic petroleum solvent, together with n-hexane, polyurethane and trichlorocyanuric acid. There is likely to be contamination with benzene in the preparation of methyl ethyl ketone, acetone toluene and light alphatic petroleum solvent.

This resulted in inhalation of these hazardous substances and also skin contact with additional absorption by skin to increase the toxic exposures internally.

These hazardous exposures occurred on a daily basis for up to 6 hours a day, 5 days a week for years.

As a result of analysing the content of MSDS, assessing the substances to which he was exposed, the extent of exposure, the biological plausibility, the recent current literature, the IARC data for occupationally related cancers, I conclude that Mr Karam, more likely than not, has sustained plasmacytoma as a result of his occupation and the hazardous substances to which he was exposed over a prolonged period in his occupation at Palmone Shoes.[103]

I consider that Dr Sutcliffe's opinion set out in her report of 9 August 2008 is of limited value to the plaintiff's case. Whilst she states that the IARC classification for boot and shoemaking is that it is occupationally associated with cancer, this does not go to the narrower issue of whether there is a relationship between benzene exposure and the development of multiple myeloma. She provided no analysis of the unidentified studies she had read and offered no reason for her preference for the "multi centred case control study from Italy".[104] Her opinion was offered without (at the time) actual knowledge as to whether benzene was present as a contaminant in the glues, and expressed the broader view that the exposure to "hazardous substances" resulted in the plasmacytoma.

In evidence, she outlined her qualifications in occupational medicine[105] with, in addition to the normal qualifying degree (with honours), a graduate diploma of occupational health and a diploma in pain medicine and fellowship of the AFOM.[106] She has practised in occupational health for many years. She said that the exposure described to her by the plaintiff was excessive.[107]

As observed earlier she expressed the view that this exposure to benzene was excessive[108] and this level of exposure was three, four or five parts per million:

Looking at it and listening to what the plaintiff had to say to me and understanding the process he was involved in, I would have to say that I think it is three or four, maybe five parts per million that he was breathing in....[109]

As I have indicated earlier, I do not accept that the plaintiff was inhaling benzene at or near this level.

In cross-examination Dr Sutcliffe accepted that she was not an epidemiologist but stated that she practised it on a daily basis and was "a practical epidemiologist''.[110] On the issue of whether there was a relationship between benzene exposure and plasmacytoma she stated that in the absence of studies on that precise nexus, she extrapolated plasmycytoma to multiple myeloma and applied what she stated to be the "Bradford Hicks criteria".[111] These criteria are:

She accepted that epidemiological evidence of the relationship is sparse. She accepted that she did not have a clear picture of the latency period,[112] and that the higher the dose of benzene the more likely the condition will occur.[113]

She agreed that the dose is partly determined by the duration of exposure and partly by the concentration of the substance.[114] Dr Sutcliffe was pressed about her reliance on the World Health Organisation's IARC classification of boot and shoemaking. In her reports she stated, "IARC has classified boot and shoe manufacturing as a hazard for the development of occupational cancer category 1" In cross-examination she conceded the cancer identified by the IARC was in fact nasal cancer.

Dr Sutcliffe was asked about the "Italian study" she referred to in her report. She accepted it was a paper by Fu et al. She was taken to a copy of it.

The abstract of this study starts "Objective to examine the cancer risk of shoe manufacturing workers and evaluate whether the risk was associated to exposure of leather dust and solvents. Is that the paper you have? --- Yes.

In the abstract to that paper it says about three-quarters of the way down the first column that: "Mortality in leukaemia was not increased in the English cohort but was increased in the Florence cohort. The highest risk was found amongst shoe workers in Florence who were first exposed between 1950 and 1959 when exposure to benzene was substantial"? --- That's correct, yes.

Do you have any idea of what is meant by 'substantial' there? --- I know that the levels were reduced but I cannot recall the levels that they looked at. Of course, I didn't retain it in my mind. I would have to check the paper through to see whether they have the exposure levels reported.

We can check the paper through but do you accept that between 1950 and 1959 benzene was frequently used by itself as a solvent? --- Yes, at some stage in the early 50s it was used as a solvent and probably before that as well.

If you were using benzene as a solvent the exposure would be enormously greater than it is when benzene is just a contaminant of toluene and other solvents? --- Correct, yes. Yes, of course.

It says in this paper further to that: "Some evidence of an excess risk of stomach, bladder and kidney cancer as well as multiple myeloma was also found in the Florence cohort only among workers employed in jobs with the highest exposure to solvents"? --- That's correct, yes.

Again, subject to whether we can find it in the paper you don't know what that highest level exposure was? --- I don't know.

That's correct, isn't it? --- I don't think it is recorded.[115]

After some discussion the cross-examination continued:

The conclusion in the abstract, perhaps one should go instead of to the extract to the summary at the end of the paper so as to avoid that potential risk: "The findings of this study confirm findings of previous study that there is association between exposure to leather dust and nasal cancer and between exposure to benzene and leukaemia in the shoe manufacturing industry. Do you see that there? --- Yes.

"Some evidence for an excess risk of stomach, bladder and kidney cancer as well as multiple myeloma and non-Hodgkin's lymphoma was found among workers employed in jobs with the highest exposure to solvent. Did you take into account that report in this paper, that it was the highest exposure to solvents at a time when exposure to benzene was very much greater than it would be now in forming your opinion that there was a relationship between the plaintiff's exposure and the development of his plasmacytoma? --- I understand this paper and that it indicates that the highest concentrations were used. That doesn't exclude the fact that smaller concentrations can cause the problem as well.

It may not exclude it but it doesn't establish it? --- It doesn't establish it, no.

And you have worked on this paper as being powerful supportive evidence for the plaintiff's exposure having been causative of his plasmacytoma, haven't you? --- One of the papers that I rely on.

Would you rely on it as powerful support for your opinion? --- That's one of the papers that I relied on. Not powerful mainly because the exposure was so high and it was at a time before there were controls brought in.[116]

Mr Gorton took Dr Sutcliffe to the scientific testing conducted by Mr Addison of Noel Arnold and Associates. She accepted that the sampling strategy was likely to produce an accurate assessment of what the exposure was at the time the sampling was undertaken.[117]

Dr Sutcliffe did not accept the accuracy of Mr Addison's tests and maintained that all solvent readings were surprisingly low to her[118] and that she thought this was explicable by the subject, Mr Palmone, in carrying out the tests not holding the shoe as close to the breathing space as the plaintiff said he did when carrying out his work.

As I have indicated earlier, I prefer Mr Addison's testing to Dr Sutcliffe's estimates.

I consider that Dr Sutcliffe's evidence provided some support for the proposition advanced by Associate Professor Wolf that there is a link between exposure to benzene and the development of multiple myeloma at a high exposure level. I do not consider that Dr Sutcliffe's evidence assisted the plaintiff, in any material way, in demonstrating that the actual exposure that I have found the plaintiff was exposed to led to his risk of developing multiple myeloma actually being increased, or to the conclusion that, on balance, that exposure was a cause of his multiple myeloma.

63 Professor Christopher Winder is a Professor of Toxicology and Professional Health at the University of New South Wales. He prepared a report of 23 September 2009 for the plaintiff's solicitors which he adopted in his evidence.[119]

64 His report was received in evidence subject to objection by Mr Gorton, who reserved the right to make submissions about certain parts of it in due course, such objection pertaining to the limits of expertise of a toxicologist when expressing opinions ostensibly of a medical nature. It was agreed that his evidence should be received and that submissions as to the admissible extent of the evidence would be made during final submissions.

65 Professor Winder's opinion (relevant to the issue of increased risk) also merged the issue of increase in risk with ultimate causation:

I agree with Mr Akram's medical advisers, that Mr Akram's employment as a shoe maker and his exposure to high levels of chemicals while working at Palmone Shoes Pty Ltd from 2002-06 are a material factor in the development of his plasmacytoma/multiple myeloma.[120]

Professor Winder stated that benzene has been known as a haematological toxicant since the nineteenth century and many haematological diseases have been reported to be the result of benzene exposure:

Multiple myeloma is listed as one of the haematological conditions associated with exposure to benzene.[121]

Benzene exposure (and in some cases, other organic solvents) has been associated with multiple myeloma in a number of studies.[122]

(a) Rinsky et al "Benzene & Leukaemia. An epidemiological risk assessment." A cohort with exposure to benzene identified a standard mortality rate to leukaemia as 409 (relative risk = 100).[123] The four deaths had "a latency period based on the estimated time of exposure of 40ppm years".[124]

(b) La Vecchia et al "Occupation and lymphoid neoplasms". A case control study of 100 multiple myelomas found a significant risk of multiple myeloma from exposure to benzene and other solvents.[125]

(c) Ireland et al "Cancer mortality among workers with benzene exposure". A 1997 study of 4172 chemical plant workers reported elevated rates of leukaemia and multiple myeloma in production workers with benzene exposure.[126]

(d) Lundberg et al "Mortality and cancer incidence among Swedish paint industry long-term exposure to organic solvents". A 1998 study of 411 Swedish paint workers exposed to solvents from 1955-1995 reported a marked increase in deaths from multiple myeloma.[127]

(e) Silver et al "Effect of follow up risk on time estimates: A longitudinal examination of the relative risks of leukaemia and multiple myeloma in a rubber hydrochloride cohort" A 2002 study of rubber hydrochloride workers showed increased risks of leukaemia and multiple myeloma with benzene exposure.[128]

(f) Collins et al "Lymphohaematopoietic cancer mortality among workers with benzene exposure". A 2003 study of 4417 workers exposed to benzene in a chemical plant showed an association between exposure and multiple myeloma.[129]

(g) Infante et al "A detailed meta-analysis of benzene cohort studies". This yielded a "statistically significant risk of 2.13 (that is, over double the risk in non-exposed populations) of multiple myeloma in relation to benzene exposure".[130]

(h) Costantini et al "Risk of leukaemia and multiple myeloma associated with exposure to benzene and other organic solvents: Evidence from the Italian Multicentre Case-control study". An Italian-based case-control study of 263 cases of multiple myeloma supported an association between benzene and multiple myeloma.[131]

66 Professor Winder stated that limitations in study quality, particularly exposure assessment pervaded all studies reviewed. "Nonetheless, the epidemiological evidence linking benzene to malignancies of the blood forming tissues is compelling".[132]

67 He also stated that there were also studies that did not report an association such as (Wong, Bezabeh and Pyatt). He did not refer to those. This was because, he said, for a matter to be reported epidemiologically as having an association, it needed to be assessed at a probability of greater than one in twenty as compared (so he said) with the near one in two probability of the civil standard.

68 I understood Professor Winder to be saying no more than this: for these studies to have accepted an association between benzene and multiple myeloma, statistically, the authors needed to be satisfied of a probability of 95% before they would report on their findings. Therefore, studies which found no association were merely studies that did not reach the 95% statistical satisfaction required.[133]

69 Professor Winder also considered that the development of multiple myeloma after benzene exposure was biologically plausible.

70 As to the levels of exposure necessary to establish multiple myeloma, Professor Winder observed that the oil refinery workers study referred to above demonstrated that the lowest level of exposure associated with the development of leukaemia is 0.7 to 1ppm.[134] Professor Winder deferred issues of latency to medical and oncology experts. Towards the end of his report, at paragraph 45, he stated

I disagree with the statement by Professor Richard Fox that 'the literature consensus is that benzene exposure is not associated with multiple myeloma'. As noted above in paragraph 27, there are sufficient literature reports to indicate that exposure to benzene is associated with multiple myeloma. Evidence continues to increase about this, and meta-analyses of multiple studies are confirming this association further (see for example, Infante's paper, which concludes 'The analysis demonstrates a significant excess in the relative risk (RR) of MM (multiple myeloma) in relation to benzene exposure'). Additionally, authoritative health agencies such as IARC have come to the same conclusion.

71 In cross-examination, Professor Winder agreed that he had no information about the degree of exposure to benzene by the plaintiff. He agreed that there was a legitimate view of the epidemiological papers that no relationship between benzene exposure and plasmacytoma had been established. He did not, however, accept that there was a legitimate medical view that exposure to benzene was not a cause of multiple myeloma.

72 Mr Gorton then asked further questions about the plaintiff's levels of exposure and the latency period:

Is the likelihood of benzene being the cause of a particular multiple myeloma dependent upon the extent of the exposure? --- Yes.

So to form the view that it was a probable cause of the plaintiff's multiple myeloma it would be necessary for you to have some view as to the actual extent of exposure to benzene, wouldn't it? --- Can I qualify my answer before I answer it?

Can you answer it and then qualify it after that? --- Okay.

The answer is yes but the human population shows a variable response to the effects of chemicals. One part per million as an exposure standard protects nearly all workers and not all workers and therefore, whether it's one part per million or a lower number would be debatable in an individual case.

In the epidemiological papers about multiple myeloma there is frequent reference to a latency period between the time of exposure or the beginning of the time of exposure and the development of the multiple myeloma? --- Yes.

That latency period is frequently expressed as being something in the region of 20 years? --- I accept your observation but that's a medical issue I don't have any expertise to comment on.

If you are not taking into account the existence of the latency period how can you answer his Honour's question when you don't know when the plasmacytoma first began? --- In at least one of the papers I read a shorter latency period was suggested.

Were you taking into account a shorter latency period when you answered his Honour's question that in this case it was probable that the exposure to benzene played a role in the plaintiff's plasmacytoma? --- No.

Then how could you answer it as probable without taking into account a latency period? --- When you said "a latency period" I believe you meant 20 years. I believe from my reading the latency period may not be 20 years. I think it may be some other number.

You said you didn't take into account a latency period. You were limiting yourself in that response to 20 years, were you? --- No. If it's 20 years I would say not. I don't think 20 years is an appropriate latency period. Again, that's something I can't answer. It's just an opinion I am giving.

If you can't answer a question as to what the latency period is how can you say that it is more probable than not that exposure less than six years before the discovery of the plasmacytoma was a cause of that? --- Because I don't believe that you can say the latency is any number. Pardon? --- I don't believe you can say the latency for any particular cancer has any particular number.

People can develop multiple myeloma or plasmacytoma without any exposure to benzene, can't they? --- Yes.

Have you got any reason for saying that this plasmacytoma did not develop independently of exposure to benzene? --- No.

Do you have any information as to the rate of growth of plasmacytoma tumours? --- No.

In giving your answer to his Honour about it being more probable than not would it not be important to know what the size of the tumour was at the time of discovery and what its rate of growth was? --- Again, they are medical questions.

So that your answer that it's more probable than not does significantly depend on medical questions which are not in your expertise? --- That's correct.

How then can you say it is more probable than not when you don't have the expertise that allows you to answer the question? --- In the reading of the papers for this case I was not of the view that the latency of the disease was any particular number.

You also didn't have any regard to the rate of growth or the size of the tumour. That's a medical question? --- (The witness nodded).

Your answer depends on both your expertise and knowledge of the medicine relating to plasmacytoma, doesn't it? --- To multiple myeloma. The plasmacytoma was what was first diagnosed? --- But it grew no - - And at that stage there was no multiple myeloma. You understand that? --- Yes.

Well, there may not have been.

MR GORTON: No identified multiple myeloma? --- Yes.

It is essential for a determination as to whether there was a cause from exposure at Palmone Shoes to form a clear view as to when the plasmacytoma commenced to be? --- Yes.

And whether it commenced to be before or after 2002 is something that depends on medical opinion rather than toxicological opinion, isn't it? --- Yes.

So that you are not in a position to express the view that it is more probable than not within your area of expertise, are you?

[There was then discussion about the limits of the witnesses expertise.]

[Previous question read out by his Honour.]

THE WITNESS: I have formed my opinion based on my reading of the literature which did not indicate to me, necessarily, that there was a fixed latency period of 20 years and therefore, my opinion is based on the possibility that this condition could have grown in less time than the time you are specifying.

HIS HONOUR: I do hesitate to ask more questions but I do have a couple more. As a toxicologist you have already told us your discipline often requires you to study epidemiology and the works of epidemiologists? --- Yes.

Which is a fancy way of saying looking at the statistical analyses of the incidence of medical conditions? --- Yes.

Are you able to say from your researches how much more likely the incidence of multiple myeloma is after exposure to benzene as compared to its natural incidence within the normal population? --- No.

73 Mr Gorton submitted that I should regard Professor Winder's evidence as unreliable and extreme, and that he showed a bias against the defendant and a marked lack of scientific balance. I did not form that view of Professor Winder. I considered that he was a conscientious and widely researched witness whose answers to all questions asked of him were considered and measured. I do accept, however, that there are some limitations to his evidence.

74 Mr Gorton submitted that Professor Winder's training and expertise permitted him to give evidence about the risk factor presented by the plaintiff's employment but that he could not legitimately express a medical opinion about the cause of the plaintiff's illness. As mentioned above the evidence was received under cover of objection by Mr Gorton. A question asked by me at T 346 which elicited the answer that the plaintiff's exposure to benzene was a probable cause of the plaintiff's multiple myeloma, Mr Gorton argued, also suffered from the same vice. In my view, there is substance in Mr Gorton's objection that Professor Winder's expertise falls short of a capacity to offer a medical opinion on the cause of the plaintiff's illness, or more broadly expressed opinions on pure medicine. This was illustrated when Mr Gorton pressed him about the latency period and its potential impact on the issue of causation: "I accept your observation, but that's a medical issue I don't have any expertise to comment on."[135](See also para 106 of these reasons on the issue of the limits of toxicological expertise). Having said that, Professor Winder was quite entitled to and did admissibly comment on the toxicological risks of benzene exposures to workers. I found his opinions on the risks presented by benzene as offering support to the opinions expressed by the plaintiff's medical witnesses, particularly Associate Professor Wolf. Like every other witness in the case, however, Professor Winder was hamstrung by the relative lack of research on the area and could not assist on the issue as to what level of exposure to benzene actually increased the risk of development of multiple myeloma.

75 The defendant called two witnesses as part of its case. Professor Fox is Director of Research at St Vincent's Hospital. He has the normal medical qualifying degrees. He holds a Doctor of Philosophy in Medicine from the University of Sydney and is a Fellow of the Royal Australian College of Physicians. He has specialised in the field of clinical haematology and medical oncology since about 1971.[136]

76 Professor Fox saw the plaintiff on one occasion and, like other witnesses in the case, a large part of his evidence-in-chief was elicited by tendering his various reports.[137] He took a full history from the plaintiff and was provided with statements from Dr Wassouf, Dr Sutcliffe and Associate Professor Wallin.[138] He was also supplied with the plaintiff's records from the Royal Melbourne Oncology Clinic and notes from Associate Professor Wolf. At page 3 of his first report (22 May 2009), he stated:

I do not believe the tumour is work-related. In general, the cause of multiple myeloma is not known. Plasmacytoma is a rarer variation of multiple myeloma and its cause is not known. There is very extensive literature on lymphohaemopoietic malignancies and relationship to various chemical exposures.

He then referred to Dr Wassouf's reliance on the Fu study "Cancer mortality among shoe manufacturing workers". It will be recalled the Fu study dealt with two shoemaking cohorts, one Italian (Florence) and the other English.

There was an increased risk of nasal cancer found in the English cohort[139] ... There was an increase of mortality from leukaemia in the Florence cohort and was (sic) the highest risk was found amongst the shoe workers in Florence who were first exposed between 1950 and 1959 when exposure to benzene was substantial. This, however, is only based on three cases of leukaemia.[140]

There was some evidence for an excess risk of stomach, bladder, kidney as well as multiple myeloma seen in the Florence cohort and the 95% confidence limits showed that that was not statistically significant. There was no increase in the English cohort.

There is a very extensive literature on the potential for benzene in various solvents or in petroleum workers, and its potential capacity to cause acute myeloid leukaemia as well as multiple myeloma.

I note a paper by Kirkeleit published in Cancer Causes and Control, Vol.19, p 13-23 in 2008. It notes that previous studies report that time from first exposure until diagnosis or death of multiple myeloma possibly related to benzene exposure is above 20 years. This comes from the reports of Rinsky published in the American Journal of Medicine in 2002, as well as the reports of Collins and colleagues published in Occupation and Environmental Medicine, in 2003 and the report of Infante published in 2006....

On the other hand there have been many papers reporting no relationship between exposure to benzene and the development of multiple myeloma (See the Wong paper). As well studies in mortality and cancer incidence on the Australian petroleum industry have not shown an increased risk that is significant ...

I would therefore consider that Mr Karam's plasmacytoma was not caused by his work exposure. My reason for this is the lack of clear cut evidence for that type of exposure to cause plasmacytoma, and as well the latency period and duration of his employment is too short and too close to the time of discovery of his tumour.

78 On 7 September 2009, Professor Fox commented on the five studies relied upon by Associate Professor Wolf:

(1) The Decoufle paper was an historical cohort of 259 male employees at a chemical plant where benzene was used in large quantities. The study group was all employees at one company between 1947 and 1960. Four deaths from lymphoreticular cancers were reported (three leukaemia, one multiple myeloma, where 1.1 deaths would be expected on the basis of national mortality rates). Professor Fox stated that "the paper states this [the multiple myeloma death] raises the possibility that multiple myeloma could be linked to benzene also".

(2) Sonoda. An increased rate of multiple myeloma in the occupational category of agriculture and fisheries showed a significantly associated increased risk (5.89). "... [O]ccasional exposure to chemical products including organic solvents or petroleum showed a significan[t] association with an increased risk of eight fold, but with a confidence limit of 1.01 to 64". Professor Fox noted "that these studies have never been confirmed in any other studies in Japan or elsewhere".

(3) "The Berlin Paper". The cohort comprised 5791 individuals exposed to organic solvents in Sweden. "The total cancer incidence was slightly elevated with a standard incidence ratio of 1.2, that is, a 20% increase. They said that malignancies of the lymphohaemapoietic system ... had an increased risk." There was no mention in particular of multiple myeloma.

(4) The "La Vecchia" paper dealt with individuals in the agriculture and food processing occupations. Multivariant relevant risks were twofold for multiple myeloma. In the "chemical industry" a "significant trend in risk [was] observed between duration of exposure to benzene and other solvents and multiple myeloma".

(5) The Walrath paper studied 4734 deaths amongst shoe workers. "There was a mortality from leukaemia slightly lower than expected (if benzene was involved you would expect an increase in leukaemia). There was a significant increase in death from multiple myeloma among both men and women.

79 Professor Fox noted that these were all individual and relatively small studies and that Associate Professor Wolf had not commented on the "so called negative studies". Professor Fox commented that the meta-analysis studies were published studies that "are considered distinct from just negative or just positive".

80 Professor Fox then referred to "Risk of Acute Myeloid Leukaemia and Multiple Myelosis in Workers exposed to Benzene", a paper by Wong published in the Journal of Occupational and Environmental Medicine Vol 52 in 1995. The data was derived from a cohort of workers employed at two Goodyear plants in Ohio. "No increased risk of acute myeloid leukaemia was detected for cumulative exposure to benzene below 200ppm years. For multiple myeloma no relationship to exposure to benzene was detected."

81 Professor Fox referred to a study by Bezabeh "Does Benzene Cause Multiple Myeloma - An analysis of the published case control literature" published in Environmental Health Perspectives Vol 104. This is a meta-analysis.[141] It referred to case studies from 1970s and 1980s which suggested that benzene exposure might be a risk factor for multiple myeloma. "An analysis has now been conducted by the published population based and hospital based case studies published through mid 1995 on examination of the relationship between multiple myeloma and benzene exposure or surrogates for benzene exposure. No increased association was found between multiple myeloma and benzene exposure or exposure to chemical groups that included benzene. The odds ratio from these analyses approximated 1. Exposure to petroleum products and employment in the petroleum occupations did not appear to be risk factors for multiple myeloma. Cigarette smoking as a surrogate of benzene exposure was not found to be associated with multiple myeloma while some studies of products of combustion described as engine exhaust did show a significant association with multiple myeloma. In toto the population based and hospital based (criteria) indicated benzene exposure was not a likely cause for multiple myeloma".

82 Professor Fox adhered to his opinion that the plaintiff's work with Palmone Shoes was not causative of his multiple myeloma.

83 I note that it does not appear that when Professor Fox wrote his substantial reports of 22 May 2009 and 7 September 2009, he had actual information as to whether benzene was actually contained within the solvents the plaintiff was dealing with or indeed what amounts were in the atmosphere in the vicinity of the breathing space.

84 By 15 September 2009, he had received the Intertek Probe[142] analysis which reported benzene levels "up to 80 micrograms per gram of materials". Professor Fox observed that the average cigarette contained 50 micrograms of benzene per 1 gram of substance, a "similar" level of benzene, and that "cigarette smoking is not associated with multiple myeloma, but has an association with Acute Myeloid Leukaemia".[143]

85 On 27 November, Professor Fox issued his final report. He had been provided with the CT scans of the plaintiff's plasmacytoma dated 24 June 2008 and "16/12/08".[144] These, he said, showed no effective growth in the tumour. Plasmacytoma and multiple myeloma are slow growing tumours and Professor Fox hypothesised that with the tumour the size it was in early 2008, even allowing for a doubling every four months, it still would have been present in 2002, that is, before the plaintiff started work.

86 He stated "To assume his employment was causative, one has to postulate an initial rapid growth and then a cessation of growth. This would be speculative". I consider that this particular argument is of no persuasive worth. Professor Fox postulates himself a doubling in size every four months from 2002 onwards. Any retrospective hypothesis predicated on the 2008 sizes of the tumour is necessarily speculative itself. Professor Fox estimates the tumour weight would be 35 to 60 grams in 2008, which in turn would contain approximately 35 to 60 billion cancer cells. Working backwards from 2008 applying (presumably) a halving formula every four months, results, according to Professor Fox, in a tumour in 2002 of 20,000 to 30,000 cells. That is, a miniscule tumour, if one at all.

87 Finally, Professor Fox referred to a paper by Bergsagel. (This in fact is a meta-analysis and was referred to frequently in Professor Fox's oral evidence). This paper was published by major North American cancer centres including Harvard University and the Mayo Clinic. On reviewing the epidemiological evidence, the paper stated, "There is no scientific evidence to support a causal relationship between exposure to benzene or other petroleum products and the risk of developing multiple myeloma".

88 In oral evidence, he stated that based on the literature he had reviewed, he disagreed with the view that benzene exposure was a risk factor in relation to multiple myeloma.[145]

89 He accepted that there was a medically recognised relationship between sufficient exposure to benzene and myeloid leukaemia, which is a blood-related cancer, but that that was a fundamentally different condition to multiple myeloma.[146] Plasmacytoma is essentially a localised version of multiple myeloma and they are essentially the same disease. As observed earlier he accepted that it was likely that if something were causative of multiple myeloma, it would likely be causative of plasmacytoma.

90 The latency period, he stated, in the papers which postulated an increase in relative risk of the development of multiple myeloma from benzene exposure was between 10 and 20 years.

91 In cross-examination, he reiterated his view that the Bergsagel review was a definitive review written recently (in 1999).

92 A theme of cross-examination was that the Bergsagel review was not objective and in fact, it was put, was merely an expansion of a statement prepared in support of litigation concerning "causality of multiple myeloma by benzene" and prepared on behalf of Amoco, a petroleum manufacturer.

93 The source for this cross-examination was a letter to the editor of a publication entitled "Blood", and in fact this letter to the editor, together with a response from Daniel Bergsagel, was tendered as an exhibit.[147]

94 Professor Fox defended the objectivity of his colleague. I did not regard this cross-examination as undermining Professor Fox's opinion, as I did not consider it undermined in any material way the Bergsagel study.

95 Mr Adams took Professor Fox to an unidentified article by Peter Infante[148] and invited his comments. It appears in that article, Infante was criticising Wong (a benzene/multiple myeloma refuter). Professor Fox accepted that there were arguments for and against the link, but said that the balance of the comprehensive meta-analyses suggested there was no link. He stated:

This is the Sonoda paper from Sapporo University in Japan, which is published in the Journal of Epidemiology and there was no significant association. It says here 'These results suggest that benzene itself was not likely to be a risk factor for multiple myeloma.

Professor Fox also cited Bezabeh in the Journal of Environmental Health:

They go on to say 'The odds ratios from these analyses approximated one and exposure to petroleum products in employment related occupations did not appear to be risk factors for multiple myelomas.[149]

96 Professor Fox again asserted that the amount of benzene in the plaintiff's work environment approximated that in a cigarette. He was then asked:

If that be correct, if that be the correct position - what you are saying is that it's so minor and so minuscule to be irrelevant? --- What?

In terms of the production of the cancer that this man has? --- I think that's what I am trying to say.[150]

97 The Infante meta-analysis was tendered.[151] Professor Fox stated that the problem he had with this paper was that it relied on the exposure of Florence shoe workers who dealt with glue that was 70 per cent benzene.[152] Professor Fox said that the level of exposure as demonstrated by the testing was 70 parts per million,[153] as opposed to 700,000 parts per million.

98 Professor Fox, in his answer to me, accepted that if Fu (upon whom Infante relied) was correct, then there was an increased risk of multiple myeloma from benzene exposure, albeit at very high levels. He went on to say that that link did not show up in later studies when the concentrations came down:[154]

You have three meta-analyses that say there is nothing there and you have one that says there is something there.[155]

99 When asked whether he thought that a link between benzene exposure and multiple myeloma was biologically plausible, he stated (in effect) that he had once held that view, but did not hold it now.

100 The witness was taken back to the benzene content and calculated that the glue used in Florence until 1963 had 10,000 times the concentration of benzene as compared to the glues in the defendant's factory.

101 Ultimately, when presented with four alternatives, he stated that there may possibly be a relationship between benzene and multiple myeloma, "but the evidence does not get you to any form of probability."[156]

102 I regard Professor Fox also as an impartial, widely read and impressive witness.

103 The remaining witness called by the defence was Dr George Crank. He holds a M.Sc (Organic Chemistry) from Queens University, Ontario, a Ph.D (Organic Chemistry) from Monash University and is a Chartered chemist. He has taught in universities for most of his career and for 20 years taught a post graduate course in chemical toxicology at the University of New South Wales.

104 Mr Adams took a similar objection to Dr Crank's evidence as Mr Gorton took to Professor Winder's evidence. I take the same view of the boundaries as I expressed in para 76. I take the view that Dr Crank is well qualified to speak about the chemical and toxicological effects of benzene and other solvents, but I disregard any medical opinions he offers as to the actual cause of the plaintiff's multiple myeloma. Toxicology, by definition, investigates the toxic effects of chemicals in humans and so there is a significant overlap between that discipline and medicine - the boundary, as I see it, commences when Dr Crank (or Professor Winder) moves from abstract epidemiology to the plaintiff and the actual cause of his current illness.

105 Dr Crank was provided with, among other documents, a history of the plaintiff's work practices (it varies slightly from the plaintiff's evidence; Dr Crank was told the plaintiff glued about 200 shoes daily and the gluing process took almost 50% of his working time)[157] the reports of witnesses Wolf, Fox, Sutcliffe, chemical files from Royal Melbourne Hospital, the National Safety Data Sheets and the analytical report of Intertek Probe dated 17 August 2009. Dr Crank's report became Exhibit D2.

106 Paragraphs 34 to 44 of Dr Crank's statement offer his endorsement or otherwise (and the reasons for same) of the opinions of Drs Wallouf and Sutcliffe and Professors Wolf and Fox.

107 Mr Adams took objection to this process; I doubt that it is truly objectionable except insofar as Dr Crank may have relied on medicine instead of toxicology in order to endorse or refute the opinions, and it does not appear to me that he has done this. There is substantial disagreement in the evidence on risk and causation and each witness, either directly or by implication, has commented on the validity of other witnesses opinions in any event.

108 Dr Crank reviewed the relevant toxicology literature and noted that different conclusions had been reached about the role of chemical exposure and multiple myeloma. He said however, that "...recently the literature has been reviewed by experts and definite opinions have been made"[158]

He then referred to the Bezabeh and Bergsagel studies of 1996 and 1999 respectively. Referring to the Bergsagel studies Dr Crank states:

...the authors conclude the following 'there is no scientific evidence to support a causal relationship between exposure to benzene or petroleum products and the risk of developing multiple myeloma

Dr Crank referred to a report by the Agency for Toxic Substances and Disease Registry, a department of the U.S. Government. In a June 2000 publication entitled "Case Studies in Environmental Medicine" - Benzene Toxicity it reported:

Several studies relate benzene exposure to a variety of tumours including multiple myeloma. Although this is plausible there is no scientific proof of such a relationship.

Dr Crank also referred to a paper by Y Takeuchi[159] which examined the general risk of cancer arising from chronic exposure to benzene. Takeuchi quotes figures for lifetime risks of exposure to benzene.

For example a person with 225 parts per million years would have an increased risk of from 1.4 to 9.6 depending on the statistical method used.

In relation to latency Dr Crank noted that in leukaemia produced by benzene exposure, the latency period was between 5 and 15 years with a median period of 9 to 11 years from exposure to diagnosis. Another report[160] he noted offered a mean latency period of 11.4 years.

On the issue of the plaintiff's actual exposure to benzene Dr Crank relied upon the Intertek Probe Report of 17 August 2009.[161] He expressed the opinion that the actual amounts of benzene in the Black Neoprene adhesive and the PA5000 were extremely low: 40 ppm and 80ppm. He compared these figures to petrol where benzene is present at greater than 10,000ppm or 1%.

He proposed that any significant exposure to benzene from the glues would require an enormous exposure to toluene and certainly bring on narcotic side effects; he offered a similar opinion in relation to n-Hexane. In the absence of significant solvent exposure symptoms Dr Crank thought that there could not have been significant benzene exposure.

In the summary to his report, Dr Crank was invited to go further and express an opinion as to whether the plaintiff's multiple myeloma was caused by his benzene exposure. For reasons I have explained I do not propose to act upon this. He concluded that the benzene content of the products was too low to be hazardous.

In evidence-in-chief Dr Crank was asked the following

You were asked to speak about the latency period between the exposure to carcinogenic substances and the development of cancer. Do you have a view, having looked at the papers yourself as to whether exposure to benzene is a risk factor for the development of multiple myeloma? --- Well, I was unable to find any convincing evidence in the scientific literature that it was.

There were some papers claiming a risk factor and other papers claiming no risk factor and there was a lack of sound scientific evidence linking the two.

When asked about the literature he had reviewed he said:

Yes. I went into this with an open mind looking for an opinion one way or the other and I was convinced that the weight of scientific evidence was against the proposition (that benzene was causative of multiple myeloma).[162]

Mr Adams put to Mr Crank that he was biased and he did not approach his task as a strictly scientific witness.[163] Like Professor Winder. I considered Dr Crank was a thoughtful and measured witness with no particular bias either way. I accept his evidence that he approached this with an open mind and only formed an opinion after reviewing the weight of the scientific evidence.

Dr Crank considered that it was biologically plausible that benzene exposure could lead to the development of multiple myeloma.[164]

109 I have embarked upon a relatively comprehensive review of the evidence because of its complexity and because, by and large, it is evidence that is based on the interpretation and application of epidemiological studies of others. These are epidemiological studies which have been pored over by the witnesses called and used as the foundation for their opinions, but which have been reproduced often only in snapshot form in this case.

110 The court in a case like this is not called upon to form an opinion of its own. Judges are not qualified to do so. This court cannot tell the plaintiff what has caused his illness any more than it can offer him treatment for it. All it can do is answer the question - has the plaintiff proved on the evidence before the court that his exposure to benzene has been a cause or material factor in the development of his plasmacytoma/multiple myeloma.

111 As I foreshadowed in para 23, a number of issues bear upon that issue of causation. I am satisfied on the evidence that it is at least highly possible, if not probable, that occupational exposure to benzene in significant levels increases the risk of a person developing multiple myeloma and by extension, plasmacytoma. The scientific community appears to be divided. Drs Wassouf and Sutcliffe, Professors Winder and Wolf, all argue for the "probable" conclusion on this issue.[165] All based their evidence on the published studies, as did Professor Fox and Dr Crank who argued against that conclusion. The published studies are also divided. Most of them are smaller studies and many of some antiquity. I accept that the meta-analyses which bring together the smaller studies offer more comprehensive and persuasive analyses. They too are divided. Infante proposes a risk factor of just over 2, but Bezabeh concluded the odds ratio approximated 1. Bergsagel found 'no causal relationship' and Sonoda concluded there was no significant association. As Professor Fox put it:

"You have three meta-analyses that say there is nothing there, and you have one that says there is something there"

Professor Winder was prepared to dismiss or at least devalue the studies that found there was no link. These were, he said, merely examples of a lack of the 95% satisfaction required for statistical certainty. It is hard to see how this sits with the Bezabeh positive finding that no increased association was found between benzene exposure and multiple myeloma and that the odds ratio approximated 1 (ie the same as the normal population). The major meta-analysis, relied on to establish the link, was Infante whose risk factor (of 2) was based upon Fu's study of the Florence cohort. As observed earlier, the exposure of those workers was to very high levels of benzene that was a component of the glue, not merely a contaminant of other solvents in the glue. The other meta-analyses dealt with less intense exposure but found no causative link.

112 Even if it could be concluded that very high exposures to benzene did increase the risk of developing multiple myeloma I do not consider that the plaintiff has proved in this case, that his exposure to benzene increased his risk of developing the illness. The foundation of the arguments for such a relationship rest with Infante, who in turn relied on the Fu study of the shoemakers from Florence.

113 As I have indicated earlier I accept that for 39 months the plaintiff was directly exposed to either PA5000 Adhesive or Black Neoprene Adhesive for approximately 5 hrs 20 minutes of an eight hour day. I accept that that exposure was to fumes from those adhesives entering his breathing space. I accept that the concentrations of benzene in those glues was 40 to 80ppm and that the presence of benzene in the breathing space was no less than 0.4ppm, but not as high as 1ppm/twa.

114 It follows that I consider that the plaintiff's exposure to benzene was less (on a time weighted average) than that prescribed by the Australian Standard (1ppm twa for an 8 hour day) and at a level that, when compared to the Florentine shoemakers, can only be described as miniscule. The relevant glues used by the plaintiff were between 17500 and 8750 times less concentrated with benzene than the glues used by the Florence cohort (up until 1963).

115 There is no epidemiological evidence that there is any increase in the risk of developing of multiple myeloma at the levels to which the plaintiff was exposed, or at anywhere near those levels. The evidence is in fact to the contrary

"Yes, but they failed to find (the risk) when they brought the concentrations down"[166]

Professor Fox when making this statement was referring to the three meta-analyses Bezabeh, Bergsagel and Sonoda.

116 Whilst not determinative in itself, the time taken between the employment period and the diagnosis of the plasmacytoma supports a lack of association between the benzene exposure and the plainitff's plasmacytoma/multiple myeloma. The plaintiff commenced work with the defendant in November 2002 and ceased in February 2006. His plasmacytoma was diagnosed in February 2008. Thus any potential latency period is between 2 years and 5 years 3 months. All witnesses were hamstrung by a relative lack of research on this issue (and on the broader issue of benzene/multiple myeloma risk generally) however the plaintiff's treating haematologist/oncologist Associate Professor Wolf, considered that this latency period was at the extreme low end of the range[167] even assuming that the tumour came into existence almost at the commencement of the plaintiff's exposure.

117 I consider that the plaintiff has failed to prove that his risk of developing multiple myeloma was increased by his actual exposure to benzene in his workplace. It follows that no Bennett and Naxakis process of reasoning ought be undertaken, predicated as it is upon a finding of actual increase in risk to the plaintiff.

118 Mr Adams argued that the causation issue was proved by direct opinion evidence and that the plaintiff only relied on the Bennett and Naxakis process of reasoning "if necessary". I have indicated that I consider that the toxicologists' expertise does not extend to offering opinions on what is ultimately a medical issue, although their evidence on toxicological risk is obviously relevant to such an opinion expressed by an expert medical witness. Of the medical witnesses who were prepared to offer such an opinion, for reasons already expressed, I am not prepared to accept Dr Wassouf or Dr Sutcliffe as offering properly informed opinions. Dr Wassouf's opinion seemed to have been formed before he conducted selective reading designed to support it. It will be recalled that[168] in August 2008, he did not feel qualified to offer an opinion and recommended seeking the advice of an industrial oncologist, but by late October 2008 he felt qualified to offer an opinion. He looked "for the positive side effect, not the negative. [He] just stopped there." Dr Sutcliffe's opinion was initially expressed as causation arising from exposure to "hazardous substances", was then predicated upon a several times greater estimate of the ppm benzene concentration in the breathing space than that that I have found, and in the absence of having "a clear picture of the latency period." Associate Professor Wolf, as indicated earlier in this judgment, expressed a causative link between the plaintiff's benzene exposure and his illness as a high possibility and did not clearly express it as a probability.

119 I consider that any properly expressed opinion on an issue such as this must be based on biological plausibility, an understanding of the actual levels of exposure, an understanding of the latency periods and a broad reading and understanding of the epidemiology studies. I am not satisfied that the opinions of Drs Wassouf and Sutcliffe on causation were based soundly on these considerations and I do not accept them. I consider both the evidence of Professor Fox and Associate Professor Wolf was based upon a sound reading and understanding of the issues and although their opinions differed, neither was prepared to elevate the causative link to greater than a possibility. Both opinions were necessarily hamstrung by the relative lack of research in the area. Associate Professor Wolf's opinion must also be qualified by the fact that there is no study that has found an increase in risk at the low levels of exposure that I have determined. For these reasons, and the reasons expressed in paragraphs 110-118, I am not satisfied that benzene exposure at the levels and for the duration that I have found was a cause or contributing factor in the plaintiff's development of plasmacytoma or subsequent multiple myeloma.

120 Given my findings it is unnecessary to consider whether the plaintiff's plasmacytoma and multiple myeloma was a reasonably foreseeable consequence of the defendant's wrongdoing.

121 The Asthma Case proceeded as an assessment of damages. From November 2002 to February 2006, the plaintiff was subjected to solvent fumes emanating in large part from the washing and gluing process described earlier. He was not offered any breathing apparatus and when he had the temerity to complain, Mr Palmone Jnr assaulted him. Dr Wassouf describes the plaintiff as developing a cough and wheezing in November 2004, which persisted thereafter, the symptoms varying in intensity but becoming worse up until the time the plaintiff ceased work in February 2006.[169] A diagnosis of asthma was made. Dr Wassouf provided a letter to the defendant which strongly recommended that the plaintiff avoid working with glue. This letter was ignored by the defendant.

122 In February 2006, when he last worked, the plaintiff was complaining of shortness of breath. On examination, Dr Wassouf found his lungs to be congested and wheezy.[170] Medication was prescribed and another certificate was provided, recommending again that he not be exposed to glue fumes. He left work on 22 February 2006 and has not worked since.

123 Dr Wassouf, on 17 March 2006, thought the plaintiff's physical symptoms had improved in the month or so since he had ceased work. The plaintiff had no respiratory symptoms prior to his work at Palmone Shoes. Dr Wassouf was then of the opinion that the plaintiff's condition was permanent, but would only flare up if exposed to glue fumes. Dr Wassouf thought then that the plaintiff had a capacity for duties "which do not involve glue fumes". The plaintiff's condition was under "good control with ... medication". The medications prescribed were bronchodilatory (Ventolin) and a preventer (Alvesco).

124 By July 2006, Dr Wassouf reported to the workers compensation insurer:

Mr Karam has developed a state of anxiety and distress as a result of his illness, loss of job and reduction of his wages by the WorkCover insurer. His asthma got worse and he became restless, nervous, cannot sleep and cannot concentrate. He tried to look for an alternative job, but was hindered by other medical conditions like poor vision and back pain ...[171]

It has been established that the exposure to glue fumes which he has been dealing with at work for many years contributed to his current condition. The development of anxiety, stress and frustration is indirectly related to his employment ... The plaintiff is not able to perform any work. His incapacity is totally related to his employment as a shoemaker dealing with irritating glue over many years.[172]

Dr Wassouf thought the level of distress was such that the plaintiff was not ready to participate in a rehabilitation program.

125 By October 2006, Dr Wassouf thought the plaintiff's psychological instability played a major role in his then incapacity. He had been referred to a psychologist, Dr Fox, who reported only slow improvement to treatment - "not encouraging", considered Dr Wassouf. Dr Fox continues to treat the plaintiff.[173]

It is to be noted that this level of distress was observed 16 months before any diagnosis of plasmacytoma. Dr Wassouf observed that, understandably, the plaintiff's level of distress became worse after his cancer diagnosis,[174] although antidepressants were prescribed in August 2007 and I accept that his pre-cancer level of distress was sufficient to preclude him from undertaking any work.

126 The plaintiff was evaluated by Dr Kaplan, a psychiatrist, at the request of his solicitors. He gave a history of becoming intensely anxious[175] since developing his respiratory problems. Prior to being diagnosed with multiple myeloma, he experienced suicidal thoughts, however since this diagnosis, he has become frightened of death. He complained of insomnia, diminished appetite and libido and social avoidance, although I am unable to determine whether these were pre or post cancer diagnosis symptoms.

127 Dr Kaplan's view was that the asthma condition gave rise to an Adjustment Disorder with Mixed Anxiety[176] and Depressed Mood as a result of his respiratory condition, the way he was treated by his former employer and the assault by his employer's son.

His psychiatric condition has been aggravated by the more recent diagnosis of multiple myeloma.

He is likely to remain prone to depression and anxiety as long as his respiratory condition persists, and his depression is likely to intensify if his multiple myeloma progresses.

128 The defendant tendered reports from Professor Richard Pain, a respiratory physician.[177] Professor Pain saw the plaintiff twice. In March 2007, he confirmed the diagnosis of asthma and that it was ongoing, but satisfactorily controlled with medication. He thought that the "occupational asthma in response to polyurethane exposure at work" had symptomatically improved since the plaintiff ceased work and received therapy. "He could work in suitable 'protected' environments". This was from a physical perspective only and Professor Pain stated that he was not qualified to comment on psychological aspects.

129 In May 2009, Professor Pain saw the plaintiff again. The plaintiff was clearly "agitated and depressed"and refused to undergo simple spirometric lung tests. "He had difficulty providing a coherent history". He was not distressed by climbing onto the examination couch and auscultation of his lungs demonstrated normal breath sounds.

130 Professor Pain thought the plaintiff's asthma was either in remission or well controlled by medication. He said, "The present clinical examination which is essentially normal in terms of the respiratory system does not allow me to positively state that he has asthma now". He accepted that from a physical perspective, there is an ongoing limitation for working in certain occupations which would expose the plaintiff to dusts, fumes, extremes of temperature or which demanded heavy physical exertion.

131 Sadly, it becomes necessary, in assessing damages, to try to reach an understanding of the plaintiff's life expectancy. The evidence about this was uncontradicted and came solely from the plaintiff's treating haematologist and oncologist, Associate Professor Wolf. The plaintiff has so far declined treatment but proposes to receive treatment shortly.[178] In the absence of treatment, the plaintiff's life expectancy is between six months and two years.

132 With treatment (which will consist of intravenous chemotherapy or thalidomide in combination with corticosteroids), the plaintiff "can have a good quality of life and have a life expectancy of eight to ten years or even longer". Eventually, the disease recurs and complications can develop.[179] In evidence, Associate Professor Wolf expanded on this. Two thirds of patients with multiple myeloma have a good response to the initial treatment.[180] He did not know whether the delay in seeking treatment would make it less effective.[181] Treatment will take six to eight months.[182]

The plaintiff would be unfit for any employment for that time.[183] If he were in good health, otherwise, he might get back to work after six to eight months.[184] A normal remission period after treatment is three to five years, after which the same sort of treatment is offered again.[185] Some will get back to work after the second treatment.[186] Associate Professor Wolf repeated that overall, the plaintiff's life expectancy is now eight to ten years.[187]

133 In cross-examination, Mr Gorton established the unsurprising proposition that any psychiatric reaction the plaintiff had to his diagnosis of cancer and his treatment would compromise his work capacity during remission. In the absence of asthma and its psychological sequalae, or of a disabling psychiatric reaction to his cancer, he would start work part-time and build up hours, avoiding heavy lifting in the process.

134 In summary, in this part of the case I make the following factual findings.

• The plaintiff has suffered asthma as a consequence of exposure to fumes at his workplace.

• His asthma is now well controlled with medication, but no doubt it was unpleasant and debilitating from 2004 until after he ceased work in 2006.

• His asthma is permanent, in the sense that absent medication, or in the presence of fumes, extremes of temperature or dust it is likely to flare up.

• The plaintiff has suffered a significant psychiatric/psychological reaction to his asthma illness. This reaction is an "Adjustment Disorder with Mixed Anxiety State and Depressed Mood".

• The plaintiff has been incapable of any form of work since February 2006, initially, and for a short time, as a direct result of his asthma. His mental state since about the middle of 2006 is such as to preclude him from any form of work.

• The plaintiff's psychiatric state has obviously been affected by his cancer diagnosis, but I do not accept that it has been overwhelmed by it. "Aggravated" is the word used by Dr Kaplan.

135 The plaintiff is a single man, aged 50, who since his asthma illness, I accept, has led a solitary life. He no longer socialises, has given up playing the lute at social functions, and leads an illness focussed life. It is impossible to quantify, with any precision, the impact the asthma and psychological sequalae have on his current state, but I accept it is significant.

136 Counsel for the Defendant submitted that pain and suffering damages for the asthma condition and its relevant consequences ought be assessed at $75,000 to $100,000. The plaintiff's counsel declined to make submissions on this aspect. In my opinion, the range suggested by the defendant is too low and does not give proper expression to the relative permanency of the asthma condition or the significance of the psychological sequalae. I assess the plaintiff's pain and suffering damages at $150,000.

137 The plaintiff is entitled to damages for loss of earning capacity caused by the negligently occasioned asthma condition and its sequalae. In assessing this amount, both from the date of injury to the date of trial and into the future, I am required to take into account the plaintiff's plasmacytoma/multiple myeloma. This is an unrelated illness (to the asthma) which has limited or eliminated the capacity of the plaintiff to earn income.

138 The High Court is Malec v J C Hutton Pty Ltd[188] laid down the approach to be adopted in these circumstances

When liability has been established and a common law court has to assess damages, its approach to events that allegedly would have occurred, but cannot now occur, or that allegedly might occur, is different from its approach to events which allegedly have occurred. A common law court determines on the balance of probabilities whether an event has occurred. If the probability of the event having occurred is greater than it not having occurred, the occurrence of the event is treated as certain; if the probability of it having occurred is less than it not having occurred, it is treated as not having occurred. Hence, in respect of events which have or have not occurred, damages are assessed on an all or nothing approach. But in the case of an event which is alleged would or would not have occurred, or might or might not yet occur, the approach of the court is different. The future may be predicted and the hypothetical may be conjectured. But questions as to the future or hypothetical effect of physical injury or degeneration are not commonly susceptible of scientific demonstration or proof. If the law is to take account of future or hypothetical events in assessing damages, it can only do so in terms of the degree of probability of those events occurring. The probability may be very high - 99.9 per cent - or very low - 0.1 per cent. But unless the chance is so low as to be regarded as speculative - say less than 1 per cent - or so high as to be practically certain - say over 99 per cent - the court will take that chance into account in assessing the damages. Where proof is necessarily unattainable, it would be unfair to treat as certain a prediction which has a 51 per cent probability of occurring, but to ignore altogether a prediction which has a 49 per cent probability of occurring. Thus, the court assesses the degree of probability that an event would have occurred, or might occur, and adjusts its award of damages to reflect the degree or probability. The adjustment may increase or decrease the amount of damages otherwise to be awarded. The approach is the same whether it is alleged that the event would have occurred before or might occur after the assessment of damages takes place. (Citations omitted).

139 Thus a distinction is drawn between proof of historical facts (to which the civil standard applies) on the one hand and past and future hypothetical situations and events on the other (to which the civil standard does not apply).

140 In Seltsam[189] Ipp JA (with whom Mason P agreed) held that Malec required the application of the following principles:

(a) In the assessment of damages, the law takes account of hypothetical situations of the past, future effects of physical injury or degeneration, and the chance of future or hypothetical events occurring.

(b) The Court must form an estimate of the likelihood that the alleged hypothetical past situation would have occurred.

(c) The Court must form an estimate of the likelihood of the possibility of alleged future events occurring.

(d) These matters require an evaluation of possibilities and are to be distinguished from events that are alleged to have actually occurred in the past, which must be proved on the balance of probabilities.

141 Recently in this Court these principles have been applied by J Forrest J in Acir v Frosster[190]

142 Another issue of principle has arisen concerning the treatment (in the pecuniary loss sense) of the plaintiff's independent supervening illness of plasmacytoma/multiple myeloma. In Jobling v Associated Dairies Limited,[191] Lord Bridge said

But when the supervening illness or injury which is the independent cause of loss of earning capacity has manifested itself before trial, the event has demonstrated that, even if the plaintiff had never sustained the tortious injury, his earnings would now be reduced or extinguished.

143 The same principle has been applied in Australia for many years. In DNM Mining v Barwick[192] Giles JA (with whom Santow JA and Windeyer J agreed) said:

Since the Court acts on facts rather than speculation where it can, if prior to the hearing there has been an event which would independently have caused loss in whole or part of the lost earning capacity, that event must be taken into account in determining the duration or extent of the exercise of a lost earning capacity and so in arriving at the plaintiff's damages.

144 Again recently this principle has been applied in Victoria in Acir v Frosster Pty Ltd.[193]

145 Counsel for the plaintiff sought to adopt Particulars of Special Damages and Particulars of Loss of Earning Capacity ("the Particulars") as representing the submissions of the plaintiff on both past loss and loss of future earning capacity. More recently, I have been supplied with a revised set of particulars which (a) correct some arithmetical errors in the original set and more importantly (b) provide updated net weekly wage figures. I understand that the net weekly wage rates (inclusive of superannuation) are agreed as follows:

146 The plaintiff's particulars were filed in respect of both the cancer case and the asthma case as one document, with the one proposed figure for past economic loss - $105,649 with interest at PIR on past loss claimed at $9099.

147 The defendant, whilst agreeing with the wage rates cited above, argues that the plaintiff's past economic loss ought be confined to the period February 2006 to February 2008.

148 It is implicit in the defendant's submissions that as at February 2008, the plaintiff's asthma condition was such as to preclude him from working but that the independent event of the cancer had supervened and would have destroyed the plaintiff's work capacity independently of his asthma condition.. For the defendant to contend that the plaintiff is not entitled to past loss from February 2008 onwards, I consider that I would need to be completely satisfied that his cancer and associated psychological disturbance would have excluded him from employment immediately. Put another way, I would need to be satisfied that he had no chance of working from this date onwards. I am not satisfied of this. From a physical perspective, the cancer has so far produced few symptoms

"There are no physical signs related to his malignant tumour at this stage. (Dr Wassouf, 15 August 2008)

"Mr Karam has mild physical symptoms arising from his multiple myeloma. (Dr Wassouf, 16 November 2009)

"He complains of painful areas in his body, particularly the pelvic bone and legs. (Dr Wassouf, 16 November 2009)

When asked about the plaintiff's work capacity insofar as the asthma was concerned, Dr Wassouf (in November 2009) expressed the view that the asthma and associated psychological condition rendered the plaintiff not fit for any duties. He was also of the view that, looking into the future, the plaintiff's cancer treatment and associated stress would preclude him from employment

During this period (the period of treatment) which could last several years Mr Karam would be severely incapacitated and unable to work. Furthermore, the stress related to his condition is severely disabling and will prevent him from engaging in any form of employment

I understand in this passage that Dr Wassouf is referring to the future and not the past.

149 In relation to past economic loss, the plaintiff is entitled to be compensated for the entire past loss between February 2006 and February 2008. That much is agreed between the parties. I calculate this part of past loss (on the inclusive of superannuation net weekly wage agreed) at

150 An assessment of past loss after February 2008 involves an assessment of the chance of the plaintiff, absent his asthma and psychological sequalae, working on in the face of his cancer diagnosis. March 2008 to mid January 2010 is a period of approximately 98 weeks. In that time, had he have been able, the plaintiff would have earned $57,187 net made up as follows:

(b) 1 July 2008-30 June 2009 52 weeks at $555.96 net per week $28,910

151 I have reviewed the plaintiff's physical capacities in this period at paragraph 148. I do not consider them to be of such magnitude that, in themselves, they would have prevented him working during this period. I do consider, however, that given the degree of psychological reaction to the plaintiff's much milder illness of asthma, that the chances of him working much beyond February 2008 have to be tempered considerably by his vulnerability to bad news. Obviously the chances of a psychological reaction to cancer precluding the plaintiff from work increase as the months roll on from February 2008. It is impossible to quantify this chance by any more than impression and intuition. I think it is appropriate to discount the plaintiff's past loss from February 2008 to 17 January 2010 by 60%, Accordingly, I allow the plaintiff 40% of $57,187 for this period.

I award the plaintiff $22,875 for the loss of the chance that he would have worked during the period February 2008 to date.

152 In total therefore I award the sum of $73,753 for past economic loss. This figure represents $50,878 total past loss to 28 February 2008 together with $22,875 for the loss of the chance of working since that date to the present[194].

153 The plaintiff's chances of returning to work, absent asthma and psychological sequalae, I assess as modest. Contingencies that impact upon the chances of his return to work in these circumstances are as follows:

• He has a 67% chance of a positive response to the initial treatment. In other words there is a 33% chance of an adverse outcome which would preclude him from working again.

• Assuming a positive response there is a lesser chance of a second treatment being successful. This treatment would be required after approximately 3 to 5 years.

• Any return to work would need to be initially on a part-time basis, of light nature and graduated, if possible, up to full time hours.

• Any return to work would need to be delayed by at least 6 months to enable treatment and recovery to occur.

• Any return to work may be precluded by a psychiatric reaction to his cancer of the same or greater degree than that which he suffered to his industrial asthma. It is impossible now to measure what degree of his current mental state is due to asthma or cancer, but it seems clear that the fact of the diagnosis of his cancer has significantly aggravated his psychiatric illness. Absent the asthma psychological/psychiatric sequalae, there must be a very significant chance that a response of similar or greater magnitude would have occurred consequent upon his cancer diagnosis. Dr Wassouf certainly foreshadowed such a reaction.

• The normal vicissitudes of life, above and beyond the above contingencies.

154 In discussion and encouraged by a question from the bench, Mr Gorton submitted that if there were to be any allowance for future economic loss (which the defendant opposed), it would be a modest amount awarded either for the loss of chance of future employment or to reflect the chance of less remunerative employment both as contemplated in Victorian Stevedoring v Pty Ltd v Farlow.[195] The plaintiff made no separate submissions on future loss of earning capacity relating to the asthma case.

155 I considered assessing this aspect on the more transparent Malec basis but am of the view that the number of contingencies that impact upon any return to the work force (absent asthma and psychological sequalae) taken in combination make such a calculation inordinately cumbersome and confusing. I am of the view that the plaintiff, after treatment, may possibly have been able to work at least in a part-time capacity for 3 or 4 years, subject of course to his being able to deal with his cancer related psychological problems. I assess that loss of chance at $12,000, together with a further $1000 which represents the loss of chance to earn superannuation in this period.

156 Thus I assess damages for future loss of earning capacity at $13,000.

157 The total amounts of taxation paid or worker's compensation payments is $7,453. This figure is not in issue.

158 I have reached the following conclusions in relation to the plaintiff's claims:

(a) The plaintiff's plasmacytoma and subsequent multiple myeloma is a serious injury within the meaning of the Act.

(b) The plaintiff has failed to prove that his employment with the defendant was a cause of or material contributing factor in his development of plasmacytoma and subsequent multiple myeloma.

(c) As a consequence of the defendant's negligence the plaintiff has developed industrial asthma and a significant associated psychological condition.

(d) The plaintiff's damages in the asthma case are to be assessed at $244,296.

(e) The plaintiff is entitled in the asthma case to judgment in the sum of $244,296, together with any interest that may be awarded on past economic loss.

(f) Subject to hearing from counsel I propose to give judgment in favour of the plaintiff in the asthma case of that sum together with any interest that the plaintiff may be entitled to in respect of past economic loss.

(g) I propose to give judgment in favour of the defendant in the cancer case.

[14] They are described in considerable detail at T 20-T 43.

[15] In other words up to 5 hrs 20 minutes every day were occupied that way. See T 43.

[16] The Safe Work Australia national standard on a Time Weighted Average, for an 8hr day was 1 part per million.(1ppm)

[17] In particular Regulations 302(2), 308(1), 312, 313(1)(b), 313(1)(c), 313(2), 313(3), 315 and 316(1).

[18] The defendant disputes that the atmospheric concentration of benzene was greater than 1ppm. This is the subject of consideration later in these reasons.

[19] [1999] HCA 22; (1999) 197 CLR 269, at para [31].

[20] [2007] VSCA 16, at para 20.

[21] Which consisted largely of epidemiological studies and medical opinions based on them.

[28] Halo Primer was not found to have any measurable benzene content. Ng/g translates to parts per million (Exhibit D2 para 56); Exhibit P13 p 14.9.

[32] Mr Pinda was referring to the solvents in the glue itself i.e. acetane, tolueme, MEK and the aliphatic petrol solvents.

[44] The tests were conducted for the purposes of the asthma case. The plasmacytoma had not been diagnosed as at December 2007.

[46] Exhibit D3 page 1. The full testing regime is set out in the exhibit.

[47] White Neoprene Adhesive was used on some shoes - its constituents are effectively the same as Black neoprene which was also used. T 441.

[65] See Exhibit D3, appendix (i), specifically photos 2, 13.

[70] Meta-analyses are comprehensive studies where the results from previous smaller studies are gathered together and analysed.

[71] "Benzene Exposure and Multiple Myeloma - a Detailed Meta-Analysis of Benzene Cohort Studies" by Peter Infante. Exhibit P18.

[74] See paragraph 13 of these reasons.

[76] Report of 27 October pps 4ff; references are contained with Exhibit P9.

[77] He also referred to other studies that dealt with the broader cytogenic and haematological studies. The complete references for these studies are annexed to these reasons.

[85] Exhibit P9, at the bottom of the 3rd page of the report of 27 October 2008.

[88] Exhibit P11, report 24 October 2008 p 2-3.

[104] Other than perhaps the studies that have found no link are funded by "the powerful petroleum industry lobby." (Exhibit P12, p 5).

[106] Australian Faculty of Occupational Medicine.

[123] That is, a relative risk of four times the norm.

[131] Exhibit P13, p 10. The full references can be found at footnotes 13-20 of Professor Winder's report.

[133] The witness explained this further at T335-336.

[134] From the later context in the paragraph, I infer that the witness is speaking of a Time Weighted Average over an eight hour shift. See Exhibit P13, pp 11-12.

[137] Exhibit D4 comprises five statements from Professor Fox.

[138] Associate Professor Wallin was not called as a witness. Neither side made any submissions as to his absence and I draw no conclusions from it.

[140] The Florence cohort was 2008 shoemakers.

[143] Exhibit D4, report of 15 September 2009.

[144] The "16/12/08" CT scan was in fact dated 16/2/08. This is a typographical error in Professor Fox's report. He comments further on about the (correct) 4½ month period between scans.

[148] T399 ff. It subsequently became Exhibit P17.

[153] T417. In fact either 40 or 80 ppm, depending on the glue.

[157] Exhibit D2 page 2. I do not regard this variation as significant.

[159] Health Effects from Exposure to Chronic Levels of Industrial Chemicals 2004, in Encyclopaedia of Life Support Systems.

[160] S.N.Yin et al, British Journal of Industrial Medicine (1978).44 (2).

[165] On the issue of actual causation though Professor Wolf did not really go beyond high possibility - "C plus".

[169] Exhibit P9, report of 17 March 2006 p 1.

[170] Exhibit P9, report of 17 March 2006 p 1.

[171] Exhibit P9, report of 24 July 2006, p 1.

[172] Exhibit P9, report of 24 July 2006, p 2.

[173] Exhibit P15, report of Dr Kaplan pp 2-3.

[175] Exhibit P15, report of Dr Kaplan dated 28 October 2009, p 5.

[176] Exhibit P15, report of Dr Kaplan dated 28 October 2009, p 7.

[179] Exhibit P11, report of Associate Professor Wolf dated 9 November 2009.

[188] [1990] HCA 20; (1990) 169 CLR 638, 642-3.

[189] [2000] NSWCA 29; (2009) 49 NSWLR 262.

[190] [2009] VSC 454 at para 263ff.

[191] [1981] UKHL 3; [1982] AC 794.

[192] [2004] NSWCA 137, [39].

[194] In his revised particulars, the plaintiff claims a figure for interest on past economic loss. I will consider submissions on interest at the further hearing of the matter.

[195] [1963] VicRp 80; (1963) VR 594.

[196] [1981] HCA 41; (1981) 148 CLR 438.