HEARD : 24, 26-28 SEPTEMBER, 2-5, 8-11, 15, 17 & 18 OCTOBER 2007 (FINAL WRITTEN SUBMISSIONS FILED 4 DECEMBER 2007)

Torts - Negligence - Personal injury arising from exposure to asbestos - Whether duty of care exists - Defendant manufacturer or supplier of cars with brake linings containing asbestos and supplier of such brake parts - Whether risk of injury to professional mechanics foreseeable

Torts - Negligence - Personal injury arising from exposure to asbestos - Whether breach of duty of care - Whether reasonable care called for defendant to give warnings - If so, to whom, in what form and by what means

Torts - Negligence - Personal injury arising from exposure to asbestos - Causation - Whether plaintiff's pulmonary fibrosis arose from exposure to asbestos or is idiopathic

1 The plaintiff suffers from serious fibrosis of his lungs. The plaintiff's case is that his condition is asbestosis and that it was caused by his exposure to asbestos in the course of his work as a motor mechanic. Asbestosis is, by definition, pulmonary fibrosis caused by asbestos. The defendant's case is that the plaintiff's condition is not asbestosis but is a pulmonary fibrosis of unknown cause (termed idiopathic pulmonary fibrosis).

2 The defendant manufactures Ford motor vehicles. It is common ground that during the period 1970 to 1987 (the relevant period) Ford motor vehicles had brake linings which contained asbestos.

3 The plaintiff worked as a motor mechanic for two Ford dealerships in Western Australia from 1970 to 1987.

4 The plaintiff claims damages for the tort of negligence. He claims that his asbestosis was caused by the failure of the defendant to warn of the dangers of working with brake linings containing asbestos and of the need to take measures to prevent or minimise the release and inhalation of asbestos dust and fibres.

5 The defendant raises issues in relation to all three of the elements of the tort of negligence: duty, breach and causation. The major groups of issues arise in relation to the questions of duty and of causation.

6 The parties have agreed the quantum of damages at $840,000.

7 It is convenient to begin by outlining some background facts, which are largely uncontroversial, before turning to the pleadings to identify the issues raised.

8 The plaintiff was born on 9 July 1949 in Sicily. He left school at the age of 11 and commenced an apprenticeship as a motor mechanic. His apprenticeship was with a motorcycle dealership. He continued working there until 1970. He was not aware of any exposure to asbestos in that employment and none was suggested in evidence at the trial.

9 There is no evidence of any specific exposure to asbestos outside the plaintiff's work as a mechanic from 1970 onwards.

10 In 1970, when he was 20, he migrated to Australia.

11 After he arrived in Australia he obtained employment with Anderson Ford, then located at 151 Adelaide Terrace in Perth. He worked as a mechanic for Anderson Ford from 1970 to 1975.

12 For the first two or three years of his employment with Anderson Ford he worked in the main workshop. This was a large workshop where dozens of mechanics worked performing a range of repairs and services to vehicles.

13 There was no mechanical ventilation in the workshop.

14 A number of issues arose in the course of the trial as to the extent and frequency of the activities by which asbestos dust was said by the plaintiff to have been generated in the workshop. The evidence in this regard will be analysed in more detail later in these reasons. At this stage I propose only a general outline.

15 In the course of servicing cars, the brakes were checked. This did not occur on all services, but did occur for 'major' or 'big' services. In the course of checking the brakes, the wheels and brake drums were removed and both the brakes and the drums were blown with compressed air. (Dust from within the brake drums would be blown out in the course of this.)

16 In the 1970s and 1980s, Ford motor vehicles were fitted with brakes lined with a friction material that included asbestos, of the type known as chrysotile. There are two main groups of asbestos: serpentines, which include chrysotile, and amphiboles, which include crocidolite and amosite. The risk of contracting cancer from exposure to asbestos varies according to the type of asbestos fibre. Chrysotile gives rise to the least risk; then amosite, then crocidolite.

17 The friction material was embedded in resin and bonded to metal brake shoes for use in drum brakes. In the case of vehicles fitted with disc brakes, the friction material was bonded to a metal backing plate for brake pads used in the disc brakes.

18 The defendant led expert evidence that the heat generated in the course of the braking process caused the breakdown of the vast majority of the asbestos in the friction material into non-fibrous material including forsterite. This evidence will be referred to further when I give consideration to the question of the level of exposure of the plaintiff to asbestos.

19 In the course of servicing vehicles, brakes were also, on occasion, rubbed with emery paper, a rough sandpaper-like cloth. There is also mention in the evidence of the need, from time to time, to chamfer or file the edge of a new brake lining to ensure it fitted correctly.

21 For about two years, from 1973 to 1975, the plaintiff worked in a designated area known as the 'Quick Service area'. This was a smaller separate area with enough room for four vehicles.

22 As the name suggests, the purpose of the Quick Service area was for as many cars as possible to be serviced each day. A team of five men worked in the Quick Service area. One man was in the pit underneath the two cars, one man worked on the wheels, one man did the 'lubes', with another two doing the motors. There was also a supervisor.

23 Substantially the same tasks relevant to this case were undertaken in the Quick Service area. They were done in a more confined area and at a greater speed. The Quick Service area was very dusty.

24 The plaintiff did not know that the brake linings contained asbestos and did not know or believe that inhalation of the dust could be hazardous and that steps should be taken to reduce any exposure and inhalation. Nor did his workmates at Anderson Ford.

25 In 1975 the plaintiff left Anderson Ford. He moved to a small country town in Western Australia called Narembeen. For about six months he worked on a wheat farm, assisting his father-in-law.

26 He then returned to work as a motor mechanic. From late in 1975 until 1988 he worked as a mechanic for Col Commons & Son in Narembeen. Col Commons was a Ford dealership.

27 At Col Commons the plaintiff did a wide range of mechanical work. He worked primarily on cars and occasionally on trucks.

28 Compressed air was used to blow out the brakes of cars in the course of servicing them. If the brakes were glazed, emery paper was used to rub them down.

29 The workshop would be swept at the end of the day.

30 In 1988 the plaintiff left Col Commons and returned to Perth. He worked in a service station as a mechanic from 1988 to 1994. This service station did not service Ford vehicles exclusively.

31 In 1994 the plaintiff commenced worked at Tom's Auto Repair in Osborne Park as a mechanic. At Tom's Auto, different procedures were used in the course of servicing brakes. Brakes were washed out with water. Compressed air was not used.

32 When the plaintiff used compressed air on the first day of his job at Tom's Auto, his employer told him that compressed air was not to be used and that water was used instead. The employer said that compressed air was dusty and dangerous.

33 Before that, the plaintiff did not know (or believe) that exposure to brake dust and fibres was or might be dangerous and that measures should be taken to reduce the generation and inhalation of dust.

34 Until the late 1990s the plaintiff was an active man in good health. He enjoyed boating, fishing and gardening (among other things).

35 The plaintiff described that in the late 1990s he noticed that he would become tired and breathless.

36 His medical records (exhibit L) reveal that he saw his general practitioner Dr Angelo Carbone in March 1997 on account of coughing and having a wheezy chest. An antibiotic was prescribed and a description of the problem as 'bronchitis and bronchiolitis, acute' was recorded.

37 The plaintiff saw Dr Carbone again twice in July 1999. He described having been short of breath on exertion for two months. Bibasal crepitations (crackling sounds) were recorded as having been heard on examination.

38 In March 2000 he spent some days as an in-patient at St John of God Hospital in Subiaco. The records suggest that the reason for admission was that the plaintiff had been struck in the face by an object at work. Chest x-rays taken at this time were recorded as suggesting some changes in the left lower lobe consistent with bronchopneumonia.

39 The plaintiff referred in his evidence to having spent a week or so in St John of God Hospital. He thought that that was in 1998 but when questioned in cross-examination he was, understandably, unsure of the dates. He is likely to have been referring to his admission in March 2000.

40 In September and October 2000 the plaintiff saw Dr Bernard Hockings, a cardiologist. Medication was prescribed to attempt to lower the plaintiff's high blood pressure.

41 In the course of the year 2000, the plaintiff saw Dr Carbone on occasions. There were continued references to feeling tired and having a cough. Bibasal crepitations were recorded. Further chest x-rays were done.

42 There were considerable further investigations during the first half of 2001, including further radiological examination.

43 In June 2001 Dr Carbone referred the plaintiff to Professor Bruce Robinson, a consultant chest physician.

44 In July 2001 Professor Robinson diagnosed the plaintiff as suffering from asbestosis.

45 The plaintiff stopped work, because of his poor health, in September 2001.

46 The plaintiff has become substantially disabled from leading a normal life by his condition. He requires oxygen 24 hours a day. His breathlessness is continuing to get worse, as is his condition generally.

47 The defendant is, indirectly, a wholly owned subsidiary of Ford Motor Company (Ford US). There is and at all relevant times was also a Ford company operating in Britain called Ford Motor Company Limited (referred to at trial as Ford UK).

48 I turn to the pleadings and to the identification of the major issues in the trial of this action.

49 The plaintiff pleads that in the course of working as a motor mechanic at Anderson Ford between 1970 and 1975, and Col Commins between 1975 and 1987, he handled and cleaned asbestos brake linings and components and was exposed to and inhaled asbestos dust, particles and fibres.

50 In the particulars it is said that, in the course of servicing vehicles, the plaintiff would use compressed air to blow the dust from each brake drum, would inspect, remove and replace asbestos brake linings, and would handle asbestos brake linings by filing or grinding back the edges to enable them to be fitted into the brake drum. Further, it is said that his work duties included regularly dry sweeping the floor of the work areas after vehicles had been serviced. Fellow employees also cleaned, handled and worked with asbestos brake linings and components, and the plaintiff worked in the vicinity of these employees.

51 The defendant denies that filing and grinding occurred but otherwise admits that the alleged activities occurred, but without any admission as to the regularity or frequency of the sweeping.

52 The plaintiff puts his negligence case in two alternative ways. First, he sues the defendant as the manufacturer of the brake linings or of the vehicles fitted with the brake linings. Secondly, he sues the defendant as the supplier of the vehicles containing the brake linings and components and as the supplier of brake spare parts.

53 The defendant denies any role in the manufacture of any brake linings or brake components. It admits that various motor vehicles manufactured by it were fitted with brake linings containing asbestos but denies that any other brake component in vehicles manufactured by it contained asbestos.

54 The defendant admits that from time to time during the relevant period it supplied brake linings containing asbestos to its licensed dealers and distributors, but denies that it supplied any other brake component containing asbestos.

55 The alleged duties of care as manufacturer and supplier are pleaded in corresponding terms in par 6 and in par 10 of the statement of claim respectively. Each is built upon a foundation of what it is said that the defendant knew or ought to have known. In summary, it is pleaded that the defendant knew or ought to have known that:

(a) inhalation of asbestos fibres and dust was extremely injurious to human health and caused diseases including asbestosis, lung cancer and mesothelioma;

(b) the asbestos brake linings and components manufactured or supplied by it, or contained in vehicles manufactured by it, would, in the course of cleaning, handling and working, be likely to release asbestos fibres and dust;

(c) persons working as motor mechanics would be exposed to asbestos fibre and dust as a result of cleaning, handling or working of the brake linings and may suffer injury unless measures were taken to prevent or minimise the release and/or inhalation of asbestos fibres and dust;

(d) if the defendant did not provide warnings, it was unlikely that any sufficient measures would be taken to prevent the release of asbestos fibres and dust and inhalation by mechanics.

56 Three sets of detailed particulars have been provided of the facts relied upon in alleging that the defendant knew or ought to have known the matters pleaded in par 6 and par 10 of the statement of claim. I do not propose to detail them here.

57 The defendant admits that, by 1970, it knew that exposure to certain types of asbestos fibre, in sufficiently large quantities and duration, could cause asbestos related disease. However, it denies that it knew (or that it was the case) that exposure of the kind claimed by the plaintiff would, or could, increase his risk of contracting any asbestos related disease.

58 The duty of care said to arise as manufacturer or supplier of the asbestos brake linings and components or vehicles which included asbestos brake lining is pleaded in corresponding terms. In substance, the duty is said to be to take all reasonable care to give two categories of warnings: first, a warning to motor mechanics and/or their employers that handling, working and cleaning asbestos brake linings and components was extremely injurious to health and caused diseases including asbestosis and mesothelioma; secondly, to issue warnings to motor mechanics and/or their employers that it was essential that measures be taken when handling, cleaning or working with asbestos brake linings to prevent or minimise the release of asbestos dust and fibres into the atmosphere and their inhalation.

59 It can be seen, therefore, that the pleaded duty of care is in terms of a duty to warn, rather than a more general duty to avoid foreseeable risk of injury to mechanics.

60 It is then pleaded that the defendant negligently exposed the plaintiff to the risk of inhalation of, and to the actual inhalation of, asbestos dust and fibres. The particulars of negligence complain of five failures:

(a) the failure to warn the plaintiff and his fellow employees who cleaned, handled and worked with asbestos brake linings against using compressed air to clean brake drums, against filing and grinding asbestos brake linings and components, and against dry sweeping work areas in which asbestos brake linings and components were cleaned, handled and worked;

(b) failing to warn the plaintiff's employers, as receivers or purchasers of asbestos brake linings and components, against those matters;

(c) failing to advise the plaintiff and fellow employees of appropriate safety measures; namely using wetting or damping down cleaning methods; using an industrial vacuum cleaner with an adequate filter system; and using a respirator when handling, filing, grinding or cleaning asbestos brake linings and components;

(d) failing to advise the plaintiff's employers of those matters; and

(e) failing to warn the plaintiff, his employers and his fellow employees of the risks and dangers of asbestos inhalation, including the risks of asbestosis, lung cancer and mesothelioma.

61 It is pleaded that as a result of the alleged breaches of duty the plaintiff suffered injury, namely asbestosis and other problems.

62 The defendant denies that the plaintiff's injuries are caused by his inhalation of asbestos from brake linings manufactured or supplied by the defendant or by the defendant's negligence. Further, the defendant says that the plaintiff is not suffering from asbestosis but suffers from lung fibrosis of an idiopathic nature.

64 First, there are issues whether the defendant owed any duty of care to the plaintiff and, if so, issues as to the content of that duty. There are both factual and legal issues in that regard. The factual issues relate to what the defendant knew or ought to have known or foreseen as to the risks to motor mechanics arising from the presence of asbestos in brake linings.

65 Secondly, there are issues respecting the question of breach of any duty of care. Did reasonable care on the part of the defendant require it to give any warnings and, if so, by what means, in what terms, and to whom?

66 Thirdly, there are a number of issues concerning the question of causation. Most fundamentally, there is a diagnosis related causation issue: is the pulmonary condition from which the plaintiff suffers asbestosis, or is it of an idiopathic nature? The parties invite attention to evidence relating to a number of topics as being relevant to this question, including the following:

(a) evidence of lay witnesses, including the plaintiff, as to the activities which occurred in the course of the plaintiff's work as a motor mechanic, and the extent to which and circumstances in which he was, in that context, exposed to asbestos fibres;

(b) evidence from occupational hygienists who provided estimates of the level of exposure to asbestos fibres experienced by the plaintiff;

(c) expert evidence as to whether there was any threshold exposure level below which it is accepted that asbestosis will not occur;

(d) epidemiological evidence as to whether there is any association between work as a motor mechanic and the level of incidence of asbestos related diseases including mesothelioma, lung cancer and asbestosis; and

(e) expert medical opinion relating to whether the plaintiff's condition is asbestosis or is idiopathic in nature.

67 It is convenient to begin by making factual findings, based upon the evidence of the lay witnesses, in relation to the plaintiff's work as a motor mechanic and the frequency of those activities undertaken which gave rise to exposure to asbestos and associated topics. Thereafter, I propose to deal in turn with the issues of duty, breach and causation.

The plaintiff's work exposure to dust during the relevant period

68 The plaintiff gave evidence regarding his work environment at Anderson Ford and at Col Commons during the relevant period. He called four other witnesses who had worked at Anderson Ford: Mr Ian Hinkley, Mr Kenneth Hood, Mr Giuseppe (Joe) Lenzo and Mr Colin Bushby.

69 Mr Hinkley worked at Anderson Ford from 1969 to 1999. (At some stage during this period, subsequent to the plaintiff's departure from Anderson Ford, the business name changed to Centre Ford). Mr Hinkley was the supervisor of the Quick Service section for the whole of the time that the plaintiff worked at Anderson Ford.

70 Mr Hood worked for Anderson Ford from 1969 to 1979. Until 1974 he spent most of his time in the general workshop, with short periods in the Quick Service section. From 1974 to 1979 he worked in the Quick Service section. When Mr Hinkley was away, Mr Hood deputised as the Quick Service supervisor. Mr Hood was cross-examined on very few aspects of his evidence.

71 Mr Lenzo worked at Anderson Ford from 1968, where he started as an apprentice, until 1987. He spent some of his time in the Quick Service area and worked there with the plaintiff. He was not cross-examined.

72 Mr Bushby worked for Anderson Ford/ Centre Ford, for some 18 years. His recollection was that he started work at Anderson Ford in about September 1975. From his commencement at Anderson Ford he worked in the Quick Service area. He was unable to put a face to the name of the plaintiff and was, in the end, unsure of whether they had both worked at Anderson Ford at the same time (ts 343, 361 - 362).

73 The defendant submits that it should be concluded that Mr Bushby commenced work at Anderson Ford after the plaintiff left and that, consequently, his evidence is of no assistance. I accept the first part of that submission but do not accept the second part of it. The tenor of the evidence of the other witnesses who worked at Anderson Ford through the 1970s and 1980s seems to me strongly to support a conclusion that there were few, if any, changes of substance in the relevant work practices and environment between 1974 and 1975 and in the years shortly thereafter. Of course, if and to the extent that Mr Bushby's evidence is materially different in a given respect from the evidence of those working at the time the plaintiff worked, I would rely upon the evidence of those working with the plaintiff. However, insofar as Mr Bushby gave evidence which is generally consistent with the others, while fleshing out or explaining matters in more detail than other witnesses, it seems to me that Mr Bushby's evidence is of assistance.

74 Leaving aside the plaintiff, there was no suggestion, in cross-examination or submissions on behalf of the defendant, that any of the lay witnesses called on behalf of the plaintiff were doing other than giving their best recollection of the working conditions which they experienced and observed and of the other matters the subject of their evidence.

75 There was no challenge, in the course of cross-examination, to the credibility of the plaintiff. In closing submissions the defendant submitted that the plaintiff's estimates of the mix of work done and the number of cars worked on and matters of that kind were estimates 'made in hindsight with the obvious incentive of financial reward'. I do not consider that the plaintiff was influenced, in his evidence as to his work practices, by any tendency, conscious or unconscious, to maximise his exposure to dust in order to assist his case. In that regard his evidence was supported by and consistent with the other witnesses who worked at Anderson Ford. For example, other witnesses gave descriptions of the level and intensity of the dust which were as vivid and graphic as those given by the plaintiff.

76 Unsurprisingly, the witnesses' evidence was not to identical effect in all respects. On matters of detail, there were some differences.

77 On the basis of the evidence of the five witnesses, I make the following findings of fact in respect of the plaintiff's work at Anderson Ford.

78 From 1970 until 1973 (or perhaps late 1972) the plaintiff worked in the main workshop at Anderson Ford. In the main workshop there were 15 car bays and up to that number of cars would be worked on at one time. About 40 to 50 cars per day were done in the workshop.

79 Approximately 50% of cars serviced received what was called a 'big' service, with the other 50% having a 'small' service. Brake work was done on big services but not in the course of small services.

80 In the course of a big service, the brakes would always be removed, 'de-dusted' and checked. The de-dusting process involved removing brake drums, tapping them on the floor to remove some of the dust, blowing them out with compressed air and then blowing out the wheels with compressed air. The plaintiff described the generation of dust in this way in par 27 of his witness statement (exhibit 3A):

When I used compressed air to blow out the brakes it would generate large amounts of dust containing asbestos which would blow up into my face and stick to my clothes and hair. It would cause a cloud or haze in the air and fall down in the area where I was working. The dust would get stirred up as I worked in it. The same would happen when the men beside me blew out brakes too, or anywhere else in the building. Sanding and filing the shoes would also cause asbestos dust.

See also ts 287; the evidence of Mr Lenzo at exhibit 10 par 12; and the evidence of Mr Hinkley at ts 309 - 310.

81 If, on inspection, the brakes were glazed, they would be rubbed back with emery paper, so as to roughen them up and prevent squeaking (exhibit 3A par 25, see also ts 248 - 249).

82 Further details and descriptions of the process of rubbing brakes with emery paper were given by Mr Hinkley and Mr Bushby. The evidence was given in the context of work in the Quick Service section but seems to me to be of general application. Mr Hinkley said that emery paper was used in about 50% of brake services to give the pads and the drum 'a hell of a rub' which created 'tons of dust' (exhibit 5 par 30). See also Mr Bushby's evidence at ts 351, 368.

83 Sometimes, when a new set of brake shoes was being installed, the edge of the shoe and lining would be chamfered or filed off (see exhibit 3A par 27, exhibit 5 par 31 - Mr Hinkley; and the evidence of Mr Bushby at ts 349 - 350).

84 The workshop would be swept, generally at the end of the day, at least if time permitted.

85 The bulk of the detailed evidence regarding the plaintiff's exposure to dust related to the Quick Service section, to which I turn.

86 The Quick Service workshop was small and unventilated. A large number of cars were serviced each day. Several witnesses said that they would often service up to 40 cars per day. Mr Hood said that in Quick Service they got through about 40 cars per day (exhibit 9 par 8). He was not cross-examined in that respect. Mr Lenzo said that it was pretty common for them to get through 40 cars a day in Quick Service (exhibit 10 par 7). He was not cross-examined. See also Mr Bushby's evidence at ts 345.

87 The defendant's submissions fixed on evidence of the plaintiff, in cross-examination, to the effect that he estimated that it took them one hour to do a small service and three hours to do a big service. The defendant submits that 40 is an unrealistically high number of cars to service in one day.

88 The plaintiff's evidence as to these estimates was, it seemed to me, directed to the question of the expected or permitted estimate of time for these tasks upon which the charge to the customer was calculated. I refer to the plaintiff's evidence in re-examination (ts 290) and to the evidence of Mr Hinkley explaining the way in which those working in Quick Service were remunerated based upon the estimated or permitted time for the service (see exhibit 5 pars 11 - 14).

89 While no doubt the number of cars serviced in a given day varied, I accept that it was not uncommonly in the region of 40 and, at other times, somewhat less.

90 As in the main workshop, the processes of using compressed air to remove dust, sanding brake shoes and, from time to time, filing brake shoes all created dust in the Quick Service workshop.

91 Something more than half of the cars that came through the Quick Service section had their brakes checked, and thus de-dusted, using the compressed air as already described.

92 Mr Lenzo described the creation of dust in the Quick Service area. He said as follows (exhibit 10 par 12):

The way it actually happened is that you would pull the drums off and tap them on the floor and get all the dust out on the floor and then blow out the wheels and then you would even blow the dust away from around you. There was so much of that dumping of dust and blowing out during the day that as the day wore on there would be more and more asbestos dust around and you would be blowing out not just the dust out of the drum that you were taking out but all the other dust that had accumulated around you.

93 The brakes on about half of the cars having their brakes serviced would be rubbed with emery paper, as already described.

94 The evidence of all the witnesses who worked in the Quick Service area was to the effect that it was an extremely dusty environment. Mr Hinkley said that 'lots of dust was being blown up into the air and into the pit. There was heaps of dust and you could see it in the air. You would often get it in your mouth and your teeth and up your nose and in your hair and everywhere' (exhibit 5 par 34). See also the evidence of Mr Hinkley (exhibit 5 pars 29, 37), Mr Hood (exhibit 9 par 9), the plaintiff (exhibit 3A pars 37, 41) and Mr Bushby (ts 346, 354).

95 The room did not have any mechanical ventilation and had poor natural ventilation. There were walls on three sides of the room. One wall partitioned the Quick Service area from the main workshop. This wall was solid except for an area of mesh at the top. There were high windows on one of the other walls. Those windows opened only partially and did not allow much natural ventilation. See, in this regard, the evidence of Mr Lenzo (exhibit 10 par 8) and Mr Bushby (ts 343, 378).

96 The dust was not removed in the course of the day. Accordingly, and given the lack of ventilation, the dust accumulated in the course of the day.

97 There were regular complaints about the dust. In response, the only thing that was done was that some fans were provided. These provided some relief from the heat but merely kept the dust airborne without removing it.

98 Five men worked in the Quick Service section. One was on wheels. He was responsible for the work on the brakes. Another was in the pit. The person on wheels was most exposed to the dust. The pit was also very dusty. But the Quick Service workshop as a whole was a very dusty environment. Dust would cover Mr Hinkley's desk in the corner of the room.

99 The evidence in the witness statements was to the effect that the plaintiff rotated between the five tasks but spent a higher proportion of his time on the brakes because he was short and worked fast on the wheels. However, the evidence of both the plaintiff and Mr Hinkley, in the course of cross-examination, was to the effect that the plaintiff did one week in five on the wheels. See the plaintiff's evidence at ts 267 and Mr Hinkley's evidence at ts 306 and, especially, at ts 308, where Mr Hinkley was asked, in plain terms, whether the plaintiff took his part in the rotation and did one week in five like each other person, to which he answered yes. I have not overlooked the evidence of Mr Hinkley in re-examination at ts 317 - 321, upon which reliance is placed by the plaintiff. However, I am not satisfied that the plaintiff spent the majority of his time on wheels, although he may well have spent a little more time in that role than in other roles.

100 The accumulated dust was, generally, swept once a day, mostly at the end of the day. If time did not permit sweeping to occur at the end of the day this may be done in the morning. There was also evidence that, at least on some occasions, a hose was used in the sweeping process.

101 Disc brakes were also de-dusted with compressed air. However, they did not accumulate dust to the same extent, and so released less dust in the process of cleaning.

102 Some attention was given, in the evidence and in cross-examination, to the question of the relative proportion of cars serviced which had disc brakes as distinct from drum brakes.

103 By the mid-1970s virtually all new Ford vehicles had disc brakes installed on the front wheels. However, according to Mr David Ford, a witness called by the defendant, there would, in that period, still have been 'lots and lots' of vehicles with drum brakes at front and back (ts 734).

104 The evidence of those who worked at Anderson Ford as to the distribution of drum brakes and disc brakes in the first half of the 1970s was not consistent. Mr Hinkley and Mr Hood said that most cars had disc brakes at the front (ts 314, 317, 332). The plaintiff thought that the majority of cars, around 60% to 70%, had drum brakes at the front (as well as at the back) (ts 243). Mr Bushby's evidence was that when he started work there were predominantly drum brakes on the front wheels (ts 347). Mr Hinkley and Mr Hood both worked for Anderson Ford for extended periods which spanned the early and late 1970s. By contrast, Mr Bushby did not commence until 1975. On balance, I consider that Mr Bushby's evidence as to the position when he commenced is likely to be reliable. Mr Hood and Mr Hinkley may well be identifying the position as at a later time, rather than during the first half of the 1970s.

105 Accordingly, I find that the majority of cars serviced at Anderson Ford while the plaintiff worked there had drum brakes both at the front and back of the vehicle.

106 The only evidence respecting the 11 years during which the plaintiff worked at Col Commons was the evidence of the plaintiff himself.

107 The plaintiff said it was common practice to use compressed air to blow out the brake drums while he was working at Col Commons. He estimated that he blew the drums on every second car that he worked on (exhibit 3A par 68). If the brakes were glazed, he would use emery paper to rub them down (exhibit 3A par 69). He estimated that he would change a set of brakes twice a week on average, and would service three or four cars a day, using compressed air on two of them on average (exhibit 3A par 72).

108 In cross-examination he acknowledged that by the 1980s more cars had disc brakes at the front (ts 275).

109 He also described in some detail the work which would be done on the brakes of trucks. I accept his evidence in that regard. However, given his evidence that the brake linings on a truck were replaced only two or three times a year (ts 276), this is not of great significance.

110 The workshop floor would be swept at the end of the day, either by the plaintiff or by an apprentice if there was one.

111 I turn to the question of whether the defendant owed a duty of care to the plaintiff.

112 It is convenient to begin with some relevant general principles.

113 The well known dictum of Lord Atkin in Donoghue v Stevenson [1932] AC 562, 580 remains relevant to the question of identification of persons to whom a duty of care is owed. In Tame v New South Wales [2002] HCA 35; (2002) 211 CLR 317 [9], Gleeson CJ observed that it is the reasonableness of a requirement that a defendant should have certain persons and certain interests in contemplation that determines the existence of a duty of care.

114 In general terms, a necessary, but not sufficient, condition of the existence of a duty of care is reasonable foreseeability by the defendant of the kind of injury that has been suffered by the person to whom the duty is owed: Tame [12]; Amaca Pty Ltd v Hannell [2007] WASCA 158; (2007) 34 WAR 109 [299]. Reasonable foreseeability is to be understood and applied with due regard to whether it is reasonable to require a person to have in contemplation a risk of the kind of injury that eventuated: Tame [12].

115 The 'kind of injury' which must be foreseeable is a reference to the different categories of injuries such as personal injury, property damage or pure economic loss. The particular injuries suffered need not be foreseeable: Mount Isa Mines Ltd v Pusey [1970] HCA 60; (1970) 125 CLR 383, 402; Amaca Pty Ltd v Hannell [299].

116 In Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307, 332 the New South Wales Court of Appeal held that it was not necessary for the plaintiff to prove that it was foreseeable that he might contract the particular injury of mesothelioma from the asbestos exposure of which he complained. It was sufficient that he could contract an injury of the kind which he suffered, namely personal injury from the inhalation of asbestos.

117 In deciding whether the defendant owed the plaintiff a duty of care, the tribunal of fact must first ask itself whether a reasonable man in the defendant's position would have foreseen that his or her conduct involved a risk of injury to the plaintiff or to a class of persons including the plaintiff: Wyong Shire Council v Shirt [1980] HCA 12; (1980) 146 CLR 40, 47.

118 A risk of injury which is remote, in the sense that it is extremely unlikely to occur, may nevertheless constitute a foreseeable risk. A risk which is not far-fetched or fanciful is real and therefore foreseeable: Wyong Shire Council v Shirt (48); Dovuro Pty Ltd v Wilkins [2003] HCA 51; (2003) 215 CLR 317 [60]; Amaca Pty Ltd v Hannell [300].

119 The test of reasonable foreseeability is to be applied at the time of the alleged breach and thus without hindsight: Amaca Pty Ltd v Hannell [301]; Homestyle Pty Ltd v Perrozzi [2007] WASCA 16; (2007) 33 WAR 209 [143].

120 In Bendix Mintex the New South Wales Court of Appeal held that a plaintiff does not have to show that the particular asbestos fibre type (there, as here, chrysotile) was known to be dangerous (332). If that approach is adopted the task of the plaintiff in establishing a duty is thereby made less onerous, given that the type of fibre here is the least dangerous. However, in the light of the factual findings I make, it is not necessary to decide whether that approach ought be taken on the foreseeability question.

121 The plaintiff invited my attention to findings of foreseeability, in respect of the hazards of asbestos, in numerous decided cases. For example, in EM Baldwin & Son Pty Ltd v Plane (1998) 17 NSWCCR 434, Fitzgerald AJA referred to other decisions of the New South Wales Court of Appeal, including CSR Ltd v Young (1998) 16 NSWCCR 56, in which it was accepted that 'the known toxicity' of asbestos dust, and 'the known uncertainty' as to the effects of exposure to asbestos dust, together with knowledge that injury or illness might not emerge for many years, give rise to a risk which could not be dismissed as remote, slight, far-fetched or fanciful [110].

122 Similarly, it has been observed that foreseeability can turn on knowledge of the dangers of any exposure to asbestos, including in the calculus for breach of duty, and is not confined to knowledge of the dangers of exposure to high levels of asbestos or levels of asbestos above any particular standard: Julia Farr Services Inc v Hayes [2003] NSWCA 37; (2003) 24 NSWCCR 138 [125] (Giles JA). In that case Spigelman CJ agreed with Giles JA and observed [2] that decisions of the New South Wales Court of Appeal established the proposition that breach of duty can be made out on the basis that there was no known safe dose of asbestos, taking into account the test of foreseeability enunciated in Wyong Shire Council v Shirt.

123 However, the conclusion that, in a particular case, a particular hazard was found to be foreseeable is a fact-based conclusion derived from the evidence in the particular case; it is not a conclusion of law. See, for example, Julia Farr Services [106] - [110]. The same point was made in relation to decisions on the question of breach of duty by Gleeson CJ and Kirby J in Vairy v Wyong Shire Council [2005] HCA 62; (2005) 223 CLR 422 [2] - [4].

124 Of course, that is not to say that decided cases are not of assistance in relation to questions of the existence and scope of duty of care. To the contrary, where the existence and scope of a duty of care is settled by authority it is unnecessary to identify and apply the legal principles that govern the determination of those questions (see, for example, Amaca Pty Ltd v Hannell [348]). Whether a duty of care arises from given facts is a question of law: Vairy [62].

125 The plaintiff invokes general principles respecting the duty of care of a manufacturer and a supplier. It is well established that a manufacturer owes a duty to a consumer to take reasonable care to prevent the product causing injury to a consumer: Dovuro Pty Ltd v Wilkins [2003] HCA 51; (2003) 215 CLR 317 [29]. In Amaca Pty Ltd v Hannell [354] there was reference to the manufacturer's duty to take reasonable care to avoid injury being suffered by persons using the product in an intended or normal way. See also CSR Ltd v Wren (1997) 15 NSWCCR 650, 655.

126 The question is, however, as to the scope of the class of persons to whom the duty is owed. The duty is owed only to those in respect of whom it is reasonably foreseeable that injury or harm might result. In Amaca Pty Ltd v Hannell, for example, the factual conclusion (at [347]) on foreseeability of harm to the home handyman, favourable to the plaintiff, in the joint reasons of Steytler P and McLure JA was the foundation for the duty of care found by their Honours in that case.

127 In the same way, reasonable foreseeability of the risk of harm to motor mechanics is a critical factual foundation of the plaintiff's case on duty of care. If that factual foundation is made out it seems, contrary to some of the submissions on behalf of the defendant, a small step to find that a duty of care arose. If (and only if) reasonable foreseeability of harm to mechanics is established, mechanics thereby become one of the classes to whom the manufacturer or supplier of vehicles fitted with asbestos brake linings or of brake lining spare parts owed a duty to take reasonable care to avoid the product causing injury.

128 Both parties accepted that the question of reasonable foreseeability was significant to whether the defendant owed a duty of care to a class of persons of which the plaintiff was a member. However, the parties appeared to differ as to what it was that was required to be foreseeable, in order that a duty of care arose.

129 The duty of care pleaded by the plaintiff is said to be owed to motor mechanics. In the course of opening, counsel for the plaintiff specified that that was intended to refer to professional motor mechanics.

130 The plaintiff submitted that the foreseeability question is whether the defendant ought reasonably to have foreseen a possibility of asbestos inhalation injury from asbestos exposure to mechanics as a result of working with Ford vehicles with asbestos in the brake linings, and that such possibility was not far-fetched or fanciful (no matter how unlikely).

131 The defendant submitted that the question of foreseeability was whether it was reasonably foreseeable by the defendant that a motor mechanic might contract an asbestos related disease as a consequence of exposure to the level or quantities of asbestos associated with his working on brakes fitted to the defendant's vehicles.

132 The plaintiff took particular issue with the reference, in the defendant's formulation, to 'the level of asbestos'. The plaintiff contended that there was no necessity to foresee any particular level in order that a duty of care arises. Insofar as the reference to a level is intended to refer to a specific numerical level, I accept the plaintiff's submission that such is not required.

133 On the other hand, I accept that, in determining whether the defendant owed a duty of care to professional mechanics, regard is to be had to the extent of exposure of mechanics which might foreseeably arise from asbestos dust and fibres released from asbestos in brake linings. If, having regard to that, and taking into account what was known or believed at the time, harm to mechanics was not reasonably foreseeable, no duty of care would be owed to mechanics.

134 Of course, in taking account of the extent to which mechanics might foreseeably be exposed to asbestos from brake linings, account must be taken of the wide range of possible work practices and environments, and of the prospect that a mechanic may work on servicing and changing brakes on Ford vehicles for many decades.

135 In short, what must have been reasonably foreseeable by the defendant is that a professional motor mechanic might contract an asbestos inhalation disease arising from the release of asbestos from the brake linings of Ford vehicles.

136 The duty of care pleaded by the plaintiff is expressed as a duty to give warnings. That invites attention to the question of the particularity of the formulation of a duty of care. A duty of care should not be formulated with such particularity as has the effect of obscuring the proper inquiry into the reasonable response to a foreseeable risk at the breach stage of the analysis: Graham Barclay Oysters Pty Ltd v Ryan [2002] HCA 54; (2002) 211 CLR 540 [191] - [192].

137 In some cases the duty question involves a determination of whether a defendant owes the plaintiff a duty to warn. That may be the position in novel situations where a more general formulation of the duty would be at such a high level of abstraction as to be of no practical assistance. See the discussion in Amaca Pty Ltd v Hannell [350] - [352]. If that occurs, the duty analysis must take account of the same considerations as are relevant in determining whether the specific breaches relied on would constitute a breach of any duty however formulated.

138 Ordinarily, the question whether the provision of a warning is within the scope of a duty of care in a particular case is determined at the breach stage of the analysis, by assessing whether a failure to warn constitutes a breach of duty: see Amaca Pty Ltd v Hannell [353] and cases there cited. However, as is there remarked, the result should be the same regardless of the approach.

139 I will return to those issues in the course of stating my conclusions in respect of the duty issue.

140 That brings me to the evidence as to whether it was reasonably foreseeable by the defendant that, if no protective measures were taken, professional mechanics might be at risk of contracting an asbestos inhalation injury or disease arising from the release of asbestos from the brake linings of Ford vehicles.

141 An enormous volume of evidence was tendered by the parties in relation to the issue of what the defendant knew, or should have known, or reasonably foreseen as at 1970, and during the period from 1970 to 1987.

142 By way of overview, the plaintiff relied upon the following main categories of evidence:

(b) various items of evidence bearing upon what the defendant knew;

(c) knowledge of Ford US and Ford UK, which was said to bear upon the defendant's position in two ways:

(i) knowledge of the foreign companies was said to be attributable to the defendant because of common directorships or senior executives within those organisations;

(ii) alternatively, knowledge held by Ford US and Ford UK was part of what the defendant ought to have known, because such information was readily available to it in the circumstances calling for inquiry by the defendant; and

(d) expert evidence as to readily available information regarding the hazards of asbestos, said to be supported by voluminous scientific literature and other publications tendered by the plainitff.

143 The plaintiff's claim is that the defendant owed him a duty from 1970 through to 1987. That being so, the question of the actual or constructive knowledge of the defendant falls to be determined, first, as at 1970, and, then, throughout the period from 1970 to 1987. Much of the evidence relied upon by the plaintiff as to what the defendant knew, and as to what Ford US and Ford UK knew, pertains to the period from 1970 to 1987. Very little of it bears on the position as at 1970.

144 The defendant led very little evidence as to what it knew regarding asbestos and the brake linings used in its vehicles and supplied by it. Substantially the only evidence led by the defendant in this regard was the evidence of Mr Ford, a former senior executive of the defendant. Although he worked for the company from about 1969, his evidence as to the defendant's relevant knowledge related primarily to the period from 1980 onwards.

145 Given that there appears to be little evidence bearing directly upon what Ford knew, as at 1970, the question of what Ford knew, at that time, will, it seems to me, overlap to a significant degree with what the defendant ought to have known at that time. The subject matter, source and circumstances of publication of some matters may (or may not) give rise to an inference that the defendant knew of them, as well as to (or not) a conclusion that the defendant ought to have known of them. In any case, it is sufficient for the plaintiff to establish that the defendant either knew or ought to have known of relevant matters.

146 The defendant's case in respect of foreseeability relied on the following main categories of evidence:

(a) expert evidence, primarily from Dr Dennis Paustenbach and also from Mr Alan Rogers;

(b) scientific and other literature relied upon by those experts as supporting their views; and

(c) a bundle of material (exhibit W) containing documents regarding threshold limit values for asbestos between 1970 and 1987 and setting out legislative and regulatory duties of occupiers of premises between 1970 and 1987.

147 The plaintiff points to admissions made by the defendant. In the course of the trial, senior counsel for the defendant made the following admission on its behalf (ts 456):

The defendant accepts that it understood or knew, if you wish, that there was asbestos in brake linings and it knew also that in a general sense if there was sufficient exposure of asbestos to people occupationally exposed, asbestos related disease could result. Those admissions are plain and we don't resile from that.

148 It was, plainly, foreseeable by the defendant that motor mechanics who serviced and repaired Ford vehicles would, in the course of so doing, service, clean, install and replace brakes. It did not appear to be in dispute that Ford was aware of the various steps involved in servicing and repairing Ford vehicles and I so find. It was foreseeable that work by mechanics might involve blowing brake dust from brake drums and filing or grinding the edge of a brake shoe to ensure that it fitted, for example.

149 The question is whether it was reasonably foreseeable by the defendant that a mechanic might suffer an asbestos inhalation injury caused by the asbestos in the brake linings of vehicles manufactured or supplied by the defendant, or from brake parts supplied by the defendant.

150 The level of risk required in order that a risk be reasonably foreseeable is not high. It is enough that it is not far-fetched or fanciful and thus is real, even though it may be extremely unlikely to occur.

151 I propose to begin the review of the evidence relating to foreseeability issues with the expert evidence. In undertaking that review it should, it seems to me, be borne in mind that the question of foreseeability is not limited to the question of risk of asbestosis. It is broader than that and extends at least to reasonable foreseeability of any life threatening disease, including mesothelioma (see Bendix Mintex). At times, the defendant's submissions on foreseeability approached the question by reference only to the foreseeability of asbestosis.

152 I will deal first with the experts called by the plaintiff.

153 Dr James Leigh is a consultant occupational physician. He has extensive qualifications in medicine and mathematics. He is a fellow of the Australasian Faculty of Occupational Medicine and the Australasian Faculty of Public Health Medicine. In 1999 he was a consultant to the World Trade Organisation on asbestos issues. He was the head of the Epidemiology and Surveillance Unit of the National Occupational Health and Safety Commission from 1988 to 1996 and head of the Research Unit of that Commission from 1996 to 2001. He was co-ordinator of the Australian Mesothelioma Register from 1988 until 2001.

154 His first report (exhibit 24A) dealt at length with the development of knowledge about the risks of health arising from exposure to asbestos. Some of the points made in the report may be summarised as follows:

(a) by 1955 the issue of asbestos exposure as a cause of lung cancer was put beyond doubt in a published study by Doll;

(b) an article in Industrial Medicine by Cooke in 1942 pointed out the need for physically measuring dust concentration of asbestos, and not relying on sight only, because the then applicable 5 million particles per cubic foot risk level would not necessarily be visible to the naked eye; and

'Since we did not know the minimum effective dose of any of the many occupational carcinogens it seems obvious that they should be completely eliminated wherever that is practicable. This can be done by using or producing suitable non-carcinogenic substitutes.

Hueper went on to describe other control measures including enclosure, wetting and ventilation.

Dr Leigh also referred to a conference in England in 1969 at the Essex offices of Ford UK. The chairman of the conference was the chief medical officer of Ford UK. The conference was on the subject matter of exposure to asbestos during brake and clutch maintenance. The hazards and appropriate control measures were discussed. Control measures such as dilution and exhaust ventilation, vacuum funnels and brushes and respirators were described and their effectiveness demonstrated. The conference papers were published in 1970 in the journal the Annals of Occupational Hygiene, 1 - 41. That publication was document 30 within the bundle of documents comprising exhibit 37, which I will denote as exhibit 37/30. Further reference to these conference papers will be made later in these reasons.

155 At pp 7 - 12 of his report Dr Leigh referred to substantial scientific literature relating to short or low asbestos exposures and mesothelioma. The following summarises some of the points made:

(a) In the course of the 1960s various reports were made of occurrences of mesothelioma from asbestos exposure, in many of which no fibre type distinctions were made.

(b) In 1964 an editorial in the British Medical Journal drew attention to the occurrence of mesothelioma at low exposures and did not distinguish between the hazards of different fibre types.

(c) In 1965, in the British Journal of Industrial Medicine, Newhouse & Thompson (exhibit 37/216) described 83 mesothelioma cases, 40 of which gave a history of occupational or domestic exposure.

(d) In 1965 and 1971 two authoritative reviews of the epidemiology of asbestos cancers were published. Both recognised the possible differential effects of different fibre types but neither claimed that chrysotile did not cause mesothelioma.

(e) By 1970 the dangers of asbestos in causing mesothelioma were well known in Australia. All types were thought to cause mesothelioma with, from 1965, a common theory held by the majority that crocidolite was the most potent, followed by amosite and then chrysotile. However, there was a fairly strong minority that felt that all types should be regarded as equally potent in causing mesothelioma, based on animal inhalation and implantation studies showing roughly equal effects per unit dose. This is reflected in the International Agency for Research on Cancer (IARC) Evaluation (1976 p 80). (The IARC Evaluation is exhibit 37/141).

(f) A 1982 report by the Australian National Health and Medical Research Council (NHMRC) on the health hazards of asbestos commented on the impossibility of determining a safe threshold below which no adverse effect of asbestos exposure existed, and recommended as a result that exposure to all forms of asbestos be kept as low as reasonably practical. (The 1982 NHMRC report is exhibit 41/15 and will be referred to later in these reasons.)

157 Professor A W (William) Musk is an eminent respiratory physician and research scientist who has specialised in the area of asbestos related diseases for many decades. He gave evidence in relation to the diagnosis of the plaintiff, to which reference will be made later in these reasons. At that stage more will be said about his expertise.

158 At pp 8 - 36 of his substance of evidence (exhibit 18A) Professor Musk gave evidence relating to the development of knowledge in relation to asbestos related diseases and as to standards and regulations applying to asbestos exposure. By the mid-1960s Professor Musk said that it was widely accepted that asbestos could cause asbestosis, lung cancer and mesothelioma. It was accepted that small doses, particularly of crocidolite, could cause mesothelioma. The need for the protection of workers exposed to all forms of asbestos was known. Following a 1964 conference (held in New York) on the biological effects of asbestos, the overview of proceedings was said to be that 'it is abundantly clear from the evidence presented at the conference that in future much greater care must be taken to eliminate unnecessary exposure to asbestos dust wherever it occurs'.

159 Professor Musk referred to the British Occupational Hygiene Society Hygiene Standards for Chrysotile Asbestos Dust published in about 1968 (1968 BOHS Standards) (exhibit 37/50). He pointed out that the committee considered the standards were the best that could be obtained from scanty data and hoped to supplement them in due course. It was unable to specify any air concentration of asbestos which was known to be free of risk from cancer. New United Kingdom asbestos regulations came into effect in May 1970. These regulated all activities where asbestos or asbestos-containing compounds were used, and required that where asbestos might be liberated into the atmosphere capable of causing harm, exhaust ventilation or personal protection was to be used.

160 Professor Musk concluded as follows. The material he had referred to would have led a reasonable employer, occupier or product supplier to have been aware of the necessity to minimise the risk of inhalation of asbestos well before 1970 onwards and to warn of the potential dangers. By 1961 the serious dangers to health occasioned by even small exposures should have been known by persons responsible for exposing other persons to asbestos and appropriate warnings and safeguards should have been implemented. By the mid-1960s, no person should have been exposed to asbestos, especially (but, by implication, not exclusively) blue asbestos (ie crocidolite), without exposure being reduced to a minimum and appropriate warnings of the risks being given to those exposed. The amounts of asbestos to which persons were being exposed could and should have been quantified during the 1960s as a consequence of these serious dangers and risks to health. By the 1970s medical researchers in the field were considering not whether there was a safe level of exposure, which had never been asserted, but whether asbestos should be banned completely.

161 Professor Musk was not cross-examined in relation to these matters.

162 The defendant submitted that Professor Musk's evidence did not take account of three critical factors and their impact on an assessment of what hazard may have existed for mechanics. The factors were: asbestos type; exposure levels and duration; and characteristics of specific asbestos-related diseases.

163 I do not accept that submission. The summary set out above reflects Professor Musk's opinion that, at the relevant time, no safe level of exposure for any variety of asbestos had been demonstrated or was believed to exist, and that all exposure to any asbestos (of whatever type) should, consequently, have been reduced to a minimum, with appropriate warnings. As to the third factor referred to by the defendant, the foreseeability issue is, as I have already found, not to be tested only by reference to asbestosis.

164 Dr Eva Francis is an occupational hygienist with almost 30 years of practical experience in the area. She has had a particular interest in the area of asbestos since the early 1970s. She gave evidence estimating the asbestos dose experienced by the plaintiff. That evidence will be referred to later in these reasons. Some of the points arising from her evidence as to foreseeability may be summarised as follows:

(a) By 1970, and through to 1987, asbestos was recognised among occupational health specialists as causing asbestosis and as a carcinogen.

(b) Mesothelioma occurrence in garage workers was reported in the UK and in Canada by Newhouse & Thompson (1965) (exhibit 37/216), McDonald et al (1970) (exhibit 37/182) and by Greenberg & Lloyd Davies (1974) (exhibit 37/177).

(c) As a result, the United States National Institute for Occupational Safety and Health (NIOSH) recommended a procedure for asbestos brake and clutch servicing requiring respiratory protection, vacuuming of brake drum dust and localising of grinders and machinery in a workshop with dust extraction in its Current Intelligence Bulletins of 8 August 1975 (1975 NIOSH bulletin) (exhibit 37/75).

(d) In a United States publication by Lorimer et al in 1976 (exhibit 37/295), asbestosis and pulmonary function loss was said to have been demonstrated in 25% of automotive workers examined.

(e) In 1970, and up to and including 1987, it was recognised by health scientists and occupational health specialists that all exposures to carcinogens, and hence to asbestos, should be minimised as far as practical. It was accepted that there was a need to reduce all exposure to carcinogenic agents to the lowest achievable level of exposure (Dr Francis referred in this respect to a publication by Conklin in 1949). There was the view that carcinogens were extremely dangerous and should be treated with comprehensive care.

(f) A comprehensive compilation of the international medical literature has always been available in Index Medicus, and the Industrial Hygiene Digest has provided abstracts of findings in occupational health. Major industrial companies in the 1970s would have been abreast to these two sources of references, with the latter being sent monthly to members of the Industrial Hygiene Foundation;

(g) Thus a prudent and responsible producer, user or manufacturer and distributor of asbestos and products containing asbestosis would have known in 1970 and through to 1987 that the inhalation of asbestos dust could be injurious to persons using, repairing and maintaining asbestos products.

165 Dr Francis was not cross-examined in relation to this aspect of her evidence.

166 The plaintiff also relied upon evidence from Mr Gordon Stewart. From 1953 to 1966 Mr Stewart worked in the industrial hygiene section of the Department of Health and then from 1966 - 1985 for a private company. Since then he has worked in the industry as a private consultant.

167 Mr Stewart referred to publications in the United Kingdom and in New South Wales in the 1940s which emphasised the need to minimise exposure to asbestos, even if the exposure arose only from temporary work or the exposure was only intermittent. He referred to the 1970 Queensland Rules under the Factories and Shops Act which prescribed measures to be taken whenever a process involved asbestos or an article partly comprising asbestos, or any work involved the use or handling of asbestos or any article containing asbestos. He referred to the 1975 NIOSH bulletin to which reference has already been made. He concluded that there was significant knowledge available throughout the period 1970 to 1987 as to the significant risks from asbestos inhalation, and that exposure and inhalation of dust derived from the manipulation, drilling, grinding and shaping of asbestos containing products such as brake and clutch parts and from cleaning by sweeping or blowing out such parts could give rise to such risks.

168 The brief cross-examination of Mr Stewart did not touch upon these matters.

169 Finally, in this respect, the plaintiff relied upon evidence from Dr David Egilman. He canvassed a very large volume of academic literature, some of which was referred to by various others of the plaintiff's experts. I have not found it necessary to rely upon his evidence and, accordingly, do not propose to review his evidence.

170 I propose, next, to review some of the literature and other documents to which reference was made by the plaintiff's experts, before turning to the defendant's evidence.

171 It is not practical to summarise, in these reasons, the contents of voluminous material relied upon by the parties' experts. I propose to set out excerpts from, or summarise, only a small selection of the material. Wherever, in the summary of the plaintiff's expert evidence set out above, I have referred by number to a particular exhibit, I have considered it and am satisfied that it supports the proposition for which it is relied upon in the summary I have given.

172 I start with the 1968 BOHS standards (exhibit 37/50). The defendant emphasised pars 1 - 3 of the summary and recommendations at the commencement of the document. These were in the following terms:

1. As long as there is any airborne chrysotile dust in the work environment there may be some small risk to health. Nevertheless, it should be realised that exposure up to certain limits can be tolerated for a lifetime without incurring undue risks.

2. The committee believes that a proper and reasonable objective would be to reduce the risk of contracting asbestosis to 1 per cent of those who have a lifetime's exposure to the dust. By 'asbestosis' this committee means the earliest demonstrable effects on the lung due to asbestos.

It is probable that the risk of being affected to the extent of having such early clinical signs will be less than 1 per cent for an accumulated exposure of 100 fibre years per cm3. That is, for example, a concentration of 2 fibres per cm3 for 50 years, 4 fibres per cm3 for 25 years or 10 fibres per cm3 for 10 years.

3. It is recommended that exposures which lie in certain ranges of dustiness be designated by categories according to the following scheme:

DUST CATEGORY CONCENTRATION AVERAGED OVER

3 MONTHS (FIBRES/CM3)

Negligible 0-0.4

Low 0.5-1.9

Medium 2.0-10.0

High over 10.0

173 However, as was common ground between the experts, and as anyway would appear to be common sense, regard must be had to the whole of the contents of the document, which included the following passages:

CRITERIA OF RISK

As long as there is an appreciable amount of dust in the air, the committee recognises that there may be some risk to health.

If there is a threshold concentration, below which nobody is adversely affected, one could not argue from a limited number of dust measurements that a worker will never be exposed to this concentration, but only that the possibility is remote. Thus, in practice, one can show only that the risk of a worker's exposure exceeding such a threshold is small. Consequently, whether or not there is a threshold exposure, one can show only that the risk of a worker being affected by asbestos is minimal.

Knowledge of the relationship between airborne dust exposure and the risk of asbestosis is not in itself sufficient to establish a hygiene standard. Another important problem, and one which is very difficult to resolve, is that of balancing the risks to health against the consequences of demanding excessive dust reduction.

However, the committee believes that it is reasonable to reduce to 1 per cent the risk of getting asbestosis through having worked for a lifetime with asbestos. By 'asbestosis' the committee has in mind the existence of the earliest demonstrable effects on the lung due to asbestos.

ESTIMATION OF THE STANDARD AIR CONCENTRATION

The way in which risk and dust concentration are related is not fully understood. However, it seems reasonable to assume that at zero concentration of asbestos there will be zero risk and that there will be an increase in risk corresponding to an increase in concentration. (p 4)

...

Good industrial hygiene practice tends towards controlling exposures below the hygienic maximum rather than maintenance at the maximum. (p 6)

...

PERIODIC MEDICAL EXAMINATIONS

In all types of pneumoconiosis too little is known about the variability of the response of different individuals to a given dose of dust to allow complete reliance on dust monitoring as a means of reducing the risk to a specified level ...

CANCER

...

There can be little doubt that these risks will be least in the lowest concentration (Knox, Doll and Hill 1965), but the quantitative relationship between asbestos and cancer risk is not known, nor is it known exactly why these two are related, nor even whether all kinds of asbestos present a risk. Consequently it is not possible, at this time to specify an air concentration which is known will be free of risk in this respect. (pp 7 - 8)

174 Consideration of the whole of the document seems to me to provide support for the conclusions about it drawn by the plaintiff's experts. The acknowledgement, in the concluding paragraph of the document, that it is not possible to specify an air concentration which is known to be free of cancer risk is of some significance.

175 The papers which were presented at the conference held at the central office of Ford UK in March 1969 were published at pp 1 - 41 in the 1970 Annals of Occupational Hygiene, a journal published for the British Occupational Hygiene Society (exhibit 37/30). It was, I think, common ground between the parties that these papers are part of what the defendant knew or ought to have known, as from around the time of its publication. In any event, I would so find.

176 In a preface, the context in which the conference arose is set out. Pages 17 - 21 are an article on exposure to asbestos during brake maintenance by Hickish & Knight. Further reference to this article will be made later in these reasons in the context of analysis of exposure levels. The conclusion of the authors was as follows:

Our investigations show that exposure to asbestos during brake maintenance is not as severe as was anticipated, and in the situations we examined, the personal exposure of the operators was below the limit corresponding to 50-year exposure [a reference to the 1968 BOHS standards already referred to in these reasons].

It is however recommended that care should be exercised during brake cleaning to avoid inhalation of the dust produced, and the development of cleaning procedures which would reduce air contamination is desirable. The present trend towards the introduction of 'flow line' servicing at dealers works, in which one individual may be engaged in almost entirely on brake servicing, emphasises this point.

Our environmental studies have not included maintenance procedures which involve the filing or grinding of brake lining material, and we would envisage that these would give rise to considerably increased air contamination by chrysotile asbestos, with the attendant need for strict precautions to prevent the inhalation of fibres.

177 The Hickish & Knight study also referred to the observed fact that the percentage of asbestos fibres in the drum dust and airborne dust was much lower than in the dust formed from the original lining material (about 1% as against 40% - 60%). There is reference to enquiries about how that occurs.

178 A reasonable person reading the Hickish & Knight paper would conclude that the asbestos in brake linings would or might lead to respirable asbestos fibres in brake dust and would lead to respirable asbestos fibres in any dust formed from the original brake lining material, such as by grinding or filing.

179 Pages 23 and 24 are a paper by Luxon of the Factory Inspectorate of the Department of Employment and Productivity. The paper sets out a number of cautionary notes respecting questions of measurement and dose. The paper describes the figures produced by Hickish & Knight as, to a large extent, reassuring in that they indicate that the exposure levels of those servicing braking systems are likely to be below the level of 2 fibres per cm3 considered, in the light of past knowledge, to be a safe one for chrysotile. The author went on to note the increasing tendency to carry out brake overhauls on a production line basis making the development of adequate precautionary measures even more important. He states, 'Certainly we should not be blowing out brake dust, even if it contains only a few per cent of asbestos'.

180 The 1975 NIOSH bulletin was issued on 8 August 1975 (exhibit 37/75). It referred to a meeting on 21 July 1975 convened by NIOSH to discuss the present state of knowledge with respect to the potential health hazards for persons exposed to asbestos during the servicing of motor vehicle brake and clutch assemblies. It stated that data from the Mount Sinai School of Medicine in New York indicated that workers engaged in the maintenance and repair of automobile and truck brake linings are exposed to potentially hazardous levels of airborne asbestos dust. It continued in the following terms:

Previous studies of the extent of asbestos emissions from automobile brake lining wear showed that only a very small fraction of the original asbestos content of the brake lining is found in brake drum dust. It was presumed that this is due to thermal degradation of the fibres during braking. The present findings indicate that enough asbestos is preserved to produce significant exposures during certain brake servicing procedures.

The full extent of asbestos-related disease in brake servicing personnel is not known at present because this particular occupational group has not been studied systematically up to now. However, a review of the scientific literature on the association between asbestos exposure and mesothelial tumors of the pleura and peritoneum has revealed at least four cases of these rare tumors in persons who were employed in jobs involving automobile brake servicing.

For your information and guidance, we are enclosing pertinent references, estimates of the population at risk, a NIOSH interim recommendation for brake and clutch servicing procedures, and a copy of the Department of Labor standard covering exposure to asbestos in the work place.

The environmental studies of brake lining servicing operations outlined above together with observations of mesothelial tumors in persons so employed affirms the necessity for instituting and maintaining recommended control measures in this industry so that the health hazards of asbestos are minimized. (references omitted)

181 Attached to the bulletin were recommended procedures for asbestos brake and clutch servicing. Attention should be given to all of the measures there referred to which included the use of a rag soaked in water to clean brake drums. It was said that 'under no circumstances shall compressed air or dry brushing be used for cleaning'.

182 The 1982 NHMRC report (exhibit 41/15) on the health hazards of asbestos was relied upon by the plaintiff's experts and also as part of the defendant's case. It included the following three passages:

Given the inability to precisely identify a threshold level and the nature of biological variations in persons exposed, it is possible that a small proportion of workers may be affected at or below a hygiene standard. Good occupational hygiene practice requires that exposures be reduced to the best practical minimum below the hygiene standard. The Sub-committee [for the report] agreed that this was particularly important where asbestos and other carcinogens were concerned ... (p 8)

The Sub-committee, having accepted the existence of a threshold of risk and taken account of the uncertainties regarding it, concluded that it is at present impossible to establish an exact line of demarcation between safety and hazard with respect to exposure to asbestos and the subsequent development of mesothelioma. The Sub-committee therefore supports the view that there should be a continuing requirement to reduce the exposure to all forms of asbestos to the minimum that is reasonably practical. (p 9)

Recommendation 1

Expert evidence suggests that it is not possible to establish a threshold value below which a carcinogenic effect of asbestos cannot be identified, although some recent evidence suggests that such a threshold may exist. The Subcommittee recommends that exposure to asbestos should, in all phases of the asbestos industry, be reduced to the lowest practicable level by the most efficient technology currently available and enforced through:

• extension of the provisions of State asbestos regulations to cover all work processes where exposure to asbestos dust may occur;
• statutory prohibition of all asbestos spraying;
• the licensing of contractors engaged in the repair, removal and replacement of asbestos-containing insulation materials;
• compliance with the NH & MRC recommended codes of practice;
• delegation of responsibility for safety precautions to principal contractors in the building industry. (emphasis in the original text) (p 10)

183 One of the recommended codes of practice was in appendix 7 and related to the handling, processing and repair of asbestos-based friction materials. Attention should be given to the whole of the contents of that appendix but I do not propose to set it out in detail. It sets out a series of recommended work procedures for employees doing a number of operations on asbestos-containing friction materials, including cutting, grinding, drilling - whether by hand or by machines, or cleaning out brake drums. A number of precautions are set out in appendix 7.

184 That brings me to the evidence relied upon by the defendant.

185 Dr Paustenbach is a toxicologist and industrial hygienist with over 20 years of experience in risk assessment, environmental engineering, ecotoxicology and occupational health. He has been involved in investigating health effects of exposure to and the remediation of carcinogenic and non-carcinogenic chemicals and many other substances. He has a PhD in environmental toxicology.

186 The following are some of the pertinent aspects of Dr Paustenbach's evidence taken from his report (exhibit Q1):

(a) Risk assessment involves identifying a potential risk, evaluating it and then determining whether the risk is such that it warrants the introduction of precautions against the occurrence of injury and, if so, what precautions are appropriate (pars 4 and 5).

(b) From an industrial hygiene perspective, the key questions which arise in the plaintiff's case are: whether during the relevant period the state of the art of industrial hygiene was such that it ought to have been concluded that brake mechanics were at risk of injury from asbestos which may be present in the dust emitted during brake repair work; if such a risk existed, what appropriate preventative measures ought to have been identified and implemented; and whether warnings were necessary (par 9).

(c) In the second half of the 1960s the professional community connected with industrial hygiene gave substantial consideration to the possibility that brake linings containing asbestos were a potential workplace hazard to motor mechanics (par 22).

(d) Until the late 1980s or early 1990s it was accepted in the industrial hygiene community that a practical safe exposure level could be identified below which there was no appreciable risk of respiratory disease occurring (par 29).

(e) Emission studies from the late 1960s and early 1970s showed that the vast majority of brake wear debris is not free asbestos fibre, because the braking process breaks down the vast majority of the asbestos fibres (pars 37 - 40).

(f) A 2003 review of worldwide exposure studies (exhibit T1) revealed that all the reliable exposure studies performed during the relevant period demonstrated that the level of asbestos fibres to which brake mechanics were typically exposed was nearly always below the applicable regulatory recommended maximum safe dose level and that even the highest measured exposures to asbestos was well below the no effect level or threshold dose that has been reported for occupational cohorts exposed primarily to chrysotile asbestos (pars 42 and 43).

(g) A 2004 review (exhibit T2) of more than 25 epidemiological studies conducted from 1975 to 2002 concluded that the weight of evidence demonstrated no increased risk of cancer, mesothelioma or asbestosis in brake mechanics (par 47).

(h) In his opinion, a competent properly informed industrial hygienist engaged in risk assessment associated with the risk of asbestos in brake linings after the mid-1960s and through much of the 1970s would have considered the possibility of an increased risk of mesothelioma in brake mechanics, but would have concluded on the evidence available to him or her that there was insufficient evidence of any such risk to require the adoption of safeguards to protect against mesothelioma; and would have considered that there was no likelihood of an increased risk of asbestosis in the brake mechanics and consequently no need to adopt safeguards to protect against it (par 48).

187 In effect, the defendant invites me to accept Dr Paustenbach's evidence in preference to the evidence relied by the plaintiff and referred to above, contending that it is more specifically directed to the key issues for this case. The defendant submits that Dr Paustenbach's conclusion at par 48 (set out above) is of crucial significance to the question of foreseeability and consequently whether there was a duty of care.

188 For a number of reasons, referred to below, I do not accept the defendant's submissions in these respects.

189 First, a reading of the whole of Dr Paustenbach's report, together with his cross-examination, suggests to me that his methodology in testing whether there existed a degree of risk requiring the adoption of safeguards is not one that accords with the approach taken in the law of negligence. The question which he poses and answers, of whether there was a level of risk sufficient to engage a duty to take precautions, is, by definition, one that involves a value judgment. The making of a value judgment in what Dr Paustenbach says is inherent in par 5 of his report and in the way in which he expresses his conclusion at par 48 (in terms of 'insufficient' evidence). It seems to me that in making that value judgment, whether there is 'sufficient evidence' to warrant the introduction of precautions, Dr Paustenbach gives great significance, if not controlling significance, to whether applicable standards as to level of exposure have been exceeded. (See, for example, his evidence at ts 1149, 1150, 1154). In the law of negligence, such standards are relevant but not determinative: Thomson v Johnson & Johnson Pty Ltd [1991] VicRp 84; [1991] 2 VR 449; Amaca Pty Ltd v Hannell [327].

190 The point is illustrated by Dr Paustenbach's response when he was questioned about the papers by Luxon and by Hickish & Knight (both exhibit 37/30), (see ts 1147 - 1149). Dr Paustenbach's focus was on the conclusion of the authors that the level of exposure was below the limits imposed by the 1968 BOHS standards. He did not appear to give any significance to the exhortations, in those papers, for steps to be taken to avoid or minimise the inhalation of dust, nor to the reference, by Hickish & Knight, to the need for additional precautions in the light of increased possible exposure arising from filing or grinding.

191 Further, in making the value judgment about whether there is 'sufficient evidence' to warrant the introduction of precautions, Dr Paustenbach did not articulate a basis for the judgment of 'insufficiency' apart from by reference to applicable standards as to levels of exposure.

192 When Dr Paustenbach was taken, in the course of cross-examination, to the works of Newhouse & Thomson in 1965 (exhibit 37/216), McDonald et al (exhibit 37/182) in 1970, Greenberg & Lloyd Davies (exhibit 37/177) in 1974, as referring to cases of mesothelioma in someone who was said to have been either a mechanic or worked with asbestos linings, his initial response was that they were case reports and were not evidence of proper epidemiological studies suggesting there was an increased risk for brake mechanics at that time (ts 1149). The law of negligence does not require that a risk be established by epidemiological studies before a duty of care arises. To the contrary, the recognition of uncertainty as to what level of risk exists, and the consequent need for further research, would support a conclusion that a risk was, at such time, reasonably foreseeable.

193 In the course of cross-examination Dr Paustenbach was referred to exhibit 37/331, a press release on asbestos and cancer, under cover of a letter, issued by the World Health Organisation and the International Agency for Research on Cancer on 23 December 1976. It included the following statements:

All commercial forms of asbestos have been shown to be carcinogenic in mice, rats, hamsters and rabbits. Human occupational exposure to all commercial forms of asbestos has resulted in a high incidence of lung cancer and mesotheliomas ...

Garage mechanics carrying out repairs on brake linings are also at risk ...

The group [a working group convened by IARC] concluded that 'at present it is not possible to assess whether there is a level of exposure to asbestos in humans below which an increased risk of cancer would not occur'.

194 When he was asked whether anything in that document should have dissuaded the competent industrial hygienist from the opinion he expressed in par 48 of his report, he responded in the negative, saying that it was consistent with what he had said. He continued as follows:

By 1975 and 1976 there clearly was a decision that more needed to be known about the exposure of brake mechanics and that's why the Dear Colleague letter [the 1975 NIOSH bulletin] came out and was issued and that's why a series of research projects were initiated in the mid-1970s to understand brake mechanics. So this is entirely consistent with what I've said. (ts 1152)

195 Thus Dr Paustenbach says that the joint press release (exhibit 37/331) and the 1975 NIOSH bulletin (exhibit 37/75, also exhibit 38/74, extracts of which are set out earlier in these reasons) are consistent with his opinion expressed in par 48 of his report. That, I think, is revealing of the reasoning underlying his opinion. It suggests that until the extent of the risk is demonstrated, there will, on Dr Paustenbach's approach, be 'insufficient evidence' to require precautionary measures to be taken. That is not the approach taken by the law of negligence. In my opinion these two publications are strong evidence that there was, following the publications, a foreseeable risk that the exposure to asbestos experienced by a motor mechanic may lead to cancer.

196 When Dr Paustenbach was taken to the concluding passages of the 1968 BOHS standards (exhibit 37/50) and asked whether that material might have dissuaded a properly informed competent industrial hygienist from expressing the opinion in par 48 of his report, Dr Paustenbach hesitated significantly before finally answering that he would say what he had said previously, namely that a competent industrial hygienist would have deferred to the various occupational hygiene standards (ts 1154).

197 Next, notwithstanding that he expresses his opinion in terms of the position as at the 1970s and thereafter, consideration of his reasoning, as it is exposed in the report and in the course of cross-examination, suggests to me that the analysis is informed by hindsight rather than by what was known at the given point in time such as 1970. His assessment is based on his analysis of what has subsequently become known through further studies. His report made little detailed reference to the information available as at 1970 and, say, 1980 and 1987.

198 Unlike several of the plaintiff's experts, Dr Paustenbach was not involved, at all, in questions of risk assessment pertaining to asbestos, during the relevant period (ie 1970 to 1987).

199 At times, Dr Paustenbach gave answers which were not responsive to the questions put and which appeared to be calculated to attempt to defend the opinion which he had expressed (see, eg, ts 1146 - 1150).

200 There is room for questioning Dr Paustenbach's independence. His involvement in questions of the knowledge of the hazards of asbestos began when Ford US approached him in 2000 and asked him to review the medical literature. His subsequent research has been funded by United States car companies including Ford US. Companies with which he is closely associated have received large sums of money (in the order of millions of dollars) since 2000. Seventy per cent of his work involves litigation. In American litigation he had given depositions in some 100 cases for motor vehicle manufacturers since 2001.

201 None of these matters were mentioned in his expert report.

202 It is to be recalled that the plaintiff's expert witnesses were not cross-examined in relation to questions of foreseeability.

203 I would summarise my conclusions in respect of the evidence of Dr Paustenbach as follows:

(a) insofar as his evidence is inconsistent with the evidence of the plaintiff's experts referred to earlier, I prefer the evidence of the plaintiff's experts;

(b) his opinion expressed at par 48 of his report, if accepted, would not, given the reasoning upon which it is based, lead to a conclusion that the risk of harm to brake mechanics arising from exposure to asbestos was not reasonably foreseeable; and

(c) in any case, for the reasons given, I do not accept his opinion at par 48 or its supporting reasoning, insofar as that reasoning is exposed.

Further, I do not accept his opinion, at par 29 of his report, that until the late 1980s or early 1990s it was accepted in the industrial hygiene community that a practical safe exposure level for asbestos could be identified below which there was no appreciable risk of respiratory disease occurring.

204 For the reasons to be developed when I give consideration to applicable standards and threshold levels, the evidence does not support a conclusion that such standards were identified as meaning that below them there was no appreciable risk of respiratory disease, or other harm. To the contrary, the evidence supports the conclusion that standards were expressed in a way that acknowledged an inability to state, in a definitive way, a level of exposure below which there was no or no appreciable risk of harm.

205 I turn to the other evidence relied upon by the defendant.

206 The defendant relies upon evidence from Mr Rogers. Mr Rogers is an experienced and very well qualified occupational hygienist. Three reports by Mr Rogers were admitted as evidence (exhibits F1, F2 and F3). The focus of those reports relates to questions of asbestos dose. I will deal with that topic later in these reasons.

207 Among the conclusions set out at the end of Mr Rogers' report of 24 December 2006 (exhibit F1) is that 'the plaintiff's contact with asbestos would have been considered as being extremely low such that the authorities, and their scientists and medical experts in the late 1960s, 1970s and early 1980s, would not have considered him as being at risk of developing asbestosis'. There is, so far as I can determine, nothing in the body of the report itself which sustains that conclusion. In answer to a question from me, counsel for the defendant identified the source of that conclusion as being what is set out in appendices to the report at pp 22 - 24.

208 Mr Rogers' conclusion set out above would not, if accepted, lead to a conclusion that the defendant owed no duty of care. That is because the conclusion is stated in terms that relate only to the risk of developing asbestosis. As already explained, the question of duty of care is not confined to whether asbestosis was foreseeable, it extends to whether any asbestos inhalation injury, including mesothelioma, was foreseeable.

209 In the light of that, it is not necessary to enter into a detailed analysis of whether the material at pp 22 - 24 sustains the conclusion stated by Mr Rogers, but I will briefly state my conclusions in that regard. I am not satisfied that the material at pp 22 - 24 sustains the conclusion stated, particularly in the light of the evidence given by the plaintiff's experts, which I accept, relating to knowledge and foreseeability of risks of asbestos exposure. Moreover, Mr Rogers' reasoning, in the appendices in question, proceeds on the basis that the British Occupational Hygiene Society view of what was 'an acceptable risk' is determinative. I have already explained that I do not share that view. Further, the relevant material (at pp 22 - 24) does not seem to me to involve the careful analysis of the known information and what it revealed at a given point in time such as 1970.

210 The other main evidence upon which the defendant relied in relation to duty of care is that contained in exhibit W, which contains two categories of material. The first is legislation and regulations regarding the duties of an occupier, applicable between 1970 and 1987. The second category is threshold limit values for asbestos exposure set by the NHMRC or other sources and applicable between 1970 and 1987.

211 The existence of duties, on the part of occupiers and employers, to take steps to prevent or eliminate hazards is, I would accept, part of the relevant context in determining whether a duty of care on the part of the defendant had or had not been breached. However, I do not consider that the existence of these duties, on the part of other parties, leads to any conclusion that, assuming reasonable foreseeability is established against the defendant, no duty of care arises. That another person may have statutory or common law duties to avoid a risk of injury does not preclude a defendant having a duty of care to avoid the same or similar risk of injury.

212 Exhibit W sets out extracts from various NHMRC documents in which there is stated a threshold value of asbestos, or chrysotile asbestos, which should not be exceeded. It can be seen that the values fell over time. The threshold values are accurately summarised in the table which is at the front of exhibit W.

213 The very limited extracts provided in exhibit W do not enable any conclusions to be drawn as to whether the standards were expressed to be a level below which there was no risk, or negligible risk, or anything of that kind. I would certainly not be prepared to infer that any such statements were made. In this regard, I note that the 1982 NHMRC report is one of the documents, an extract of which is provided in exhibit W. Further extracts of that report were tendered as exhibit 41/15 and have been referred to earlier in these reasons. Those extracts provide no support for a suggestion that the standards are stated to be levels below which there is no or no real risk. Rather they support the contrary conclusion. The same is true of the 1968 BOHS standards, also referred to earlier. See also exhibit 41/1, a publication by the NHMRC in October 1975, containing model asbestos regulations and an accompanying guide. Paragraphs 12 and 13 of the guide state that it is not possible to specify a hygienic standard for asbestos at which the risk of cancer is removed, and that wherever there is a likelihood of exposure to asbestos dust, all essential steps should be taken to ensure that employees are not unnecessarily exposed.

214 Further and in any event, as already explained, standards of this kind are relevant but not determinative of the questions of duty and breach.

215 Accepting, as I do, the evidence of the plaintiff's experts, summarised above, and the material upon which they relied, I find that, as at 1970, the defendant knew, ought to have known or ought reasonably to have foreseen that:

(a) the asbestos in brake linings in Ford vehicles, or supplied by Ford to be fitted to Ford vehicles, would release respirable asbestos fibres when it was filed, ground or otherwise worked in order to be fitted;

(b) although a substantial majority of the asbestos in brake linings would or would probably be broken down into non-fibrous material by the braking process, brake dust would or may contain measurable quantities of respirable asbestos fibres;

(c) motor mechanics would, in the course of their work, be exposed to the respirable asbestos fibres referred to in (a) and (b);

(d) while the weight of opinion favoured the view that the carcinogenic effects of different varieties of asbestos, namely crocidolites, amphiboles and chrysotile, was markedly different, there was debate about that as at 1970, which debate continued during the 1970s. In any event, science had not determined, as at 1970, that there was any threshold level of exposure for any variety of asbestos, including chrysotile, below which there was no risk, or even no realistic risk, of life threatening injury including mesothelioma;

(e) it was thought that low doses of asbestos fibres were or might be capable of causing a life threatening injury including mesothelioma;

(f) good industrial or occupational hygiene practice required that reasonable steps be taken to reduce any exposure to asbestos, at whatever level the exposure might be; and

(g) various protective measures could be taken to reduce the exposure to asbestos of a motor mechanic, including eliminating the use of compressed air and dry sweeping, and using vacuum cleaners or wet cleaning methods and respirators.

216 Thus the defendant ought to have known that, if no protective measures were taken, there was a real risk, not merely a far-fetched or fanciful prospect, that asbestos fibres released from the brake linings of Ford vehicles would cause life threatening injury, including mesothelioma, to motor mechanics.

What the defendant knew or ought to have known during the period 1970 to 1987

217 The expert evidence and supporting material already referred to seems to me to sustain conclusions corresponding to those stated in the two preceding paragraphs of these reasons, in respect of the period 1970 to 1987. I find that, at no time through that period, did science determine that there was a threshold dose of asbestos generally, or chrysotile in particular, below which there was no risk or no realistic risk of any life threatening injury, including mesothelioma. See, for example, the exhibits already referred to, including exhibit 37/75, 37/331 and 41/15.

218 Further, those conclusions are reinforced by additional evidence, including as to what the defendant knew in the relevant period. I turn to that evidence.

219 Through the relevant period, the defendant received repair and service manuals from Ford US and Ford UK. Some only of these were in evidence. There is evidence that documents may have been destroyed pursuant to a document management policy (exhibit 40A). I do not, by that observation, intend any suggestion of impropriety (and none was suggested by the plaintiff). Rather, I note the possible destruction of relevant documents only as meaning that it should not be thought that the following is necessarily a comprehensive list of those repair and service manuals with any relevant warnings received by the defendant from Ford US or Ford UK.

220 The relevant repair and service manuals before the court include exhibit E (1971), exhibit 42/6 (1974), exhibit 42/13 (1983) and exhibit 42/14 (1984). The 1971 manual, for example, states that care should be taken during all repair operations to avoid inhaling brake shoes/pad dust. The 1974 manual says never to inhale dust from brake linings as asbestos dust, when inhaled, can be injurious to health. The 1983 manual says that, under no circumstances should compressed air blow-off be used to clean brakes, brake drums, clutches and associated components. The 1984 document warns that the 'brake assembly dust and dirt should not be removed by blowing off with an air gun because a health hazard from breathing asbestos dust may develop'.

221 Repair and service manuals issued by the defendant itself during the relevant period also, from time to time, included warnings about asbestos exposure during brake repair. Exhibit 42/9 is a service manual issued by the defendant for the 1978 Ford Transit. It includes a warning, at pp 2-6, and repeated at 2-7 to 2-8 in bold lettering, that:

Never inhale dust from brake linings. Asbestos dust when inhaled can be injurious to health. Do not blow out dust with an airline. A vacuum cleaner brush or rag should be carefully used to remove dust. Any dust should be contained in a sealed bag for disposal.

Similar warnings are to be found in manuals for other cars, including the Escort, Telstar and Transit at various times through the relevant period. See annexures DF2 - DF6 to the witness statement of Mr Ford (exhibit C).

222 Further, annexure DF7 to Mr Ford's statement is an extract from a technical services bulletin issued in 1977 by the defendant. Mr Ford says the bulletin appears to be issued to upgrade a service manual in accordance with a change from drum brakes to front disc brakes. The bulletin stated under the heading 'Rear Brake Shoes - Remove and Install' to 'clean drum with a rag or brush, do not use compressed air'. See also other technical service bulletins at exhibit 42/23, 42/24 and 42/25. Exhibits 42/24 and 42/25 each states that a person should 'observe the safety precautions regarding brake asbestos dust prior to overhauling/examining the brakes'. (These documents are not dated. There is no direct evidence as to their date. They were tendered by the plaintiff, having been discovered by the defendant. The defendant adduced no evidence in relation to these documents.)

223 There are also documents of the defendant, from various points during the relevant period, evidencing an awareness of the hazards relating to asbestos and of the need for and examples of, appropriate protective measures, in relation to asbestos in contexts apart from within brake linings (see annexures JD2 - JD4 to Mr John Dalzell's statement exhibit 2).

224 The defendant called Mr David Ford. For most of the 1980s he was on Ford's Operating Committee which he said was akin to a de facto board of directors. He said that he and others at Ford were aware there was a significant percentage of asbestos in brake linings (exhibit C par 55). Based on general conversations he recalls having with other members of Ford engineering management, he understood that, once the brake linings had been manufactured and the asbestos bonded into the linings, the brake linings were safe as the asbestos was totally encapsulated within the resins (exhibit C par 68). He was not aware of any suggestion there was a health risk for mechanics from asbestos in brake linings. He recalled, although he did not know when, enquiring with a brake lining manufacturer about the type of asbestos in brake linings. He was told that it was 'white' asbestos (chrysotile) and that the general understanding at the time was that it was the 'blue' asbestos (crocidolite) that was of more concern for potential health risks (exhibit C par 73).

225 I accept Mr Ford's evidence as to his understanding at the relevant time. Of course, that does not provide comprehensive evidence of the state of knowledge of the defendant as a whole. In any case, if Mr Ford's understanding of the position reflected that of the defendant, the question then arises as to what the defendant ought to have known.

226 The defendant called Dr Michael Goodman, a well qualified epidemiologist. He expressed an opinion, based on an analysis of all the studies in epidemiology, that work as a mechanic does not give rise to an increased risk of mesothelioma or asbestosis. That evidence will be referred to in detail, later in these reasons, in relation to causation. In cross-examination, he agreed that the type of analysis which he had undertaken could not have been done before 1980. He agreed that based on papers such as Lorimer (exhibit 37/295) published in 1976, that anyone reading the literature in the 1970s would have suspected there was a risk of mesothelioma and asbestosis from brake work (ts 962).

227 On the basis of the material already referred to, namely the plaintiff's expert evidence, which I accept, the exhibits tendered in support of those opinions, and the evidence of what the defendant knew during the relevant period, already referred to, I find that my conclusions as to what Ford knew, or ought to have known or ought reasonably to have foreseen, as at 1970, apply also to the period from 1970 to 1987.

228 The plaintiff also relies upon the material in exhibit 38, evidence of knowledge on the part of Ford US and Ford UK, in support of its factual case on foreseeability. I have made findings in favour of the plaintiff, in respect of foreseeability, without reference to that material. Nonetheless, for the sake of completeness, I propose to state, in summary form, my conclusions in respect of exhibit 38.

229 Exhibit 38 contains a substantial volume of material evidencing an awareness or belief, on the part of Ford US, that:

(a) brake dust contains some asbestos and could be hazardous to health and may cause mesothelioma; and

(b) compressed air should not be used to clean brake drums, and indeed its use was banned by Ford US to its dealers.

230 The material is accurately summarised in the plaintiff's written submissions and I will not detail it here. Mr Ford said in his evidence that staff of the defendant in Australia were encouraged to contact counterparts at Ford US if they had problems (ts 727). The evidence also establishes that the defendant received information, at least in the form of service and repair manuals and technical service bulletins, from both Ford US and Ford UK.

231 The defendant knew that the brake linings in Ford vehicles, and supplied by it as spare parts of Ford vehicles, contained asbestos. The defendant knew that asbestos could be hazardous. In the circumstances, the defendant ought to have taken reasonable steps to ascertain the scope of any risk arising from the known presence of asbestos in the brake linings. (As to the duty of a manufacturer to take reasonable steps to enquire into potential hazards of a product, see Western Australia v Watson [1990] WAR 248, 267; Scanlon v American Cigarette Co (Overseas) Pty Ltd (No 2) [1987] VicRp 23; [1987] VR 281, 284.)

232 The circumstances already found called for enquiry by the defendant. In the circumstances, and given the relationship between the defendant and Ford US and Ford UK, those latter companies were a readily available source of information for the defendant.

233 Further, the material in exhibit 38 can, in the context of the evidence of regular communication between the defendant and Ford US, assist in the drawing of an inference that the defendant would, on the probabilities, have received communications from Ford US to the substance and effect already stated.

234 The plaintiff also contended that the knowledge reflected in exhibit 38 could be attributed to the defendant, by reason of common directors or executives of Ford US and the defendant. I do not accept that submission. The knowledge of Ford US reflected in exhibit 38 cannot be automatically attributed to all its directors and executives, and there is no evidence that the particular individuals in question had any relevant knowledge.

235 Having made the findings set out above, I turn to the defendant's submissions in respect of the issue of duty of care.

236 The defendant pointed to a number of matters in support of its submission that it owed no duty of care to the plaintiff.

237 Many of those submissions fall away in the light of the factual findings which I have made. In other words, many of the defendant's submissions respecting duty invite conclusions on the evidence different from those which I have reached.

238 For example, the defendant's written submissions characterise the levels of exposure to which workers could legally be exposed under applicable regulations and laws as being the subject of government consideration 'as to levels below which no risk existed'. I have found that regulations and standards were not propounded on the basis that below the stated threshold no risk existed.

239 The submission, made in written submissions, that during the relevant period, numerous studies had determined that no increased risk to garage mechanics existed; that occupational hygienists believed that asbestos bonded in resin posed no danger; and that the heat from the friction of braking converted (implicitly, all) asbestos to inert substances, is not supported by the evidence and is inconsistent with the findings I have made.

240 The defendant also submitted that a ground on which the defendant did not owe a duty of care to the plaintiff was that 'it is not the fact that the level of exposure to which garage mechanics are exposed can increase the risk to them of asbestos related disease beyond the risk to which the general population is exposed'. For two reasons, I do not accept that submission. First, in my opinion it is not supported by the evidence. Whatever may be the position as regards asbestosis (a question to which I will return), the evidence established that any increase in the level of exposure to asbestos increased the risk of mesothelioma. There was no suggestion, from any expert in the case, that there was a threshold level below which an exposure to asbestos did not affect the risk of contracting mesothelioma.

241 Secondly, the submission invites consideration of the question of duty by reference to material not known at the time of the alleged breach. The question of whether a duty exists is to be assessed by reference to what was known and foreseeable at the time of the alleged breach. Any conclusion that scientific knowledge subsequent to the breach (available by the time of trial) meant that any exposure caused by the alleged breach was incapable of affecting the relevant risk, would go to causation, not to the question of whether a duty of care existed.

242 The defendant also submitted that the hazards of asbestos generally were widely understood by the time of the 1970s throughout Australia, including Western Australia, and avoidance of inhaling asbestos dust was a common sense measure requiring no elaboration. In the latter respect the defendant relied upon the observations of Heydon JA in Van Der Sluice v Display Craft Pty Ltd [2002] NSWCA 204 [74]. However, there is no evidence that it was widely understood, during the 1970s, by mechanics or their employers that brake linings contained asbestos. Consequently, while the dust produced in the course of servicing vehicles was no doubt inconvenient and, at times, unpleasant, it could not be confidently assumed by someone in the defendant's position that any danger or hazard arising from asbestos would be understood by those servicing vehicles with asbestos brake linings or by their employers.

243 I have found that, as at 1970, and for the period from 1970 to 1987, the defendant ought reasonably to have foreseen that, if no protective measures were taken, respirable asbestos fibres released from brake linings in Ford vehicles may, as a real and not far-fetched or fanciful possibility, cause a motor mechanic to contract an asbestos inhalation disease.

244 For the reasons discussed under the heading of 'Duty of care: legal principles', that conclusion would lead me to find that the defendant owed a duty to take reasonable care to avoid injury to motor mechanics arising from the asbestos in brake linings in Ford vehicles or in brake linings supplied by the defendant.

245 However, as has already been observed in that section of these reasons, the duty of care pleaded by the plaintiff in this case is expressed not in that way, but as a duty to give warnings. Care is needed to ensure that formulation of the duty in that way is not permitted to have the effect of obscuring the proper inquiry to be undertaken at the breach stage of the analysis. Generally, the question of whether the provision of a warning is within the scope of a duty of care in a particular case will be determined at the breach stage of the analysis when considering the reasonable response to a risk identified as reasonably foreseeable. Here, the duty is expressed in terms of a duty to give two categories of warnings (summarised earlier in these reasons under the heading 'The pleadings'). The breach is particularised as a failure to give five categories of warning or advice.

246 To avoid any risk of obscuring the proper inquiry to be undertaken at the breach stage of analysis, I will state my conclusions in respect of the question of duty of care in a way that is subject to my consideration of whether reasonable care in the circumstances required the provision of any (and if so what) warnings. As will appear, I come to the conclusion, in considering the breach question, that reasonable care did require warnings to be given by the defendant.

247 Subject to that proviso, I find that the defendant owed the plaintiff a duty of care.

248 The question of whether a duty to take reasonable care has been breached is about what a reasonable person would do by way of response to the risk of injury which was foreseeable. Identifying the reasonable person's response requires consideration of the magnitude of the risk and the degree of the probability of its occurrence, along with the expense, difficulty and inconvenience of taking alleviating action and any other conflicting responsibilities which the defendant may have: Wyong Shire Council v Shirt (47 - 48) (applied in Vairy v Wyong Shire Council [2005] HCA 62; (2005) 223 CLR 422 and Mulligan v Coffs Harbour City Council [2005] HCA 63; (2005) 223 CLR 486).

249 A failure to eliminate a risk that is reasonably foreseeable does not establish negligence. In some cases the response of a reasonable person to a foreseeable risk may be to do nothing: Mulligan [3]; Aerospace Engineers Services Pty Ltd v Ibrahim [2007] WASCA 33 [20].

250 Proper inquiry at the breach stage involves identifying with some precision what a reasonable person would have done by way of response to the foreseeable risk: Graham Barclay Oysters [192]; Amaca Pty Ltd v Hannell [356].

251 It is for a plaintiff to demonstrate that there was something that the defendant could have done which would eliminate or reduce the risk complained of and which was practicable: Roman Catholic Church Trustees for the Diocese of Canberra v Hadba [2005] HCA 31; (2005) 221 CLR 161 [13]; Amaca Pty Ltd v Hannell [356].

252 When assessing reasonableness, a hindsight analysis is to be avoided: Vairy (especially at [105], [126] - [129]); Neindorf v Junkovic [2005] HCA 75; (2005) 80 ALJR 341 [93]; Homestyle [47].

253 Further, what is reasonable must be assessed by reference to all members, present and future, in the class of which the plaintiff is a member: Amaca Pty Ltd v Hannell [365]; and by reference to all the relevant risks, ascertained at the time in question: Mulligan [50]; Vairy [127].

254 Consideration of whether the defendant breached its duty of care involves identifying what reasonable care required of the defendant and measuring this against what the defendant in fact did.

255 I begin by considering the question of what, if anything, reasonable care required the defendant to do in response to the foreseeable risk of harm to motor mechanics from inhaling asbestos fibres released from the brake linings of Ford vehicles (or spare parts supplied by Ford).

256 The seriousness of the potential harm to a mechanic, arising from inhaling asbestos fibres, must be taken into account. As I have found, the defendant knew or ought to have known or foreseen at the relevant time that inhalation of asbestos fibres gave rise to a risk of life threatening disease.

257 Regard is also to be had to the degree of probability of the risk in question materialising (measured according to what was known or ought to have been known by the defendant at the relevant time). In the light of the evidence and the findings I have made, I consider the degree of probability to have been very low: the contraction of disease was very unlikely (although a real and foreseeable risk).

258 I have already found that the defendant knew or ought to have known that various protective measures could be taken so as to reduce the potential exposure of a mechanic to asbestos, including eliminating the use of compressed air and dry sweeping, and involving the use of vacuum cleaners or wet cleaning methods and respirators.

259 Further, I find that the defendant should have known that mechanics and their employers may not have been aware that brake linings contained asbestos, or of the consequent risks or need to take protective measures, or of what suitable methods were available. The evidence does not support a conclusion that the defendant had any reasonable basis to assume that mechanics and their employers all knew that brake linings contained asbestos. There is evidence of warnings about avoiding asbestos dust from brakes in certain service manuals for particular models of Ford vehicles, referred to in my earlier discussion of what the defendant knew or ought to have known during the period 1970 to 1987. However, for reasons explained shortly, when I consider the question of what steps were taken by the defendant by way of warnings, the defendant could not reasonably have proceeded on an assumption that such warnings had come to the attention of all professional mechanics or their employers.

260 On the face of things, those circumstances and that knowledge (actual or constructive) would seem to require at least consideration to be given by the defendant as to whether there were practical available means to communicate to mechanics at least the following:

(b) inhalation of asbestos dust and fibres can lead to life threatening disease;

(c) steps should be taken to eliminate or reduce inhalation of dust from brake linings, including:

(i) not using compressed air to blow out brake dust, instead using a vacuum cleaner or a wet method;

(ii) using a respirator when filing, sanding or grinding brake linings; and

(iii) not dry sweeping areas which have brake dust.

261 The defendant submits that it had no effective means of identifying or communicating directly with professional mechanics.

262 The plaintiff's case is that the defendant's duty required it to give warnings either directly, to professional motor mechanics, or indirectly, by warning the employers of motor mechanics.

263 The plaintiff submits that there were a number of methods available to the defendant for communicating appropriate warnings. The plaintiff says that warnings could have been given by way of labels or inserts with spare parts; through a variety of means of communication with Ford dealerships; through courses run by the defendant for mechanics; and through communication during the regular attendances of representatives of the defendant at Ford dealerships.

264 To my mind, a practicable and appropriate measure, available to the defendant, in the circumstances as I have found them, was to insert a warning, in an eye-catching or obtrusive style, in or on (or both) the boxes or other containers containing brake shoes and brake pads supplied by it as spare parts. Of course, such a step would not have immediately provided a warning in respect of the Ford vehicles already fitted with brakes containing asbestos lining. However, on the evidence, in the course of servicing brakes, brake shoes and pads were regularly replaced. In that way a warning as a label on or insert with spare parts could have been expected to bring the safety information respecting asbestos to the attention of mechanics and their employers.

265 There does not seem to me to be any other reasonably practicable steps available to the defendant which would have effectively communicated relevant warnings to all professional mechanics or to the employers of all such mechanics. None was suggested by the plaintiff.

266 The substance of what, I find, the defendant ought to have communicated, by way of a label or insert in its brakes spare parts, is as set out in (a) - (c) of [260] of these reasons.

267 I note that the substance of that warning is substantially similar to the warning given by the defendant in certain of its service manuals: see, eg, exhibit 42/9 and annexures DF2 - DF6 of exhibit C.

268 Such warnings should, I find, have been given from 1970 and throughout the period 1970 to 1987. That follows from my earlier findings as to what the defendant knew or ought to have known as at 1970 and through the period 1970 to 1987.

269 I turn to the question of what steps the defendant took by way of attempt to warn in relation to hazards arising from the presence of asbestos and other protective measures.

270 There was little evidence in relation to that topic. The evidence of Mr Ford is to the effect that, for a substantial part of the relevant period at least, he and others on the Operating Committee were not aware of any suggestion that there was a health risk for mechanics from asbestos in brake linings. His understanding was that because the asbestos was bonded into the linings, it was totally encapsulated within the resins and did not pose a hazard.

271 To the extent that such an understanding was held at senior executive level, it might not be surprising if little or no attempt was made to warn mechanics of any risk arising from asbestos in brake linings.

272 There is evidence of warnings in certain service manuals for particular models of Ford vehicles. These are detailed in the earlier discussion of what the defendant knew or ought to have known during the period 1970 - 1987. Similarly, there is some evidence of technical service bulletins updating specific service manuals which include some warnings or other statements about avoiding inhaling asbestos dust or means of doing so.

273 It is unclear, on the evidence before me, whether and to what extent such warnings were commonly found in service manuals.

274 In any event, in my opinion the giving of warnings in the manner given in the service manuals already referred to does not constitute a sufficient response to the risk in the circumstances of this case. The service manuals are extremely voluminous documents. The warnings are found in parts of the manuals which concern routine tasks and, as the defendant itself submitted, were unlikely to be read by professional mechanics. The risk of life threatening disease to motor mechanics, albeit very unlikely to materialise, called for the giving of warnings in a way which was better calculated to come to the attention of mechanics and their employers.

275 The defendant submitted that any warning beyond those contained in the defendant's product manuals would have been disproportionate to the relevant risk. In circumstances where the defendant ought to have known or foreseen that there was a real risk (albeit small) of life threatening injury to motor mechanics if no protective measures were taken, the expense and inconvenience of including a warning label or insert with spare part brake pads or discs would not, to my mind, have been disproportionate to the risk sought to be reduced or eliminated.

276 It is clear from the evidence that there were no warning labels or inserts on or in the boxes or other packaging of the brake shoes and discs.

277 For those reasons, I find that the defendant breached its duty of care to professional motor mechanics, including the plaintiff, by failing to insert a warning, in the terms already referred to, in or on the boxes or other containers containing brake shoes and brake pads supplied by it as spare parts.

278 That conclusion invites attention as to whether reasonable care required any other steps, by way of warning, to be taken by the defendant.

279 I have already found that there were no other reasonably practicable steps available to the defendant which would have effectively communicated relevant warnings to all professional mechanics or their employers.

280 There were, however, a range of possible means of communication by the defendant with Ford dealers. The evidence establishes that, from time to time in various ways, Ford communicated with its dealers. Bulletins or letters were sent by the defendant to its dealers. The question is whether reasonable care called for warnings to be given in such communications in circumstances where, I have found, warnings should have been provided with the parts.

281 I am not satisfied that, if warnings were provided with the relevant spare parts, reasonable care required further specific communication by the defendant to the Ford dealerships. By its one-off or occasional nature, such communication was less likely to be effectual than the regular presence of a label or insert with spare parts. Moreover, it would only have reached a subset of those to whom a warning should have been given. It would, I think, have been reasonable to proceed on the basis that one could be sufficiently confident that the warnings in or on the boxes would come to the attention of mechanics and their employers as not to require further steps to be taken.

282 If, contrary to my view, reasonable care did not require the provision of appropriate labels or warnings with spare parts, then I would have found that reasonable care required that the defendant communicate appropriate warnings to its dealers. I am aware that that would not have assisted the mechanics who worked elsewhere than for Ford dealerships. Nonetheless, that does not seem to me a sufficient reason to exclude the taking of what was a readily available step to attempt to reduce a foreseeable risk of life threatening injury to those mechanics who worked at Ford dealerships.

283 For substantially similar reasons, had I not found that reasonable care required provision of warnings by way of labels or inserts, I would also have found that reasonable care required that, at the training sessions for mechanics which it held, the defendant convey the substance of the warning already referred to to the mechanics in attendance.

284 For the reasons given, I have found that the defendant breached its duty of care to professional mechanics, including the plaintiff, by failing to insert a warning, to the effect already referred to, in or on the boxes or other containers containing brake shoes and brake pads supplied by it as spare parts.

285 There are two factual issues raised as to causation. The first is whether any required warnings would have been heeded. The second is a very substantial issue: was the plaintiff's pulmonary fibrosis caused by exposure to asbestos? As will appear, I resolve these factual issues in favour of the plaintiff. Thereafter, I apply the legal principles as to causation to the facts as found, concluding that the defendant's negligence caused the plaintiff's asbestosis.

Causation - would a warning label or insert have been heeded?

287 The defendant submitted that a warning by written material contained within the boxes in which brake shoes and pads were delivered by the defendant would be unlikely to have reached the plaintiff, who regarded brake work as simple and who, the defendant submits, it should be concluded does not read English.

288 The proposition that he cannot read English was never put to the plaintiff. I do not think the evidence supports a finding that he does not read English.

289 In any event, the question of causation in this case is not, on my analysis, confined to the issue of whether the plaintiff himself would have read a warning label or insert with brake spare parts. The plaintiff worked for many years at Anderson Ford. The work practices at Anderson Ford and the evidence of other persons who worked there over a period of decades support the conclusion that hazards associated with the presence of asbestos in brake linings, and the consequent need to take protective measures, were generally not appreciated by those working in and managing the workshop.

290 Had the risks associated with the presence of brake linings and the need to take protective measures, with such measures being identified, been known by those in management, or by at least any significant numbers of those working at the workshop then, I find, it is likely that the suggested protective measures would have been implemented and the use of compressed air would have stopped.

291 On the probabilities, had warnings of the kind already referred to been inserted on or in the boxes containing relevant brake spare parts, the contents of those warnings would have come to the attention of sufficient people to ensure that the work practices which occurred at Anderson Ford would not have been adopted. Rather, practices would have occurred in accordance with the recommendations on the warning label or insert.

292 For example, Mr Hinkley, the manager of the Quick Service at Anderson Ford, gave (unchallenged) evidence that had he been warned about the dangers he would have insisted that various measures be taken.

293 I find that had the warnings been given by label or insert in the boxes or other container containing the brake shoes or discs, the plaintiff would not have been exposed to the asbestos arising from the work practices at Anderson Ford and Col Commons. Rather, protective measures as suggested in the warning would have been implemented.

294 If such measures had been implemented then it is clear that the exposure of the plaintiff to asbestos would have been very considerably diminished (see, for example, the evidence of Dr Paustenbach ts 1123 and Associate Professor David McKenzie ts 1058).

Causation - does the plaintiff have asbestosis?

295 This action raises a substantial factual issue going to the heart of the question of causation: does the plaintiff have asbestosis?

296 The causation issue presented in this case is different in character from the causation issues often arising in claims for asbestos inhalation injury. In many such cases, the issue is whether the exposure arising from the defendant's negligence caused or contributed to the asbestos inhalation disease suffered by the plaintiff, in circumstances where other sources of exposure to asbestos are identified. In this case the question is whether asbestos caused the fibrotic condition at all.

297 Asbestosis is one of the well-known possible effects of exposure to inhalation of asbestos. There are other known consequences, some of which are malignant, including mesothelioma and lung cancer.

298 Asbestosis can be caused by crocidolite, amosite or chrysotile asbestos.

299 Asbestosis affects the walls of the air spaces in the smallest conducting airways of the lungs. The precise causal mechanism appears not to be known with certainty. It is thought that the asbestos fibres cause inflammation, leading to scarring or fibrosis of the walls of the small airways and air spaces. The fibrosis is diffuse, in that it occurs throughout the lung (although not necessarily evenly throughout the lungs). It is interstitial in that it is found between the alveolar lining cells and the cells lining the blood capillaries on the walls of the alveoli.

300 The main symptom of asbestosis is progressive breathlessness, initially during exertion but later also at rest. The breathlessness may be accompanied by cyanosis (bluish colouration of the skin due to low levels of oxygen in the blood). With more advanced asbestosis, the load on the right side of the heart is increased as the pressure in the circulation through the lungs increases. Death from asbestosis usually results from respiratory failure.

301 Pleural plaques are localised areas of thickening on the inner pleural lining of the chest wall. They may become calcified by having calcium-containing compounds deposited within them.

302 It is not in dispute that the plaintiff has pleural plaques and suffers from a serious fibrosis of his lungs. One type of pulmonary fibrosis is asbestosis. There are others.

303 Asbestos induced pulmonary fibrosis is known as asbestosis. There are a variety of pulmonary fibrotic conditions which may be caused by a number of agents other than asbestos. Some of these conditions exhibit many of the same characteristics as asbestosis. (The detail of that is one of the issues and is dealt with later in these reasons.)

304 There is a recognised disease or condition known as idiopathic pulmonary fibrosis (IPF). This is pulmonary fibrosis of an unknown cause. In Britain, IPF is termed cryptogenic fibrosing alveolitis.

305 Another pulmonary fibrotic condition, or collection of conditions, recognised in recent years, of an idiopathic nature is non-specific interstitial pneumonia (NSIP).

306 The plaintiff relies primarily upon the evidence of Professor Musk and Professor Robinson, both of whom expressed the opinion that the plaintiff has asbestosis. The defendant relies upon evidence of Associate Professor McKenzie to the effect that the defendant has IPF or NSIP, and not asbestosis.

307 The classification and nomenclature of pulmonary fibrotic conditions is, relevantly, based on what the causal agent for the condition is believed to have been. Because of that, the medical question of diagnosis has the central question of causation inherent within it.

308 Nonetheless, the question of whether the plaintiff's pulmonary fibrosis was caused by his exposure to asbestos is a question for the court, which must come to its own conclusion. In doing so, it may well (but need not) derive significant assistance from the medical evidence. Further, it is not only medical evidence which bears upon the question of whether the plaintiff has asbestosis. The parties relied upon a range of other categories of evidence as relevant to the question of diagnosis. There are issues as to whether and to what extent some of these categories are capable of assisting or do assist in determining the question of diagnosis.

309 Both parties invited attention to the plaintiff's work history. Both parties also called industrial hygienists, each of whom gave quantitative estimates of the level of exposure of the plaintiff to asbestos in the course of his work. The defendant relied upon epidemiological evidence as to whether there is any association between work as a motor mechanic and the level of incidence of asbestos related diseases including mesothelioma, lung cancer and asbestosis. The plaintiff says that such evidence is, as a matter of law, incapable of assisting in this case and, in any event, on a proper analysis provides little or no assistance. The defendant also relied upon evidence as establishing that there is a threshold level of exposure to asbestos, below which asbestosis will not occur. The plaintiff denies any such threshold exists.

310 The plaintiff submitted that in determining the question of whether he has asbestosis or IPF or NSIP, the medical evidence is of primary significance. In the end, on my analysis of the evidence as a whole, for reasons to be developed, that is the view to which I have come.

311 I have considered the evidence relied upon by the parties as to causation as a whole, not simply discretely within the particular categories I have identified. Nevertheless, for ease of exposition, it is convenient to deal with the categories in turn.

312 In this case, no lung biopsy has been done. That is for clinical reasons of avoiding unjustified risks to the plaintiff.

313 I have already made findings in relation to the plaintiff's work history.

314 I will set out my findings in relation to the evidence of witnesses who provide dose estimates, then the epidemiological evidence, before turning to the medical witnesses.

315 Both parties adduced evidence from occupational hygienists who provided estimates of the aggregate exposure to asbestos fibres experienced by the plaintiff during his work as a motor mechanic from 1970 to 1987.

316 Plainly, there are some difficulties in making accurate estimates in circumstances where no measurements were taken at the time in respect of any part of the plaintiff's employment. Both the main experts in this regard (Mr Francis and Mr Rogers) said that, even where measurements are taken, substantial error ranges are allowed for (somewhere from 30% to 50%) in the measurements.

317 The method of estimating used by the experts involved having regard to published studies in which measurements had been taken in the work environment of a car mechanic, so as to provide data as to exposure to asbestos. Of course, of necessity that means that consideration must be given to the question of the extent to which the work conditions the subject of the sampling correspond to those of the plaintiff.

318 Occupational hygienists have devised methods by which to sample and measure the concentration of asbestos fibres in given air space. That is sought to be done in a way which enables extrapolation of the results of the period of sampling more broadly to the conditions experienced, across the whole day or week, by those in the workplace in question.

319 In this regard, account must be taken of different conditions experienced in the course of performing different tasks or when different operations are occurring in a workplace. Peak exposures will be experienced during an operation which creates significant measurable asbestos dust or fibres. However, if that operation is only performed once a week, across the week the average exposure will be significantly lower.

320 These considerations are accommodated by the use of a time weighted average (TWA) exposure. This is calculated over a normal 8-hour working day for a 5-day working week. This can be done by identifying relevant tasks giving rise to exposure, monitoring each individual task for its exposure, and then estimating the proportion of time spent on each task. On that basis, a TWA exposure can be calculated. Another method of arriving at a TWA exposure is to make a series of samples throughout the period of the working day.

321 The primary method of sampling the airborne asbestos appears to be the membrane filter method. By this method, an air pump or sampler is placed in the area to tested. Measured quantities of the ambient atmospheric air pass through the sampler. Within it are filters or membranes through which the air passes. The membranes capture airborne particles of dust or other substances. By relating the number of fibres observed to the quantity of air passing through the pump a figure is derived of the number of fibres per ml of air.

322 The membrane filter method does not involve an identification that the fibres observed under the microscope are asbestos. The method counts the fibres; it does not identify what the fibres are. Other technology needs to be involved for that to occur. One available technology for this purpose is known as analytical transmission electron microscopy (ATEM).

323 A figure for a cumulative exposure can be derived by multiplying the period of the exposure by the TWA exposure. Thus, for example, a person who is exposed to a TWA exposure of 2 fibres/ml for a period of 5 years will have a total cumulative exposure of 10 fibres/ml years. The total cumulative exposure is sometimes referred to as a person's 'dose' of asbestos.

324 The plaintiff relied upon evidence from Dr Francis. She is a retired occupational hygienist who worked in the Division of Occupational Health within the Health Department of New South Wales for almost 30 years. She has a Bachelor of Pharmacy, Master of Pharmacy and Doctor of Philosophy in Pharmaceutical Chemistry from the University of Sydney.

325 Her work at the Health Department focused primarily on the investigation of workplaces where employees were exposed to respirable fibres. Her work involved her measuring the asbestos exposures of workers in a number of work environments. She has written a number of papers in the field of respirable asbestos fibres and has served on a number of committees of the NHMRC assisting in the production of guidelines relating to levels of asbestos exposure.

326 Dr Francis' report of 4 July 2007 is exhibit 14.

327 It set out that she had made assumptions as to the plaintiff's work environment and what he did, in accordance with letters from the plaintiff's solicitors dated 30 May 2006 (exhibit 12) and 12 June 2007, although apparently sent on 2 July 2007 (exhibit 13).

328 She summarised her understanding of the history and his exposure in pts 3 and 4 of her report.

329 At pt 6 of her report she set out her asbestos exposure estimates. For the Anderson Ford general workshop area she estimated an average airborne asbestos exposure in the range of .7 to 3 fibres/ml. For the Quick Service area she estimated the average would have been .7 fibres/ml for 75% of the time and 3 fibres/ml for 25% of the time. For the Col Commons' workshop she estimated the average exposure to be in the range of .5 to 2 fibres/ml.

330 From those figures, using the bottom and top figures of those ranges and applying them to the period of time the plaintiff spent in each workshop, she calculated a cumulative asbestos exposure for the period 1970 to 1987 in the range of about 11 to 34 fibre/ml years.

331 The basis of the estimates is said to be Dr Francis' personal experience, as detailed in pt 1 of the report, and the references referred to in pars 6.6 to 6.10 of the report (ts 393).

332 The plaintiff also relied upon the evidence of Dr Egilman. In his report dated 31 May 2007 he was asked whether he agreed with Dr Francis' report as to her assessment of the plaintiff's likely exposure. He said that he did, stating that in general he agreed that the average exposures were in the .7 to 3 fibres/cc (ie fibres/ml) range.

333 The defendant objected to the admission of Dr Egilman's report (MFI 16A), primarily on the ground that his process of reasoning and calculation is inadequately exposed. It was agreed by the parties that the ruling would be given after closing submissions were completed. I will return to this matter later in these reasons.

334 The defendant relied upon three reports from Mr Rogers. Mr Rogers is a very well qualified occupational hygiene consultant. He has a Bachelor of Science in Pure and Applied Chemistry (UNSW), a Master of Science in Occupational Hygiene (University of London) and a Master of Science in Environmental Chemistry (UNSW). He is certified by both the American Board of Industrial Hygiene and the Australian Institute of Occupational Hygienists.

335 Mr Rogers has, since 1978, actively researched the association between asbestos and diseases such as asbestosis, lung cancer and mesothelioma in Australia. He continues to publish the results of his research. He was a member of the research panel for the Australian Mesothelioma Surveillance Programme and the Australian Mesothelioma Register. He was responsible for assessing the occupational histories of all 3,758 Australian mesothelioma cases in terms of the degree of asbestos exposure as well as in industry and occupation. He has published a number of papers, including some which are directly relevant to the issues in this case.

336 His first report was dated 24 December 2006 (exhibit F1). In it he referred to studies showing that the heat generated by the braking process causes the vast majority of original asbestos in brake linings to brake down into non-fibrous magnesium silicates such as forsterite. For that reason, he said, figures as to the exposure of asbestos of those involved in the manufacture of brakes, or those who regularly grinded and filed brakes, ought not to be equated with the position for those in the general brake servicing and repair industries whose primary exposure is to brake dust.

337 In pt 3.2 of the report he provided an analysis of the published data regarding TWA exposures for persons working as mechanics. An overview of the published TWA exposure value is set out in a table on p 13 of his report. He concluded that the historical 8-hour daily TWA exposure of workers involved in routine brake and clutch repairs is no more than .2 fibres/ml and most likely .05 fibres/ml or less.

338 He then proceeded to use the average exposures already referred to for the various periods of the plaintiff's work. He concluded that over his years as a mechanic the plaintiff's cumulative exposure to chrysotile is estimated as no more than 3.4 fibre/ml years and most likely less than 1.7 fibre/ml years.

339 Mr Rogers' second report is dated 14 January 2007 (exhibit F2).

340 It developed in considerably more detail a point adverted to in the first report, as to the breakdown of the asbestos in brake linings in the course of the braking process. In the second report, Mr Rogers explained that the membrane filter method does not identify whether the fibres observed are asbestos. A different technique such as ATEM is required for that purpose. He referred to various studies indicating that the vast majority of the fibres found from brake dust are not of the same composition as the original chrysotile asbestos in the brake linings.

341 In consequence, Mr Rogers said, in his second report, that the figures of 1.7 to 3.4 fibre/ml years in his first report were estimates of regulatory fibres not asbestos fibres. He said that the exposure to asbestos would have been in the region of 1% to 2% of the figures in his first report.

342 His third report was dated 17 September 2007 (exhibit F3). It expanded on some of the points earlier made. It concluded that actual asbestos fibre exposures are likely to be in the range of 1 to 3 orders of magnitude (1/10th to 1000th) less than the reported total fibre values in his first report.

343 It can be seen from this outline of the competing views that the estimates of exposure provided by the parties' experts are different to a very substantial degree. On the basis of Mr Rogers' original report, his estimates were, broadly, 1 order of magnitude lower than those provided by Dr Francis. However, taking into account his second report, his estimates are about 3 orders of magnitude different from those of Dr Francis.

344 I am not satisfied that any of the dose estimates provided by the experts called by the parties should be accepted as a reliable estimate of the plaintiff's cumulative exposure to asbestos. That is so broadly because I accept, in respect of each expert, the submissions made by the opposing party as to why that expert's evidence ought not be accepted as a reliable estimate. That being so, I will not recite every detail of my reasons for so finding, but propose to deal with the matters which seem to me to be of most significance.

345 The basis of Dr Francis' estimates was not clearly articulated in her report. In particular, how the references set out in pars 6.7 to 6.10 supported the estimates given in respect of the plaintiff was not made clear.

346 When, during cross-examination, Dr Francis was invited to explain how estimates given in some of the literature she relied upon supported the estimates she had given of the plaintiff's exposure, I found her explanations of her reasoning to be, in significant respects, difficult to follow and, often, insofar as I could follow them, unconvincing. I will give some examples.

347 Dr Francis was cross-examined in relation to the study by Hickish & Knight (exhibit 37/30). In that study an estimate of the daily exposure of the mechanic engaged on brake cleaning was given, covering a work shift during which brake servicing was carried out on 11 vehicles. The TWA exposure was said to be .68 fibres/ml. Dr Francis was asked how, taking into account what was in Hickish & Knight's study, she had derived her estimate of a maximum exposure of 3 fibres/ml. She explained that by reference to the exposure associated with the use of emery paper, to which she attributed a figure of 2.3 fibres/ml. I accept that account should be taken of exposure arising from the use of the emery paper, especially as it was frequently used. The question is how to derive a reasonable basis for a reliable estimate. There were, she said, no studies estimating exposure in the context of the use of emery paper. She treated the work with the emery paper as being roughly equivalent to processes of grinding or linishing (ts 422 - 431). However, those latter processes involve the application of machines rather than hand rubbing.

348 The figures in par 6.3 of the report are based on an assumption that the plaintiff spent 75% of his time blowing out brakes and 25% of time using emery paper (ts 416). That was said to be because she understood the plaintiff said he used emery paper on about a quarter of the jobs. At one point of her evidence Dr Francis appeared to agree that the effect of her approach was to assume that he had spent a quarter of the two and a half years rubbing with emery paper (ts 428). However, she then appeared to say that it was based on intermittent occasions when he would do work of that nature.

349 In the end, I was left without a clear understanding of the basis upon which the figure of 3, especially the component of about 2.3 for the work on emery paper, had been derived, and, insofar as I understood what had been articulated, I am not satisfied that it provides a reasonable basis for a reliable estimate.

350 Next, Dr Francis had understood that there was a rotation system in the Quick Service area but had not understood that rotations occurred on a substantially equal basis. Nonetheless, she said that if she assumed that one week in five was blowing out the brake drums, that would not lead her to re-think her estimates (ts 414 - 415). The reasons given for that (ts 415) were not readily comprehensible to me. Further, Dr Francis agreed that there was a difference between the time when the plaintiff was doing a brake job and the time when he was in the workshop while others did a brake job. Dr Francis said the exposure in the first case would be at a higher level. I was left uncertain as to what estimate had been used for the lower level (while others had done brake work) and the basis for deriving such an estimate.

351 For the 11 years that the plaintiff worked at Col Commons, Dr Francis estimated the plaintiff's exposure to be in the range of .5 to 2 fibres/ml. I find that her estimate of the plaintiff's exposure in this period was based upon assumptions as to the plaintiff's activities which are not established on the facts that I have found them. In particular, she assumed that he worked on truck brakes every week or two on average (ts 439). She accepted that if, as I have found, he worked on trucks only two or three times a year, that would have an impact on her figures by considerably decreasing her estimate.

352 One of the papers upon which she relied in her report was a paper by Plato et al (exhibit 37/212). The range referred to in that paper, in the abstract, was a TWA exposure range of .1 to .41 fibres/ml in 1965 compared to much lower figures in 1985. When asked what support she derived from the paper for her estimates she said that it has been presented as an 'example of the lower range of the possible exposure' (ts 442). She did not explain how the figures in the Plato et al study supported the figure at the bottom of the range which she had used (namely .7 fibres/ml).

353 When asked to identify the paper or papers from which she derived the upper range, in addition to Hickish & Knight, she referred to a paper by Rohl. However she agreed that that paper related to peak exposures not TWA exposures.

354 For the reasons given, I do not accept Dr Francis' evidence as providing a reliable estimate of the plaintiff's exposure to asbestos.

356 Dr Egilman's reasoning in stating that he agreed with Dr Francis that the average exposures were in the .7 to 3 fibres/ml range is not exposed, at all, in his report (MFI 16A).

357 I would uphold the defendant's objection to that part of Dr Egilman's evidence. The failure to expose the reasoning means, in my opinion, that I am unable to be satisfied that Dr Egilman's opinion is admissible as expert evidence: Pollock v Wellington (1996) 15 WAR 1; Pownall v Conlan Management Pty Ltd (1995) 12 WAR 370, 390; Makita (Australia) Pty Ltd v Sprowles [2001] NSWCA 305; (2001) 52 NSWLR 705.

358 If, contrary to my view, the evidence were admissible, for reasons corresponding to those given in relation to Dr Francis' evidence, I would not be prepared to act upon it as a reliable estimate of the exposure of the plaintiff. That conclusion applies to the evidence in his report (MFI 16A). It also applies to the additional evidence given by Dr Egilman in the course of cross-examination, including his reference to the table in MFI 16C and his observation that, although he has not done a calculation, he would say that the total exposure was probably about 30 to 40 fibre/ml years (ts 473). It is not sufficiently clear to me what assumptions he has made as to the various tasks giving rise to exposure, how often they occurred, what exposure level is to be attributed to each, and so on, to enable me to act on his evidence.

359 A convenient starting point for consideration of Mr Rogers' evidence is by reference to a comparison between his first report and his second report. As outlined above, his second report provided estimates for the plaintiff's exposure to asbestos which were in the region of 1% to 2% of the exposure estimates in his first report.

360 For the reasons which follow, I do not accept the re-calculation of exposure estimates found in the second report.

361 His first report was in terms that over the relevant period the plaintiff's cumulative exposure 'to chrysotile' was estimated as no more than 3.4 fibre/ml years and most likely less than 1.7 fibre/ml years. Thus the estimate was not expressed (as Mr Rogers sought to suggest at times in cross-examination) as an estimate of regulatory fibres, but as an estimate of chrysotile asbestos fibres. Moreover, that is what Mr Rogers had been asked to provide; see exhibit 35 which sought an estimate of total cumulative asbestos exposure.

362 That invites attention to the question of why the approach taken in the second report was not taken in the first report. Mr Rogers was asked this question but, to my mind, provided no satisfactory response. His response to the question (ts 1181) was largely non-responsive, rather he sought to say things supporting his position generally. That approach to responding to questions seemed to me a not uncommon feature of Mr Rogers' evidence.

363 The re-calculation in the second report followed the receipt by Mr Rogers of a letter from the defendant's solicitors (exhibit 34). Mr Rogers did not suggest that, but for the letter, he would have undertaken the recalculation. I find that the recalculation was not an idea of Mr Rogers, but was something prompted by the letter from the defendant's solicitor.

364 One of the studies relied upon by Mr Rogers was co-authored by Dr Paustenbach (exhibit T1). In that study, the authors stated that all the studies that they had relied upon had been those which had checked their samples for asbestos fibres greater than 5 microns in length and with at least a 3 to 1 width ratio using phase contrast optical microscopy.

365 Mr Rogers could not identify any published work where the asbestos exposure had been recalculated in a fashion similar to the approach he had taken in his second report (ts 1183).

366 In all these circumstances I do not accept the recalculations of exposure in Mr Rogers' second report.

367 At various times in the course of cross-examination, Mr Rogers was asked questions about matters which might alter an element of his estimates of the plaintiff's exposure. At times, it seemed to me that Mr Rogers' response to such questions was affected by his firm view that the exposure was to be calculated as set out in his second report. That view led him to tend to see adjustments to elements of the exposure estimate as being insignificant to the overall result. See, for example, his evidence at ts 1199 - 1200 and ts 836.

368 Although a reading of Mr Rogers' written reports might be suggestive of a careful and precise approach to the process of estimation, his responses in cross-examination did not create that impression. See, for example, the passages just referred to. Other examples of this lie in the use which he made of published studies as a reliable guide for estimating the exposure experienced by the plaintiff and in his answers to questions about those studies.

369 I have set out, earlier in these reasons, my findings as to the work practices and environment experienced by the plaintiff. I will not repeat them here, but will mention a few matters. The plaintiff worked in an environment in which he and others always used compressed air to blow out brake dust. Emery paper was often used to sand or deglaze brakes. From time to time a new brake shoe and lining would be filed. I have made findings as to the extent of the dustiness of the Quick Service workshop.

370 I am not satisfied that the papers relied upon by Mr Rogers involved work practices and environments which substantially reflected the plaintiff's work practices and environment, or that Mr Rogers sufficiently took account of differences or possible differences in work practices and environment in deriving, from the published studies, his estimates for the plaintiff's exposure.

371 My conclusions in that regard are drawn from substantial and lengthy evidence in cross-examination in these respects and from consideration of various of the studies referred to by Mr Rogers. I do not propose to burden these lengthy reasons with a detailed recitation of all those matters, but refer to the following.

372 A number of the studies relied on by Mr Rogers involved a range of work environments, in some of which compressed air was used, but in others of which it was not used. These include studies by NIOSH (ts 1169, 1175), by the National Industrial Chemicals Notification and Assessment Scheme (ts 1172), by Roberts et al (ts 857 - 862) and by Lamont & Moore (ts 875). The presence or absence of the use of compressed air to blow out the brakes is significant to the level of exposure experienced. I am not satisfied that Mr Rogers had sufficient regard, in using the figures from these studies, to the differences or likely differences between the work environment of those the subject of these papers and the plaintiff's work environment.

373 Similarly, special exhaust ventilation was used during some of the blowing out of brakes in another study relied upon by Mr Rogers: Rodelsperger et al (exhibit V/2). In cross-examination Mr Rogers suggested that the study was ambiguous, in that it was not clear whether the special exhaust ventilation systems were used in some of the cases where compressed air was used, or whether they were used in all cases. To my mind, the meaning of the paper was clear. The reference to special exhaust ventilation systems is in the context of 'blowing out', which I take to be a reference to the blowing out by compressed air (see p 64 of the article). Mr Rogers conceded that if more than half of the garages using compressed air had special exhaust ventilation, as I find, then he ought not have relied upon the Rodelsperger et al study (see ts 864 - 866).

374 Mr Rogers referred, in his report, to the study by Hickish & Knight. It reported a TWA exposure of .68 fibre/ml years (and higher peak exposures). When he was estimating the historical TWA exposure for workers in routine brake and clutch repairs, Mr Rogers reduced the TWA exposure figure to .1, on the basis that the 11 cars serviced in the day for the study was atypically high. However, when it came to assessing the plaintiff's exposure, he did not increase the figure to a sufficient degree as would take account of the large number of cars often serviced while the plaintiff was working in the Quick Service area. Similarly, the study by Kauppinen & Korhonen (exhibit V/3) set out exposure figures based on cleaning out the brakes on four wheels. Mr Rogers did not increase those exposure figures in applying them to any of the plaintiff's work.

375 Another study relied upon by Mr Rogers was a study by Plato et al (exhibit 37/212). Mr Rogers agreed that, among those under the description 'car mechanics' in the study, were people who had been car electricians, car conditioners or had worked in other non-asbestos exposed tasks including as supervisor (see p 448 of exhibit 37/212). In those circumstances, the figures in that paper would seem to include workers whose situation was of no assistance in assessing the plaintiff's exposure, although Mr Rogers did not seem to be prepared to make that concession (ts 1161 - 1162).

376 A study by Burdorf & Swuste (exhibit 37/56) was referred to in Mr Rogers report, but not relied upon. It had assigned exposure levels of between 2 to 5 fibre/ml years for the period until 1975. I found the reasons given by Mr Rogers for discarding, entirely, any reliance on figures derived from Burdorf & Swuste, and particularly from the German study apparently relied upon by Burdorf & Swuste, to be unconvincing: see ts 1164 - 1167.

377 It is, I think, very doubtful whether the work environments the subject of the published studies referred to by Mr Rogers substantially replicated that of the plaintiff while working at Anderson Ford, particularly in the Quick Service area. Mr Rogers said (ts 837) that the description of the dust given by the witnesses fitted with some of the descriptions in the literature, referring to the Hickish & Knight and Kauppinen & Korhonen studies. However, he was invited later in his evidence to identify the parts of those reports upon which he relied. His answers in that regard, and consideration of the studies referred to, do not satisfy me that the conditions in the studies he referred to substantially replicated those described at Anderson Ford (ts 1187 - 1189).

378 Given the conditions in the Quick Service area, there is also a real question as to whether an allowance needed to be made, in estimating the plaintiff's exposure, for the background exposure. That is an ambient exposure that is not limited in duration to the performance of specific tasks. Mr Rogers did not allow any amount for that, saying that generally it was less than was measurable (ts 869). I am not satisfied that I could safely proceed on that basis in respect of the Quick Service area.

379 Finally, there were also aspects of the way in which Mr Rogers gave his evidence and responded to questions which militate against acceptance of his evidence. Examples of them are to be found in the passages of transcript to which I have already made reference (for example, ts 857 - 862, 863 - 866, 1161 - 1165, 1169 - 1171, 1181). Often he did not respond directly to a question. While mindful that this may occur for a variety of reasons, in the end I concluded that Mr Rogers was, at times, more inclined to want to argue or defend his position than to answer the question asked of him. He was also, on occasion, apparently unwilling to make concessions.

380 As already explained, I am not satisfied that any of the dose estimates provided by the experts called by the parties ought to be accepted as a reliable estimate of the plaintiff's cumulative exposure to asbestos.

381 The defendant submitted that, were such a conclusion to be reached, it would not be appropriate for me to attempt an estimate of my own. In the circumstances and given the findings that I have made, I accept that submission.

382 Thus I am, I consider, not in a position to make findings as to the particular level or range of exposure experienced by the plaintiff in the course of his work during the relevant period. It seems likely that it is within a range the endpoints of which are between the extremes proposed by the two experts (ie higher than the bottom of Mr Roger's range and lower than the top of Dr Francis' range). Beyond that, the most that might safely be concluded, it seems to me, is that seems likely that the plaintiff's exposure was less than 25 fibre/ml years. I say that taking into account the criticisms made by the defendant, which I have accepted, of Dr Francis' estimate, particularly as it relates to the upper limit of her range. However, it must be acknowledged that, even to draw the conclusion that, on balance, the exposure is probably less than 25 fibre/ml years involves a degree of speculation.

383 I would not be prepared to make any further, more specific findings as to the level of the plaintiff's exposure.

384 In any case, taking into account the conclusions to which I have come on the other areas of evidence relevant to causation, to be set out later in these reasons, the question of the estimated level of exposure of the plaintiff is not, on my analysis, of central significance.

385 The estimated level of exposure would be of obvious significance, were it to be accepted that there is a threshold level of 25 fibres/ml years below which clinically apparent asbestosis does not occur. However, as will be explained later in these reasons, I do not accept that there is such a threshold. Given that, a reliable estimate of the exposure would be a matter to be weighed in the assessment of the whole of the evidence, including especially the medical evidence, relevant to whether, on the probabilities, the plaintiff's fibrosis was caused by asbestos. In that regard I note that Professor Robinson, whose evidence I accept (as explained later in these reasons), was not asked any questions directed to whether exposure at a specific level would lead him to alter his view on diagnosis. Moreover, he said that he did not think an occupational hygiene study would assist in determining the diagnosis question (ts 622). Professor Musk took a somewhat different view on this latter point, although his evidence at ts 557 should not be overlooked.

386 That brings me to the epidemiological evidence.

387 The defendant relied upon epidemiological evidence to invite a conclusion that it demonstrated that there is no increased risk of mesothelioma, lung cancer or asbestosis for those working as mechanics as compared to the general population. In this regard, the defendant relied primarily upon the evidence of Dr Goodman, an epidemiologist, whose evidence was directed primarily to this topic. His report is exhibit G. The defendant also relied upon some of the evidence of Dr Paustenbach: par 47 of his report (exhibit Q1) set out earlier in these reasons, which refers to an article of which he was a co-author (exhibit T2).

388 Dr Goodman is an assistant professor at Emory University School of Public Health. He is the director of the Georgia Center for Cancer Statistics. He is a co-author of a number of published epidemiological studies and meta-analyses.

389 Epidemiology is the study of the distribution and determinants of health-related states in populations. Generally, epidemiology seeks to test whether there is an association between a particular postulated agent and a given disease. Comparison groups are used so that the risk of disease among those exposed to the postulated causal agent can be compared to the unexposed comparison group.

390 Epidemiological studies commonly use a measure called relative risk (RR) as a measure of the strength of an association. RR is the ratio of the incidence of disease in exposed individuals to the incidence in unexposed individuals. If the RR equals 1, the risk in exposed individuals is the same as the risk in unexposed individuals, which is, Dr Goodman said, interpreted as meaning there is no association. If the RR is more than 1, the risk in exposed individuals is greater than the risk in unexposed individuals.

391 To take account of the influence of chance, tests for statistical significance are applied so as to calculate a 95% confidence interval. That is the band of results within which, statistically, there is a degree of confidence of 95%. If the 95% confidence interval of a RR assessment includes 1.0 then generally, Dr Goodman said, the departure from 1.0 is considered statistically not significant and is generally not accepted as evidence of a true association.

392 Dr Goodman expressed the opinion that, based on his review of the relevant studies, there is no epidemiological evidence to support the opinion that involvement in car repair in general, or brake repair in particular, causes or contributes to the development of asbestosis.

393 Dr Goodman (with others) conducted a meta-analysis of studies evaluating the risk of mesothelioma and lung cancer among workers involved in car repair and brake replacement. The results were published in an article (exhibit V/14) referred to in his report. He expressed the opinion that the studies showed no increase in the risk of mesothelioma among workers involved in car repair and brake replacement as compared to the unexposed comparison group.

394 As to the studies regarding the risk of lung cancer among persons engaged in car repair, he concluded that these studies 'on balance' do not support the proposition that motor vehicle repair causes asbestos lung cancer. I note that in his evidence-in-chief, Dr Goodman again used the word 'on balance' in stating that the lung cancer studies as a group do not show an increase in risk (ts 906). That is also how it is expressed in the published meta-analysis (exhibit V/14).

395 Dr Goodman has not done a meta-analysis of studies in respect of asbestosis (nor did he refer to a meta-analysis by anyone else). He referred to some studies which he said suggested the lack of an increased risk of asbestosis among motor vehicle mechanics. However, as I understood his evidence, in expressing his opinion as to the absence of epidemiological evidence regarding asbestosis being caused by work as a mechanic, he relied heavily upon the epidemiological studies and his meta-analysis respecting mesothelioma and lung cancer. Those studies could, Dr Goodman said, be used to draw conclusions in respect of asbestosis. That, he said, is because those at risk of asbestosis will have a greater increase in the risk of lung cancer, and a greater again increase in the risk of mesothelioma (exhibit G p 4; ts 906 - 907 and 920 - 921). Thus, Dr Goodman said in his report, 'it would be illogical to expect an elevated risk of asbestosis in the absence of any increase in risk of mesothelioma or lung cancer'.

396 The plaintiff puts two main submissions in response to the epidemiological evidence. First, the plaintiff submits that, as a matter of law, the epidemiological evidence is irrelevant to the issues in this case. Secondly, in the alternative, the plaintiff submits that, in all the circumstances and on a proper analysis, the epidemiological evidence does not provide any significant assistance to the resolution of the particular causation issue in this case.

397 For the reasons which follow, I accept the plaintiff's second submission, but not his first submission.

398 In Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262, Spigelman CJ gave consideration to the question of how epidemiological evidence is to be approached in the context of questions of causation. In Seltsam v McGuiness the issue was whether the plaintiff's renal cell carcinoma had been caused by inhalation of asbestos. Medical science was not able directly to identify the causal mechanism leading to the disease, and whether it involved asbestos. The plaintiff relied upon epidemiological evidence to support a conclusion, by way of inference, that inhalation of asbestos had caused his disease. Spigelman CJ held [22] (Davies AJA agreeing) that epidemiological evidence can play a role both in the general question - whether an agent is capable of causing a disease - and the specific (legally critical) question - whether the agent caused the disease in the particular case.

399 Here, of course, the issues are quite different in character from those in Seltsam v McGuiness. There is no doubt that asbestosis is caused by asbestos, or that pulmonary fibrosis can be caused by asbestos. However, pulmonary fibrosis can be caused by other things and the question is whether the plaintiff's fibrosis was caused by asbestos or by something else (which may be unknown). I will return to this point after discussing the cases further.

400 A second difference is that, in Seltsam v McGuiness, the epidemiological studies were invoked to support an inference in favour of causation. Here, they are invoked to prove the absence of a causal link. That difference does not seem to me to be decisive, in the sense of meaning that epidemiological evidence cannot assist. The difficulties of proving the absence of cause may, however, be a matter to be borne in mind in assessing the weight to be given to the epidemiological evidence.

401 In Seltsam v McGuiness Spigelman CJ identified the use to which epidemiological studies can be put in the context of questions of causation [78] - [101]. He concluded that epidemiological studies were admissible as circumstantial evidence which may, alone or in combination with other evidence, establish causation in a specific case [89], [102].

402 Epidemiological evidence was relied upon in Amaca Pty Ltd v Hannell. Differing approaches to the use of that evidence were taken in the joint reasons of Steytler P and McLure JA, on the one hand, and in the reasons of the Chief Justice on the other. That, I think, arose from the differing views taken as to how the expert evidence in that case was to be understood.

403 In Amaca Pty Ltd v Hannell, the respondent had mesothelioma. It was not in doubt that mesothelioma is caused by asbestos. The evidence in that case established that there is a background risk, for everyone, of contracting mesothelioma, arising from exposure to asbestos in the general environment. The respondent had had three specific exposures to asbestos arising from home handyman work which he did using the appellant's product. The question was whether the respondent had proved that his mesothelioma was caused or contributed to by the home handyman exposure.

404 The Chief Justice held that the respondent failed on that causation question. In his view, the expert evidence was to be understood as being to the effect that the background exposure and the home handyman exposure were alternative causes of the mesothelioma. Given the expert evidence as to the relative risk, and given the inability of expert evidence to identify which one or more fibres caused the mesothelioma, the respondent failed to prove on the balance of probabilities that his mesothelioma was caused by or contributed to by his specific exposure [214] - [222].

405 In the course of his reasons [33] - [34], [40], the Chief Justice referred with approval to and applied the passages from the reasons of Spigelman CJ to which I have referred.

406 The reasons of Spigelman CJ have been followed in several appellate courts on a related but different point: see the cases referred to in footnote 12 of Freidin v St Laurent [2007] VSCA 16; (2007) A Tort Rep 81-875. See also Ellis v South Australia [2006] WASC 270 [645] - [649].

407 In contrast to the Chief Justice, Steytler P and McLure JA understood the expert evidence in Amaca Pty Ltd v Hannell as meaning that asbestos fibres from all sources, that is background exposure and handyman exposure, made a cumulative contribution to the contraction of mesothelioma. In that context, their Honours held that the epidemiological evidence was not of assistance in answering whether the appellant's negligence had contributed to the injury (although it may be of assistance in determining whether a contribution was material) [413]. However, their Honours acknowledged the role for epidemiological evidence where the range of potential causes are alternative, in the sense that they are incapable of operating jointly to produce the same indivisible injury, or where, as in Seltsam v McGuiness, there is no direct or proven connection between the breach and the particular injury.

408 The plaintiff pointed to the passage in the joint reasons at [368] that 'epidemiological evidence is purely statistical probabilistic evidence that says nothing about the cause of a disease in a specific case'. In making that observation, their Honours were, I think, describing the nature of epidemiological evidence. (A similar observation was made by Spigelman CJ in Seltsam v McGuiness [78].) They were not, by that observation, saying that epidemiological evidence was incapable, in all cases, of bearing upon the cause of a disease in a specific case.

409 The relevance and weight to be given to epidemiological evidence in determining a causation question is, in my opinion, highly sensitive to the nature and character of the particular causation issue in the case.

410 Asbestosis is a dose related disease. Not all exposure to asbestos, at whatever level, necessarily causes asbestosis. The issue is whether the exposure of the plaintiff, in the course of his work as a mechanic, caused his fibrosis.

411 In the abstract, the issue in this case seems to me to be one which is capable of being assisted by epidemiological evidence. The weight of such evidence, in the context of other evidence relating specifically to the plaintiff is, of course, another matter.

412 To the extent, and only to the extent, that there were epidemiological studies of persons who had experienced substantially similar exposure to asbestos as had the plaintiff, such evidence would be capable of assisting in determining the causation issue in respect of the plaintiff. However, in stating the relevance of epidemiological evidence in that way, it is plain that the degree of assistance to be derived from it is directly linked to the extent to which one can be confident that the persons the subject of the epidemiological studies had an exposure to asbestos substantially similar to that experienced by the plaintiff in this case.

413 For reasons to be developed, I am not satisfied that the mechanics the subject of the epidemiological studies relied upon by Dr Goodman and Dr Paustenbach experienced an exposure substantially similar to that experienced by the plaintiff. For that reason I find that the epidemiological evidence is not of any significant assistance in resolving the causation issue in this case.

414 Dr Goodman was asked a series of questions in cross-examination about whether the studies which he had relied upon involved people with the same working history in the motor vehicle industry as the plaintiff. Dr Goodman said (ts 944) that it is not unreasonable to assume that 'at least some of them did'. He accepted that it was an assumption on his part. It was said to be reasonable to make that assumption because in their paper he and his co-authors had used 'multiple studies spanning a lot of circumstances'.

415 Dr Goodman could not say how many mechanics in the studies worked without any warning of the dangers, without any precautions, or without any protective equipment.

416 Dr Paustenbach was asked questions on this topic at ts 1122 - 1123. When asked whether he agreed that there was no study referred to in his paper that assessed the exposure in situations comparable to the plaintiff's work in the Quick Service area, Dr Paustenbach said that he would say that the NIOSH studies should have encompassed people like the plaintiff but it would not be possible without looking at the studies as a body of work to identify which study best represented the plaintiff. He said some of the early studies probably would, because that was before engineering controls, although by the 1976 study there was some engineering controls. Dr Paustenbach said that there could be seen a 5 to 10 fold difference between when there were engineering controls and the era when there was not. Dr Paustenbach said that the plaintiff worked in both eras. That observation is true in the literal sense. However, on the evidence, the plaintiff worked for 17 years without any controls being implemented.

417 Associate Professor McKenzie referred to the introduction of controls in the 1960s and 1970s. Dr Paustenbach acknowledged that some controls were in place in some instances by the mid-1970s and that controls were further implemented after that.

418 The 1975 NIOSH Bulletin (exhibit 37/75) recommended a range of measures to minimise exposure to asbestos dust for mechanics. It stated in plain terms that under no circumstances should compressed air or dry brushing be used for cleaning brakes. It would not be safe to expect or assume that, following that communication, a substantial number of mechanics continued to work in the United States in conditions similar to those experienced by the plaintiff.

419 By 1970, the Hickish & Knight and Luxon papers had been published, recommending various measures and firmly stating that brakes should not be blown out using compressed air.

420 On all the evidence before me, it would, I think, be quite unsafe to proceed on the basis that a substantial proportion (at least) of the mechanics the subject of the various studies experienced conditions, including the absence of any warnings or controls, as did the plaintiff. In the absence of being satisfied that the studies relied upon involved workers experiencing similar conditions to those experienced by the plaintiff, I find that the epidemiological evidence does not provide any significant assistance on the question of the cause of the plaintiff's fibrosis.

421 There is a further matter which is, to my mind, of fundamental significance to the question of whether Dr Goodman's evidence assists in determining the causation question in this case.

422 Dr Goodman relied upon his meta-analysis of the studies relating to the incidence of mesothelioma and lung cancer in brake mechanics. He had not conducted a meta-analysis in respect of asbestosis. From the results of his analysis in respect of mesothelioma and lung cancer, he drew a corresponding conclusion in respect of asbestosis. He did that on the basis, explained earlier in these reasons, that 'it would be illogical to expect an elevated risk of asbestosis in the absence of any increase in risk of mesothelioma or lung cancer'.

423 However, I do not accept that latter proposition. Indeed, Dr Goodman qualified it, in a significant way, in the course of cross-examination.

424 Dr Goodman agreed (ts 946 - 947) that the potency in respect of causing mesothelioma was very substantially different in respect of the three main varieties of asbestos: crocidolite, amosite and chrysotile. The ratio for carcinogenicity is something of the order of 500: 100: 1 for crocidolite, amosite and chrysotile (respectively). Mr Rogers had suggested figures of 1100: 500: 1 (ts 821).

425 Dr Goodman agreed that those ratios do not relate to the fibrogenicity of asbestos. He agreed with the proposition that all three fibre types are similarly capable of causing asbestosis. He agreed that the statement in his report that it would be illogical to expect any elevated risk of asbestosis in the absence of any increase in mesothelioma or lung cancer needed to be qualified by the statement 'depending on the type of fibre exposed to', at least for mesothelioma. He said that he was 'not sure' about lung cancer.

426 As to lung cancer, it is to be recalled that he expressed his conclusion upon the meta-analysis in terms of a position 'on balance'.

427 The qualification accepted by Dr Goodman, as to the use of studies respecting the incidence of mesothelioma as a guide to the incidence of asbestosis, was similarly made by Professor Musk (ts 552) and Professor Robinson (ts 625).

428 Indeed, Dr Goodman said that he is undecided on the question of whether chrysotile can cause mesothelioma at all (ts 933). Given that he allows for the real possibility that chrysotile does not cause mesothelioma at all, while accepting that it is fibrogenic, an absence of increase in risk of mesothelioma for persons exposed to chrysotile would not necessarily say anything about the risk of such persons regarding asbestosis.

429 In the light of those matters, even if I accepted that epidemiological studies demonstrated the absence of an increased risk in respect of mesothelioma or lung cancer for the plaintiff (which, for the reason already given, I do not), I would not be prepared to conclude from that that there was no evidence of an elevated asbestosis risk for the plaintiff.

430 Thus for the two reasons given, I find that the epidemiological evidence is not of any significant assistance in the resolution of the question of the cause of the plaintiff's fibrosis.

431 If, contrary to my view, the reasons I have given did not lead to the conclusion that the epidemiological evidence is not of any significant assistance, consideration of that evidence would need to take account of the following three matters.

432 First, regard must be had to the nature and inherent limitations and uncertainties of epidemiology, which Dr Goodman acknowledged (ts 925 - 927).

433 Secondly, Dr Goodman acknowledged that proving a lack of association is 'virtually impossible'. He agreed that absence of evidence of an association does not necessarily establish an absence of association.

434 Thirdly, Dr Goodman's conclusion that there is no epidemiological evidence to support the opinion that involvement in car repair or brake repair causes or contributes to asbestosis must be viewed in the context of Dr Goodman's view of what is involved in causation. His evidence reveals a conception of causation which does not accord with the approach taken by the law. For Dr Goodman, at least where epidemiology is available, it would appear to be the sole criterion by which causation is to be determined. If epidemiological studies show no increased risk then, on Dr Goodman's view, the individual facts and circumstances of a particular person cannot overcome an absence of association. Association is seen by Dr Goodman as a pre-requisite to causation.

435 Thus, for Dr Goodman, if the same number of people in the unexposed control group contracted the relevant disease as in the exposed group then, without more, it can be said the disease contracted by each member of the exposed group was not caused by the exposure (ts 930 - 933, 968). That will be so regardless of the history of and clinical findings for the patient.

436 This point is not in itself a reason to reject Dr Goodman's evidence as to whether epidemiological studies demonstrate an elevated risk of a relevant disease for mechanics. Rather, it is a reason for treating with caution that part of his evidence which refers to the absence of causation.

437 The plaintiff pointed to a number of other matters which, it was submitted, should lead to the conclusion that Dr Goodman's evidence does not assist in resolving the issue in this case. It is not, in the light of the findings I have made, necessary to resolve these matters. I propose to mention only some of them.

438 The plaintiff pointed to the use, in his report tendered in evidence in this case, of studies which he had rejected for the purposes of his meta-analysis. More generally, the plaintiff pointed to a number of studies relied upon by Dr Goodman which, by reference to matters raised in cross-examination and submission, were said not to be reliable. It was also submitted that some studies which pointed in the opposite way were unjustifiably dismissed. There seems to me to be force in some of these criticisms (see, for example, ts 947 - 953).

439 The plaintiff also pointed to evidence of Dr Leigh (exhibit 24B) which, he submitted, was, in various respects, of contrary effect to the evidence of Dr Goodman and related specifically to Australia. The consideration and resolution of that submission would need to take account of the absence of cross-examination, in this respect, on both sides. Dr Leigh was not cross-examined at all. Dr Goodman was not cross-examined with reference to Dr Leigh's report. Mr Rogers was not cross-examined on his evidence as to the unreliability of the Australian Mesothelioma Register (ts 823 - 825).

440 Finally, even if the epidemiological conclusions as to the absence of evidence of an increased risk of asbestosis from car repair and brake replacement work were to be generally accepted, there would remain a very real question as to the degree of assistance to be derived from it in coming to the ultimate decision as to causation. Here, Professor Musk and Professor Robinson differed. Professor Robinson's evidence was that, whatever the studies might show generally, they would not help his diagnosis much when he was considering a patient with bilateral calcified pleural plaques (ts 633). His approach to diagnosis relied centrally on the features individual to the particular patient.

441 For the reasons given, I have found that the epidemiological evidence does not provide any significant assistance in resolving the question of whether the plaintiff's fibrosis was caused by asbestos.

442 That brings me, finally, to the medical evidence.

443 As already explained, the medical question of diagnosis closely mirrors the factual question of causation: is the plaintiff's fibrotic condition caused by exposure to asbestos?

444 I begin with an overview of the opinions of Professor Robinson, Professor Musk and Associate Professor McKenzie, and the other medical evidence relied upon by the parties.

445 Professor Robinson is a consultant physician at the Department of Respiratory Medicine at Sir Charles Gairdner Hospital. He has spent a large part of his career dealing with asbestos related disease and has published numerous papers dealing with the subject. He has also edited books dealing with asbestos related diseases. He has been appointed by the NHMRC as the Chief Investigator of the National Research Centre for Asbestos Related Diseases at the University of Western Australia.

446 Professor Robinson saw the plaintiff as a patient in June 2001, and diagnosed him as suffering from asbestosis.

447 In his letter of 2 July 2001 (exhibit 28A) he reported that the plaintiff had described breathlessness present for about two years and getting worse over that time. On examination he had 'inspiratory crackles most marked on the left in the axillary line and posteriorally'. Chest X-rays showed bilateral interstitial lung disease more marked on the left. Thus Professor Robinson observed, from the outset, that the disease was not evenly distributed between the left and right sides.

[the plaintiff] has quite extensive pleural disease and interstitial lung disease. Interstitial lung disease has been present for some time and has a honeycombing appearance ... there is no history of exposure to any drugs or any other agents likely to cause interstitial lung disease, nor is there any evidence of any other disease. It is unusual to have such marked interstitial disease in someone so young who has not been exposed to large amounts of asbestos.

if this is asbestos induced [the plaintiff] must be quite sensitive to it. There is no other obvious cause of interstitial lung disease and therefore cryptogenic fibrosing alveolitis would remain a possibility. But again, bilateral pleural disease including calcification and the history of asbestos exposure makes that much less likely. On balance one has to ascribe the interstitial lung disease and pleural disease to asbestos exposure.

450 Thus, from the start, Professor Robinson adverted to other possible causes of the lung disease and other possible diagnoses.

451 Professor Robinson provided two further reports, by letters of 28 November 2001 (exhibit 28B) and 8 June 2006 (exhibit 28C). These confirmed the diagnosis of pleural plaques and asbestosis.

452 Professor Robinson was given a history with regard to the plaintiff's exposure to asbestos by the plaintiff and, subsequently, by a written statement provided by solicitors. Although some parts of the statement were expressed in very descriptive terms (ts 609), I am satisfied that in substance the history described to Professor Robinson was not substantially different from the history as I have found it. (Perfect correspondence between the proven facts and those assumed by an expert is not necessary to the materiality of an expert's opinion: Makita [38], [64].)

453 Based upon the plaintiff's history and the objective evidence of the pleural plaques, Professor Robinson considered that the plaintiff had had significant exposure to asbestos, although it was, relative to the range of cases in which asbestosis is experienced, moderate or low.

454 Professor Musk is an eminent respiratory physician who has specialised in the field of asbestos related lung disease. He is a clinical professor of medicine and holds a chair in public health at the University of Western Australia. He has conducted research in relation to the cohort of people exposed to asbestos at Wittenoom for over 30 years. He has, over the past decades, seen numerous people with asbestos related disease with a range of occupational and non-occupational exposure. Most of his 250 or more publications in peer-reviewed medical journals relate to asbestos related diseases. In or about 2000, Professor Musk was selected by the World Trade Organisation as one of three world scientific experts in a dispute between Canada and France relating to imports of chrysotile asbestos. He was awarded the Order of Australia for his services to respiratory medicine in the areas of asbestos disease and smoking related disease.

455 Professor Musk provided a report by letter dated 29 June 2006 (exhibit 19). He recorded a history for the plaintiff. Although, of course, not detailed, the thrust of the history provided to Professor Musk is broadly consistent with the history of exposure as I have found it to be. (As to his evidence at ts 559 - 560, I refer to my findings that the plaintiff and his work mates did, at times, file or chamfer the edge of a new brake lining.) Professor Musk examined the plaintiff, reviewed lung function tests, echocardiograms and some CT radiography. He expressed the opinion that the plaintiff suffers from advanced asbestos-induced interstitial lung disease (ie asbestosis) and pleural disease.

456 Finally, the plaintiff relied upon evidence from Dr David McEvoy, a consultant respiratory physician based in Queensland. He was consulted by the defendant's solicitors, who provided material to him including some CT scans.

457 In a report dated 12 July 2004 (exhibit 32) Dr McEvoy set out detailed comments on what he observed from the CT scans. He expressed the opinion that the scans show evidence of asbestos related pleural disease, namely pleural plaques with calcification and extensive bilateral destructive pulmonary fibrosis. He commented:

In this setting asbestosis would have to be considered the most probable cause of his progressive pulmonary fibrosis. The histopathology and CT scan appearances of idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis) or usual interstitial pneumonia (these being different terms used to describe the same condition in the literature) are indistinguishable from those of the lung changes induced by asbestos fibre dust exposure or asbestosis.

458 He stated that, on all the evidence presented to him, the clinical features were 'entirely consistent with the diagnosis of asbestosis'. He observed that the rapidly progressive and disabling form of pulmonary fibrosis of the plaintiff had features that are a little unusual for asbestosis and commented that, from the description of his occupation, one would not have expected him to have developed asbestosis.

459 I would observe immediately that, on the ultimate diagnosis question, to my mind only quite limited assistance can be derived from the report and oral evidence of Dr McEvoy. As he was at pains to emphasise in his oral evidence, he was given only very limited material and did not examine or speak to the patient.

460 The plaintiff emphasised the passage in Dr McEvoy's report that 'It would certainly be indefensible to say that he did not have asbestosis'. In the context of the report as a whole, and taking into account Dr McEvoy's oral evidence (ts 1247), I take this as saying no more than that, on what he had available to him, one could not positively conclude that it was IPF; the position was too uncertain to do that.

461 However, some assistance can be gained from some of the general observations in Dr McEvoy's report, to one of which I will refer later in these reasons.

462 The defendant relied on the evidence of Associate Professor McKenzie. He is an associate professor of the School of Medicine at the University of New South Wales, a position he has held since 1993. He is a senior specialist and the head of Respiratory and Sleep Medicine at the Prince of Wales Hospital and is the chair of the Respiratory Clinical Network for the South-Eastern Sydney and Illawarra Area Health Service.

463 Associate Professor McKenzie has provided two reports. His first report is dated 31 January 2007 (exhibit J1).

464 He examined the plaintiff on 30 November 2006. He took and recorded an occupational history. He also took a medical history. As well as examining the plaintiff, Associate Professor McKenzie reviewed radiography and various pulmonary function tests and some of the plaintiff's medical records.

465 Associate Professor McKenzie found that the plaintiff had pleural plaques and a severe parenchymal pulmonary condition. Associate Professor McKenzie estimated that the total cumulative exposure, based on the history, would have been less than 5 fibre/ml years. He noted that he had been asked, in his letter of instruction, to assume that total cumulative exposure would have been less than 1 fibre/ml years and most likely in the order of .2 fibre/ml years.

466 At pp 8 - 10 of his report he considered the onset of symptoms, clinical features, radiographic findings, pulmonary function tests and the total cumulative exposure and concluded that the plaintiff's fibrotic condition is not asbestosis. In the course of that he identified various clinical, radiographic and pulmonary function features which he said were atypical of asbestosis. In considering the question of cumulative exposure, he stated (as amended in evidence-in-chief) that: 'It has been estimated and generally agreed that asbestosis would not progress to clinical disease at or below a cumulative lifetime of 25 fibre/ml years.' That proposition is controversial. I will return to it shortly.

467 He then postulated, as the most likely diagnosis for the plaintiff's condition, 'cryptogenic (or idiopathic) pulmonary fibrosis'. He referred to some aspects of that condition which, he said, fitted with the plaintiff's condition (ie its patchiness, the areas it tended to affect, and the frequency of ground glass opacification being seen). There was reference to an association between idiopathic pulmonary fibrosis and reflux oesophagitis, from which the plaintiff has suffered.

468 At the bottom of p 10 Associate Professor McKenzie made the following observations which, because they are relied upon by the plaintiff, I set out in full:

I cannot exclude the possibility that the presence of asbestos fibre in Mr Lo Presti's lung has aggravated or accelerated the development of fibrosis in this cryptogenic or idiopathic condition. However, I do not consider that the asbestos fibres initiated the fibrosis or that their contribution was large. On the basis of the likely asbestos exposure, the extent of the pleural disease and the possibility of a small contribution to the fibrotic process, I would allow a disability of 10% as being attributable to the asbestos exposure.

469 The plaintiff argued that if Associate Professor McKenzie's evidence is accepted, the observations just set out justify a finding that the plaintiff's asbestos exposure materially contributed to his fibrotic condition. I do not accept that submission. I find that Associate Professor McKenzie's evidence in this regard was not that he considered the process described as likely to have occurred. Rather he was adverting to something which is possible but unlikely (ts 1025; see also exhibit N).

470 In relation to prognosis, Associate Professor McKenzie referred to the absence of any known effective treatment for the plaintiff's condition and estimated his median survival at 5 years.

471 Associate Professor McKenzie provided a further report dated 10 September 2007 (exhibit J2). The plaintiff points out that no additional medical material relating to the plaintiff was available to Associate Professor McKenzie when he prepared his subsequent report. It was prepared in response to a request from the defendant's solicitors to expand on his reasons and give some more references.

472 In it, Associate Professor McKenzie provided an overview of the classification of interstitial lung diseases. Figure 1 from his report is set out below:

473 He stated that the term 'idiopathic pulmonary fibrosis' has been used in the past to describe the group of conditions under the category 'idiopathic', but is now meant to be used specifically for the UIP variety. UIP is usual interstitial pneumonia.

474 There is then set out a detailed discussion of the clinical and radiographic features of each of IPF, NSIP and asbestosis. He says (at p 2) that it is important to distinguish between the various forms of IPF because this information has prognostic and therapeutic significance.

475 In addition to the level of the plaintiff's exposure and his view as to a threshold level of exposure, in his reports, Associate Professor McKenzie relied upon a number of other matters as making a diagnosis of NSIP or IPF more likely than asbestosis. Those matters include the following:

(a) the rapid progression of the plaintiff's disease following a low level of exposure and a long latent period;

(c) various other radiographical features, including the asymmetry or patchiness of the fibrosis, the demarcation between areas of fibrosis and other areas, and the early involvement of the upper lobes;

(d) the absence of crackles being heard on the right side on occasion, said to be suggestive of the patchy or localised fibrotic process rather than a diffuse process as is typical in asbestosis; and

476 The defendant also relied upon a report dated 19 April 2002 by Dr Julian Lee, who was formerly the head thoracic physician at Royal Prince Alfred Hospital in Sydney.

477 Dr Lee examined the plaintiff on 4 April 2002. He reviewed some CT scans and other radiography. He expressed the opinion that the 'changing CT scan appearances cannot be attributed to asbestosis' and that 'a post-infectious or other inflammatory process appears likely'. After a brief summary of what he understood to be the occupational history, Dr Lee stated that chrysotile is the major form of asbestos in brake linings and 'it has been estimated that cumulative exposure levels of 100 fibre/ml years or greater are necessary to cause asbestosis'. He concluded that 'the balance of evidence does not support a diagnosis of asbestosis either by accepted exposure criteria or on radiological appearances'.

478 Dr Lee died some time prior to the trial. His report (exhibit I) was tendered (over objection from the plaintiff) under s 79C of the Evidence Act 1906 (WA).

479 I do not find Dr Lee's report to be of a significant assistance in resolving the issues. That is primarily because, unlike the other four medical witnesses, I do not have the benefit of his evidence in cross-examination. Secondly, I note his statement that it has been estimated that exposure levels of 100 fibre/ml years or greater are necessary to cause asbestosis. As will appear later, I do not accept that any threshold has been established for contracting asbestosis. Further and in any event, on my assessment of the material relating to a possible threshold, the highest threshold contended for in recent decades is 25 fibre/ml years, not 100.

480 Given the nature of the issue, and the divergence in views summarised above, a convenient starting point is the identification of the criteria by which the diagnostic decision in choosing between asbestosis and IPF or NSIP is to be made.

The matters relevant to the diagnosis question: the common ground and the issues

481 The views of the medical experts at trial differed as to what matters assisted in the diagnosis question. There was some common ground, in that it was agreed that certain matters were relevant. However, Associate Professor McKenzie suggested that a wider range of factors were of assistance in choosing between the alternative diagnoses than did the plaintiff's experts.

483 A question of choosing between the alternative diagnoses will only arise if the hallmarks of a pulmonary fibrotic condition are established. This will usually occur through evidence of structural change by, for example, radiography, pathology or through evidence of functional impairment. Functional impairment may be found through signs and symptoms including the presence of inspiratory crackles (crackling sounds heard through a stethoscope while a patient breathes in) or by other methods including testing.

484 In this case it is not in doubt that the plaintiff has a serious pulmonary fibrotic condition.

485 In 2004 the American Thoracic Society (ATS) published an official statement in relation to the diagnosis and initial management of non-malignant diseases related to asbestos (exhibit O). That statement set out guidelines for the diagnosis of asbestosis. It appeared to be accepted by all three of the primary experts on this topic that the 2004 ATS guidelines provide useful guidance for diagnosis of asbestosis.

486 All the experts agreed that a history or other evidence of exposure to asbestos is required for a diagnosis of asbestosis.

487 The relevance of the plaintiff's history of exposure and thus the extent of his exposure to asbestos is clear. Asbestos is dose responsive. The risk of asbestosis increases and decreases with the level of exposure. Consequently, the level of exposure affects the probabilities of a person suffering asbestosis, and affects the probabilities that a fibrotic condition suffered by a person is asbestos induced.

488 Thus it is not enough, in order to make a diagnosis of asbestosis, to identify that there has been some exposure to asbestos, without having any regard to the level or extent of exposure. A history should be taken to enable an assessment of the extent of exposure. With that information, the assessment can be made, on the probabilities, as to whether the patient has asbestosis.

489 Consistently with that, Professor Robinson agreed with the statement in the 2004 ATS guidelines that to diagnose asbestosis one must establish the presence of pulmonary fibrosis and determine whether an exposure has occurred that is of 'sufficient duration, latency and intensity to be causal' (ts 607).

490 Professor Robinson did not consider that an occupational hygiene study is of much assistance for the diagnosis question. Measurements or estimates of exposure are, he said, not part of the 2004 ATS guidelines because usually they are not available and, when they are available, they are not always accurate. What is required for diagnosis of asbestosis, he said, is significant exposure, not any particular number (ts 625 - 626).

491 On the other hand, Professor Musk said, in his evidence, that an accurate history of the exposure would be helpful, as would an assessment by an industrial hygienist (ts 549 and 557).

492 In cross-examination (ts 558 - 560) Professor Musk was asked questions about the fact that asbestos is broken down by the heat effect of braking so that the asbestos content in brake dust is not to be equated with the asbestos content of the original brake lining. Professor Musk said that he was aware of that issue and it was one of the reasons why his understanding of the extent of exposure would be better if advice was given by an industrial hygienist.

493 It is clear from many of Professor Musk's answers in cross-examination that he considered that the lower the level of exposure, the lower the probability that a person's pulmonary fibrosis is asbestos induced.

494 In this context some criticisms made on behalf of the plaintiff of Associate Professor McKenzie's approach should be dealt with. It was said that he had re-interpreted the 2004 ATS guidelines as requiring 'sufficient' exposure when the ATS criteria merely required a history of exposure. I do not accept that criticism. The 2004 ATS guidelines require 'an appropriate history of exposure' (p 695) and an exposure of 'sufficient duration, latency, and intensity' (p 700).

495 It was also common ground that the presence of pleural plaques in a patient is relevant because pleural plaques are a marker of exposure to asbestos. For practical purposes, it is accepted that they do not occur without there having been exposure to asbestos. However, the presence of pleural plaques does not signify the level of exposure. Professor Robinson agreed with that proposition, with the gloss that he said that pleural plaques signified a more than trivial level of exposure (ts 615).

496 The presence of pleural plaques indicates the presence in the plaintiff of asbestos which is biologically active and fibrogenic, ie able to cause fibrosis. That was explained by Professor Robinson and agreed by Associate Professor McKenzie. Professor Robinson said that the pleural plaques demonstrated the presence of biologically active and fibrogenic asbestos which had not been neutralised by the braking process (ts 629). As Professor Robinson put it, the presence of pleural plaques puts the diagnosis of asbestosis on the table, it does not make the diagnosis (ts 626 - 627). One then works through the likelihood that the condition is asbestosis rather than one of the other fibrotic conditions caused by something else identifiable, or idiopathic in nature.

497 Consistently with that approach, a report of the Adelaide Workshop on Asbestos-related Diseases published in 2004 (exhibit V/11) stated, in a passage to be set out later in these reasons, that the presence of pleural plaques 'increases the likelihood' that asbestos is responsible for the fibrosis in a particular case.

498 It was also common ground that consideration has to be given, before making a diagnosis of asbestosis, to alternative diagnoses, including IPF, and to any possible alternative causes for the fibrosis.

499 The 2004 ATS guidelines (exhibit O) recorded that there had been guidelines set out in 1986 and that the 2004 guidelines were a review and update of the 1986 criteria. Under the 1986 guidelines, the third criterion was exclusion of alternative plausible causes for the findings. That criterion was changed in the 2004 guidelines so as to become 'exclusion of alternative diagnoses'. It is stated in comparative notes, that the 1986 guidelines had mentioned smoking as a cause of obstructive disease but that non malignant diseases presenting similarly to asbestos-related disease should also be ruled out.

500 Professor Musk was of the view that there were very few other matters, beyond those already referred to, capable of assisting in making the differential diagnosis between asbestosis and IPF. Professor Musk was a participant in the Adelaide Workshop on Asbestos-related Diseases and a co-author of the report, referred to earlier, which was published in 2004 the International Journal of Occupational and Environmental Health (and, apparently, also in the Journal of Occupational Health and Safety of Australia and New Zealand) (exhibit V/11). In the report, it was said that:

In subjects who have been exposed to asbestos, IPF is indistinguishable from asbestosis clinically, physiologically, radiologically and pathologically, except that the presence of pleural plaques increases the likelihood that asbestos is responsible for the fibrosis. 'Ground glass opacity' on HRCT is seen more frequently in IPF than in asbestosis, however, and rapidly progressive fibrosis is more likely in IPF than asbestosis. Whether the condition is ultimately considered to be asbestosis or IPF may rely on an occupational history or other evidence of significant asbestos exposure.

501 Professor Musk said in evidence that he adhered to the views in the first two sentences (ts 537 and 539).

502 By contrast, Associate Professor McKenzie expressed the opinion that the diagnosis decision of asbestosis or IPF/NSIP is influenced by clinical, radiographic and pulmonary function features, as well as the degree of exposure to asbestos. He also stated that there is a threshold level of exposure (25 fibre/ml year) below which clinical asbestosis will not occur.

503 I will start with the question of whether there is a minimum threshold level of asbestos exposure before asbestosis will be contracted. I will then turn to clinical, radiological and other matters said to be relevant to the diagnosis question.

Is there a threshold level of exposure for contracting asbestosis?

504 The defendant invites the conclusion that a threshold level of exposure to asbestos exists, below which asbestosis will not be contracted, and that the threshold level is 25 fibres/ml years. It relies on evidence from Associate Professor McKenzie, Dr Goodman and Mr Rogers.

505 Associate Professor McKenzie said, at p 9 of his first report (exhibit J1), that it was 'generally agreed' that asbestos would not progress to clinical disease at or below a cumulative level of 25 fibre/ml years. He noted that there had been reports of clinical asbestosis in people with lesser exposures, which may be explained by an underestimate of the exposure level or by an enhanced susceptibility of the individual. However, Associate Professor McKenzie's report says it is clear that any cases with exposure levels less than 25 fibre/ml years would be of mild severity and with a slow rate of progression. In his second report (exhibit J2), he referred to the article in 1979 by Berry et al (exhibit V/7) which, by back extrapolation of data, concluded that asbestosis would not become clinically apparent below 25 fibre/ml years.

506 Associate Professor McKenzie was cross-examined on the report of Dr Leigh (exhibit 24A). He agreed (ts 1063) with the statement by Dr Leigh that the estimated cumulative dose of asbestos required for induction of asbestosis has diminished over the years. Associate Professor McKenzie suggested that it was not logical to think that the required cumulative dose had actually decreased and suggested that what has happened is that technology has improved the detection of asbestosis. Associate Professor McKenzie was not aware of the report by Burdorf & Swuste (exhibit 37/56), referred to by Dr Leigh, in which it is said that there is, at 4.5 fibre/ml years, a lifetime risk of asbestosis of 2 in 1,000.

507 In a note of a conversation with the defendant's solicitors on 5 and 6 February 1997, Associate Professor McKenzie is recorded as saying that at an exposure around 5 fibre/ml years, if the plaintiff were susceptible to fibrosis, then it is possible (although still unlikely) that he could have the 'beginnings of asbestosis' and a 'few symptoms' (exhibit N, see also ts 1074 and 1076 - 1077).

508 Dr Goodman gave evidence in his report that asbestosis typically occurs in circumstances of heavy exposure to asbestos, with estimated cumulative exposure levels of 25 fibre/ml years or higher reported in most studies (exhibit G p 4). That statement is, of course, quite different from a suggestion that a threshold of 25 fibre/ml years is generally accepted in the medical profession.

509 In cross-examination, Dr Goodman said that numbers being used as the threshold for asbestosis ranged from 2 - 25 fibre/ml years, although he was uncertain whether 25 was the top of the range (ts 935 - 938).

510 The defendant also relied on evidence of Mr Rogers (exhibit F1, p 17), which drew upon the work of Berry et al and of Doll & Peto.

511 On the whole of the evidence I am not satisfied that it is generally accepted within the medical profession that there is a threshold level of exposure to asbestos, namely 25 fibre/ml years, below which asbestosis will not be contracted or below which no clinically observable symptoms will occur.

512 There are, among the literature, respected studies which express the opinion or conclusion that there is a threshold for asbestos of 25 fibre/ml years, or something substantially to that effect. See the works by Berry et al in 1979 (exhibit V/7) and by Doll & Peto in 1985 (exhibit V/19).

513 However, the evidence does not lead me to conclude that those views have been generally accepted. In this regard, I note that a specific passage from the Berry et al article was read to Professor Musk, who then agreed with the proposition that the article was 'regarded as the authoritative study' for a period after its publication (ts 561). That, however, does not mean that one of its other specific conclusions, to the effect that there was or may be a no effect threshold of 25 fibre/ml years, was generally accepted and Professor Musk's evidence should not, to my mind, be taken as agreeing with such a proposition. In any event, the question of causation is to be addressed on the current state of knowledge, not on the basis of scientific understanding in earlier decades.

514 Rather than it being generally agreed that there is a threshold, the proper conclusion, it seems to me, is that the question of whether there is a threshold and, if so, what it is, remains one of continuing debate and inquiry within the medical profession. That is supported by the evidence of Professor Musk (see, for example, ts 534 - 535), which I accept in this regard.

515 It is clear from their evidence that neither Professor Musk (ts 534, 557) nor Professor Robinson themselves accept the view that there is a threshold exposure level for asbestosis. The proposition that their views in that regard were a departure from the generally held views within the medical profession was not put, or at least not squarely put, to either Professor Musk or Professor Robinson.

516 By contrast, it was specifically put to Dr Egilman (ts 473) that the view of the mainstream medical profession was that any exposure of less than 25 fibre/ml years will not give rise to asbestosis exhibiting symptoms. Dr Egilman disagreed with that proposition.

517 To the extent that either Professor Musk or Professor Robinson responded to a question regarding generally held views (rather than their individual views) on the question of a threshold, their evidence does not support the conclusions invited by the defendant. See, for example, the evidence of Professor Robinson at ts 625 - 626.

518 The statement in the 2004 Adelaide Workshop paper (exhibit V/11) that there is 'some evidence' for a threshold for asbestosis supports the view that the position remains one for debate and further enquiry.

519 All three of the main medical witnesses (Professor Robinson, Professor Musk and Associate Professor McKenzie) are of the opinion that individual sensitivity to asbestos varies to a significant degree.

520 I have also taken account of Dr Leigh's evidence (exhibit 24A) to which some reference has already been made, and upon which there was no cross-examination.

521 In determining the question of whether it is generally accepted within the profession that there is a threshold, it is relevant to take into account that both Professor Robinson and Professor Musk have been, for decades, leading experts in relation to asbestos related disease. On the other hand, Associate Professor McKenzie is not presently actively involved in that area. In that light, the views of Professor Robinson and Professor Musk as to what is and is not generally accepted within the profession are entitled to some weight.

522 Taking all these matters into account, I am not satisfied that it is generally accepted within the medical profession (or any relevant subset of it) that asbestosis will not occur, or be clinically observable, at a level of exposure to asbestos below 25 fibres/ml year. Nor am I satisfied that any other threshold has been accepted as having been demonstrated. Nor does the evidence otherwise satisfy me that there is a threshold level of exposure for asbestosis. That being so, I do not make the finding invited by the defendant, namely that there is a threshold of 25 fibre/ml years (or any other particular level) below which asbestosis will not occur or be clinically observable.

523 However, the material referred to in this discussion is nonetheless relevant to a consideration of the likelihood that the plaintiff's condition is asbestosis. The material already referred to suggests to me that it will be rare for a person who has an exposure less than 25 fibre/ml years to experience asbestosis of a very serious kind, as has occurred in this case. I have found that it is likely that the plaintiff's exposure level was less than 25 fibre/ml years. I take these matters into account in coming to my conclusion on whether the plaintiff's fibrosis was caused by asbestos.

Other matters said to be relevant to diagnosis

524 That brings me to the question of what other matters are of assistance in the diagnostic choice between asbestosis and IPF (or NSIP).

525 I begin with the question of the rate of progress of the condition.

526 Differing views were expressed on the question of whether a low dose of asbestos and a long latency period suggested a slow progression of asbestosis once symptoms emerged. Professor Musk disagreed with that proposition. He suggested that the data on Wittenoom suggested that people with light exposure are less likely to get asbestosis and have, on average, a longer latency period but, once they develop symptoms, the disease progresses at much the same rate (ts 546, see also 541 - 542 and, in re-examination, 574). The paper he referred to was tendered (exhibit 23). Professor Musk relied on figure 2 within that paper as supporting the proposition that once asbestosis started the rate of progression was the same among those with low, medium or high exposure.

527 As was pointed out in evidence of the defendant's witnesses, the text of exhibit 23 appears to suggest the contrary. On p 996 it was said that those with exposure of more than 148 fibre/ml year had 2.5 times the rate of progression from category 1 (onset) to category 2 as did those with exposure of less than 55 fibres/ml year, although it was said that this could be due to chance. See also the summary and the concluding paragraph.

528 Professor Robinson also expressed the view that a lower level of exposure gives a longer latency period, but once the disease starts it more or less progresses at the same pace as if the patient had a high intensity exposure and shorter latency period (ts 618).

529 In any event, I do not think the question to be of primary significance. It was accepted by all relevant witnesses, including Professor Musk, that the rapid progression of a pulmonary fibrotic condition is a factor in favour of a diagnosis of IPF, as against asbestosis. At ts 539 - 540 Professor Musk agreed with the statement in the 2004 Adelaide Workshop report that rapidly progressive fibrosis is more likely in IPF than in asbestosis. He said that it was a 'soft' factor, in that it was a clinical impression that had not been tested. Professor Robinson accepted that the plaintiff's condition was aptly described as rapidly progressing and that in that sense it was more consistent with IPF than with asbestosis (ts 621).

530 I find that the rapid progression of the plaintiff's fibrosis is a relevant factor in favour of a diagnosis of IPF. It is a factor which, I find, was taken into account by Professor Robinson and by Professor Musk.

531 It was also generally accepted that the presence of ground glass opacification was a factor in favour of a diagnosis of IPF. It is a consideration which was, I find, taken into account by all three of the main medical witnesses. Professor Robinson explained that the appearance of ground glass opacification reflects that the inflammation process is still going on, whereas the fibrosis is the scarring which occurs later in the fibrotic process.

532 Ground glass opacification was said to be more frequently observed in cases of IPF than in asbestosis cases in the 2004 Adelaide Workshop report. Professor Musk adhered to that view in his evidence, but said that this too is a 'soft' factor. He said that ground glass was, at times, associated with asbestosis as well as with IPF. Professor Robinson agreed that the ground glass opacity was not typical of asbestosis but was seen in rapidly progressive cases (ts 617).

533 Associate Professor McKenzie relied quite extensively upon various other aspects of what he observed from the plaintiff's radiography. This included the asymmetry or patchiness, the demarcation of fibrotic areas, the early involvement of the upper lobes and other matters. However, for the reasons which follow, I do not accept that (apart from matters already mentioned such as the presence of pleural plaques and ground glass opacification) the radiography is a factor of assistance in the diagnosis decision.

534 Associate Professor McKenzie set out a summary of some of the radiographic features of IPF, NSIP and asbestosis at p 4 onwards of his second report. I note that when he was taken to this part of his report and asked a question with reference to his 'view' he responded that it was not so much his view as a summary of what is in the medical literature. When asked whether it accorded with his own view, he said 'well yes I accept it'. That evidence suggests that in that part of his report Associate Professor McKenzie is not so much stating his own view as summarising what is to be found in certain literature.

535 Professor Musk said, in unequivocal terms, that radiography could not assist in a diagnosis between IPF and asbestosis (putting aside any indication of pleural plaques) (see ts 537, 538). In substance he was not challenged in relation to that opinion. His opinion is supported by the 2004 Adelaide Workshop report (exhibit V/11). Professor Robinson said, in effect, that features of the plaintiff's condition such as its patchiness were not typical of asbestosis but were also atypical for IPF or for NSIP (ts 616 - 617, 629) and thus did not assist in the diagnosis question.

536 Dr McEvoy said in his report of July 2004 (exhibit 32) that the CT scan appearance of IPF is indistinguishable from that of asbestosis. He was not cross-examined in relation to that proposition.

537 I accept the substantially unchallenged evidence of the plaintiff's witnesses, supported by the statement in the 2004 Adelaide Workshop report (exhibit V/11), to the effect that the radiography is not of assistance in the diagnosis decision.

538 Because I accept that evidence in preference to that of Associate Professor McKenzie, I accept that the patchiness or asymmetry of the fibrosis is not a factor of assistance in the diagnosis decision. Thus the fact that Associate Professor McKenzie and, on occasion, others, had heard crackling on one side only, relied on by Associate Professor McKenzie as indicating patchiness, is not of assistance.

539 Finally, Associate Professor McKenzie referred to the fluctuating nature of the plaintiff's condition involving deterioration, some improvement and then further deterioration. This was said to be suggestive of IPF. Professor Robinson agreed that there had been periods of improvement where he had been a bit 'up and down' (ts 621). He had said as much in one of his reports (exhibit 28C). However, he was not asked whether that was an indication in favour of IPF. Professor Musk expressed the view that the degree of fluctuation was not an indication in favour of IPF. He said that both diseases are progressive, but people with either disease may get a respiratory infection and may experience symptoms from minor infections that others without pulmonary fibrosis would be untroubled by. Thus it would be unsurprising that a person with either form of pulmonary fibrosis would feel better or worse at different times (ts 545). I am not satisfied that the fluctuating progress of the disease is a factor of any significance in the diagnosis decision.

540 As to factors and matters relevant to the diagnosis decision, my findings include the following:

(a) it is not generally agreed, nor is it established, that there is a threshold level of exposure of 25 fibres/ml years below which no asbestosis or asbestosis with symptomology will be contracted by anyone;

(b) (with the exception of the features agreed by all experts to be relevant, namely the presence of pleural plaques and ground glass opacification) radiography, including features such as the patchiness and clear demarcation of the fibrosis, does not assist in the diagnosis.

541 In these respects, Associate Professor McKenzie's opinion is, consequently, based in part upon matters which I have found not to be so (in the first respect) or not to be a material factor.

542 By contrast, there is, in my view, no matter of significant assistance to the diagnosis which Professor Robinson or Professor Musk has failed to take into account and no matter which they took account of but ought not have taken into account in their diagnosis.

543 The findings just made would, in themselves, absent countervailing reasons, lead me to prefer the opinions of Professor Robinson and Professor Musk over those of Associate Professor McKenzie. However, there are some additional considerations which reinforce my preference for the opinions of Professor Robinson and Professor Musk over that of Associate Professor McKenzie.

544 I turn to some other matters which are, to my mind, relevant to the weight to be given to Associate Professor McKenzie's evidence.

Observations on Associate Professor McKenzie's evidence

545 Questions seem to me to arise when the contents of the two reports written by Associate Professor McKenzie are considered, one against the other.

546 The first report (exhibit J1) made no mention of NSIP. Under the heading 'alternate diagnosis' (on p 10), the likely diagnosis was said to be 'cryptogenic (or idiopathic) pulmonary fibrosis'. Various comments about that condition were made including that there is an association between 'idiopathic pulmonary fibrosis' and reflux oesophagitis. A reference is made to the radiography. The concluding paragraph refers to the absence of known effective treatment for the plaintiff's condition.

547 In his second report dated 10 September 2007 (exhibit J2), Associate Professor McKenzie concluded that it is probable that the plaintiff is suffering from 'an idiopathic form of interstitial pulmonary fibrosis, probably non specific interstitial pneumonia'.

548 In cross-examination, it was suggested (ts 1074) to Associate Professor McKenzie that when he wrote his first report, the differential diagnosis of NSIP had not suggested itself to him sufficiently to be mentioned in the report. (Of course, if that had been the case, it would have significantly detracted from the weight of Associate Professor McKenzie's opinion in his second report, given that his first report was in no sense interim or said to be incomplete and given that he did not receive any additional medical information between the dates of the two reports.) Associate Professor McKenzie said that that was not the case. Rather, he said, in the first report he was using the term IPF at the categorical level in the classification in his second report, ie as including IPF, NSIP, and the several other conditions under the general category idiopathic.

549 Accepting, as I do, that to be so, some observations may be made. In his second report, Associate Professor McKenzie says that the term 'idiopathic pulmonary fibrosis' has been used in the past to describe the group of conditions under the category idiopathic but 'is now meant to be used specifically for the UIP variety'. Thus, in his first report, Associate Professor McKenzie's usage of the term IPF was not consistent with what he said was the proper usage of the term.

550 Next, the first report refers to the association between IPF and reflux oesophagitis. The second report explains the association between reflux oesophagitis and IPF (in the specific sense). There is no suggestion in the second report of any association between reflux and NSIP. In the absence of evidence of an association between NSIP and reflux, the statement in the first report of an association between IPF, in the broad categorical sense, and reflux seems somewhat imprecise.

551 Further, the second report identified radiographic differences between NSIP and IPF. Finally, it also identified that NSIP is more responsive to treatment. In that light, the concluding observation in the first report, referring to the absence of any known effective treatment for the plaintiff's condition, seems inapposite, insofar as his condition was considered to be NSIP (while being apt insofar as the condition was considered to be IPF, of the specific variety). Moreover, Associate Professor McKenzie did not state to anyone, prior to his second report of 10 September 2007, that he considered that the plaintiff's condition was (probably) treatable.

552 In making these observations I do not suggest any doubt that, in giving his evidence, Associate Professor McKenzie was performing his professional role as an expert, expressing his genuinely held opinion on a difficult issue. However, these matters seem to me to be relevant to the weight to be given to Associate Professor McKenzie's evidence.

553 The defendant submits that the specific points in the observations just made were not squarely put to Associate Professor McKenzie in cross-examination. That may be accepted, at least as to some of them. In that light I certainly would not have used the observations just made as a basis to reject (in accordance with the plaintiff's submission) Associate Professor McKenzie's evidence that in his first report he used the term 'IPF' in its broad categorical sense. As I have said, I accept Associate Professor McKenzie's evidence in that regard. The fact that these points were not squarely put to Associate Professor McKenzie is to be taken into account in having regard to the observations just made in considering Associate Professor McKenzie's evidence as a whole. However, it does not, it seems to me, mean that these points must be disregarded entirely.

554 The references in the plaintiff's medical reports to pneumonia were given some emphasis in Associate Professor McKenzie's first report. They were not mentioned in the second report. In the course of cross-examination it was put to him that the progressive nature of the fibrosis excluded a causal role for pneumonia assuming it was correctly diagnosed. He responded by saying 'I think pneumonia has played a role in him'. He was questioned for some time and in the end said that he was not happy to exclude pneumonia as a cause of the plaintiff's disease (ts 1058 - 1060). I found his evidence on this point unconvincing. I prefer the evidence of Professor Musk who said (exhibit 20, ts 555, ts 580) that post-pneumonic fibrosis is not progressive, as was the plaintiff's fibrosis (even assuming a correct diagnosis of pneumonia) (ts 548). Consequently, pneumonia can be excluded as being the cause of the plaintiff's fibrotic condition.

555 Further, in the context of a question as to whether drugs as a cause could be excluded, Associate Professor McKenzie raised, for the first time, the possibility of beta blockers (ts 1051). To my mind Associate Professor McKenzie exhibited a reluctance to exclude any possible alternative cause which might have been postulated to asbestos as the causal agent.

556 Associate Professor McKenzie relied upon a joint statement of the ATS and the European Respiratory Society (ERS) regarding IPF published in 2000 (exhibit V/13). That statement, he accepted, requires the presence of a biopsy for the making of a diagnosis. He agreed that a definite diagnosis could not be made without a biopsy but a provisional diagnosis could be made, pointing out that in the majority of cases in clinical practice a diagnosis would be made without a biopsy (ts 1050). The relevance of a biopsy to the making of a diagnosis of IPF seems to me to have been a matter which ought to have been made clear in Associate Professor McKenzie's reports, but was not.

557 At times, Associate Professor McKenzie seemed to me to interpret literature so as to support the position he was adopting. For example, at ts 1033 - 1034 he would not accept that a reference to 'disease' in a journal article was a reference to asbestosis when, given the title, subject matter and context of the article, in my view, it plainly did. The ATS/ERS joint statement required, for the diagnosis of IPF, the exclusion of other known causes of interstitial lung disease including drug toxicities and environmental exposures. When it was suggested that environmental exposures were not excluded in this case he said that one must look at the occupational history to see whether the exposure was 'sufficient'. At other times he appeared to retreat from the ATS/ERS joint statement when it suggested features of IPF which accorded with asbestosis and with the plaintiff's condition, or when it suggested general or usual features of NSIP which did not accord with the plaintiff's condition.

558 Finally, there is a very marked difference in the degree of expertise and experience respecting asbestos related disease between Associate Professor McKenzie, on the one hand, and Professor Musk and Professor Robinson, on the other. Associate Professor McKenzie has no research interest in asbestos related diseases. He has not published in the area. He does not conduct or work in any occupational health clinic.

559 In making that observation, I do not overlook that the question in this case is whether the plaintiff does or does not suffer from an asbestos related disease. Moreover, in weighing conflicting evidence of expert witnesses, the question is, obviously, not simply to be resolved in favour of the expert who is more experienced or better qualified. However, experience and expertise are among the matters to be considered. Associate Professor McKenzie agreed that where a diagnosis is not straightforward, experience is an important asset.

560 All of the matters referred to above, in addition to the findings made under the preceding heading, bear upon the resolution of the conflict in expert opinion between Associate Professor McKenzie and Professors Musk and Robinson.

561 There was nothing about the manner in which either Professor Musk or Professor Robinson gave his evidence or responded to questions which gave me any reason to question the reliability of the evidence. To the contrary, each presented as an extremely impressive witness.

562 There are, however, some observations I would make in relation to their evidence. In the course of doing so I will deal with some of the criticisms of their evidence and reasoning made by the defendant in its submissions.

Observations as to the evidence of Professor Robinson and Professor Musk

563 Professor Musk was cross-examined at some length. He was asked a number of questions relevant to the differential diagnosis as between asbestosis and IPF. However, the diagnosis of NSIP was not put to him and he was asked no questions about it. Professor Robinson was asked numerous questions as to the diagnostic choice between asbestosis and IPF. He was asked only two questions about NSIP, being the last two questions of his cross-examination (ts 629).

564 Those matters are, I think, relevant to whether the opinion of Associate Professor McKenzie, that the plaintiff has an idiopathic form of pulmonary fibrosis which is either NSIP or IPF, and more probably NSIP, should be accepted in preference to the opinions of Professor Musk and Professor Robinson.

565 The defendant pointed in submissions to Professor Musk's evidence in cross-examination (ts 557) that only two lines of investigation into the correct diagnosis were left open. The first, Professor Musk said, was to consult an industrial hygienist to look at the actual exposure of the plaintiff; the second, to look at the epidemiological evidence to see whether anything is to be learned from that area. The substance of that evidence, as I understood it, was that these were the two areas, beyond the information already available to Professor Musk, which were or may be capable of assisting in determining the diagnosis question.

566 However, I have made findings that the evidence of the industrial hygienists does not provide a reliable dose estimate for the plaintiff. I have also found that, for the reasons given, the epidemiological evidence does not assist in any significant way.

567 In that light, the two lines of inquiry contemplated by Professor Musk have, in the event, proved not to assist in the diagnosis question. That returns attention to the opinions of the experts based upon the information available to them. In any event, as already observed, Professor Robinson differed from Professor Musk on the question of the utility of dose estimates and the epidemiology.

568 Each of Professor Robinson and Professor Musk has expressed the opinion that, taking into account what he knows of the plaintiff's history and the presence of the pleural plaques, the probabilities favour the conclusion that the plaintiff's condition is asbestosis.

569 As already explained, Professor Robinson gave significant but not controlling weight to the presence of pleural plaques. Professor Musk has, I think, taken a similar approach. Such an approach seems to me to have been appropriate and open to be taken. I refer to the earlier discussion of the significance of the presence of pleural plaques.

570 Professor Robinson explained in his evidence that individual sensitivity and reaction to the presence of asbestos fibres varies substantially. He referred to it as 'host reactivity' and found it to be a relevant consideration in his diagnosis of the plaintiff (see, for example, ts 619, 627 and 631). I accept that it is appropriate to take into account variations in host sensitivity and reaction to asbestos in determining the diagnosis.

571 Each of Professor Musk and Professor Robinson approached the diagnosis question in a way which was, each considered, and, I find, consistent with the 2004 ATS guidelines.

572 In support of a submission to the contrary, the defendant argued that in order to satisfy the third criterion of the 2004 ATS guidelines: exclusion of alternative diagnoses, alternative diagnoses must be excluded as reasonable possibilities. I do not accept that submission. Rather, the criterion, as I would understand it, requires the doctor to exclude, on balance, alternative diagnoses. That is what Professor Robinson did, as he explained.

573 The defendant submitted that the reasoning of Professor Musk and Professor Robinson was at variance one with the other. However, the defendant did not, when asked, identify particular respects, of any real significance, in which their reasoning was at variance. They differed on the utility of epidemiology and of a dose estimate from an industrial hygienist to the diagnosis. However, the defendant accepted that that was not significant for present purposes. That is because neither in fact relied upon any epidemiology or dose estimate in making their diagnosis or expressing their opinion in court. Of course, given that quite different questions, at times respecting different topics, were asked of each of them, some aspects of their reasoning have been articulated in greater detail by one rather than the other. An example of this is, I think, to be found in Professor Robinson's 'mathematical approach', to be discussed shortly.

574 Next, the defendant pointed to the evidence of Professor Robinson to the effect that, because of the low level of the plaintiff's exposure, it was likely that there had been some amphibole contamination of the asbestos dust (ts 634 - 637). The defendant submits that there is no basis to postulate amphibole contamination other than working backwards from the (assumed) diagnosis of asbestosis and then having regard to the low level of exposure to asbestos. Rather, the defendant submits, the low level of asbestos exposure should lead to a conclusion that the disease is IPF rather than asbestosis. Accordingly, a fatal flaw in Professor Robinson's reasoning is said to have been revealed.

576 There is no specific evidence before me as to the composition of Ford brake linings during the relevant period, although clearly it was generally understood and accepted that they contained chrysotile (being serpentine, not amphibole, in nature). Thus the possibility of amphibole contamination, perhaps for a part of the relevant period, cannot be definitely excluded. However, there is nothing in the evidence which positively supports it having occurred.

577 Professor Robinson was, from the time he first saw the plaintiff, aware of the source and nature of the plaintiff's exposure to asbestos. The possibility of amphibole contamination of what was understood to be chrysotile asbestos was not a matter mentioned in his reports. It emerged only at the conclusion of his oral evidence. Professor Robinson said (and I accept) that his diagnosis does not hinge upon a view that there was amphibole contamination. I find that that possibility was not a central part of Professor Robinson's reasoning in reaching (and maintaining) his opinion that the plaintiff has asbestosis.

578 I accept that, to the extent that the level of exposure was thought to be so low as to suggest that there was or may have been amphibole contamination, that should lead to further consideration of the question of whether the fibrosis was caused by asbestos at all. However, I do not accept that Professor Robinson failed to do that in forming (and maintaining) his opinion that, on the probabilities, the plaintiff's fibrosis was caused by asbestos.

579 In the end, Professor Robinson says, the diagnosis question is a question of likelihood. An apparently important part of his reasoning in preferring a diagnosis of asbestosis as being more likely than IPF was articulated in the course of re-examination. At ts 631 - 632 Professor Robinson said as follows:

one makes a judgement call based really on likelihoods. For example, he has asbestos in his lung. It is causing disease. Cryptogenic fibrosing alveolitis, the alternative diagnosis, is a very rare disease. It is about 3 in 100,000. So, for example, if you have a high level of asbestos exposure, let's say you worked in the mill at Wittenoom or some intense exposure, you might have a lifetime risk of 30%. With moderate exposure it might be 3%. That means 97% of people with that exposure won't get it, so 3% is still pretty high. If you have low-level exposure it might only be .3% so that means 99.7% of people in that occupation won't get it so epidemiological studies often won't show that up but .3% is still 100 times .003%, which is the background incidence of IPF, so anyone who has got asbestos exposure who has an IPF or asbestosis-like pattern, 99 of them, on sheer mathematical grounds, who have had low exposure have probably got asbestosis and one IPF. When a patient comes to see me and I weigh this up and I make the statement, 'On balance one has to ascribe the interstitial lung disease to asbestos,' it's as much a mathematical thing; that is, that there are 99 chances out of 100 that it's due to asbestos, or something like that. I mean, IPF is a rare disease.

580 See also ts 634 - 635 where the same point was made, and where he said that even if asbestos being the cause was 10, 20 or 30 times more likely than it being a case of IPF, that would still influence the diagnosis.

581 Professor Robinson did not identify (and was not asked to identify) the sources of the probability figures which he used in his explanation of his view of the competing probabilities. There is other evidence, to which I will come, as to the incidence (more correctly, prevalence) of IPF, suggesting it is higher than the level referred to by Professor Robinson. The incidence or prevalence of the disease is a matter where there is evidently available data. However, given that the plaintiff's exposure level was, from Professor Robinson's perspective, unquantified, it would seem unlikely that there is published data from which figure for the probability of the plaintiff contracting asbestosis can be directly derived.

582 I do not take Professor Robinson's figures as to the probability of contracting asbestosis to be intended as mathematically precise. Rather, they seem to be illustrative numbers used to explain his thinking. The thrust of his thinking is that, given the presence of the plaques and the plaintiff's history of exposure, the probabilities of asbestosis exceed the probabilities of IPF by more than an order of magnitude, ie at least a factor of 10.

583 Professor Robinson's vast experience and research, over more than 20 years, in relation to asbestos related diseases might be thought to provide a reasonable foundation for making a ball park assessment of the kind which he explained.

584 A similar line of reasoning was, I think, taken by Professor Musk, although it was developed in less detail. In the course of agreeing that the lower the exposure of the plaintiff the less likely the disease is to be asbestosis, he observed, 'but IPF is not a common disease so I think virtually any measurable exposure is likely to be important' (ts 568).

585 The defendant criticised this reasoning, which it termed Professor Robinson's 'mathematical approach', in two respects. First, it pointed to evidence to the effect that the prevalence of IPF is higher than the 3 in 100,000 referred to by Professor Robinson. Associate Professor McKenzie said (ts 1006 and 1057) that the literature suggests the prevalence of IPF is somewhere between 5 per 100,000 and 20 per 100,000. He suggested that the higher figures were more recent, and that the literature suggested an increase in incidence of the disease. The ATS/ERS joint statement (exhibit V/13) had some reference to prevalence estimates varying from 3 to 6 per 100,000, with more recent figures for one county in New Mexico revealing a prevalence of 20 per 100,000.

586 There was also evidence from Dr Goodman which suggested a prevalence figure for IPF which was higher again. He referred to Table 5 of an article by Demedts et al (exhibit V/17). That was based primarily upon the study in the county of New Mexico (also referred to in the ATS/ERS joint statement) which had identified (using round figures) a prevalence for males of 20 per 100,000 and an incidence for males of 10 per 100,000. Elsewhere in the Demedts et al paper, there is reference to a study showing a prevalence of 3 - 6 per 100,000 for males; and another indicating a prevalence of 20 per 100,000 for males (see p 9).

587 I accept Associate Professor McKenzie's evidence to the effect that the prevalence of IPF is now thought to be somewhere between 5 and 20 per 100,000.

588 In this context, the defendant appeared also to place reliance on evidence to the effect that the prevalence of asbestosis generally is falling. I do not find such evidence to be of any assistance in assessing the likelihood of whether the plaintiff, with the history which he has, and with pleural plaques, has asbestosis.

589 Thus I have found that the prevalence of IPF is now thought to be higher than the 3 per 100,000 figure used by Professor Robinson. However, given the scale of the differences in the ball park figures used by Professor Robinson, that, in itself, does not seem to me to invalidate his reasoning (although, plainly, it makes the position less clear cut). Moreover, it is unclear whether Professor Robinson was referring to the prevalence of IPF in Australia specifically, as against its prevalence throughout the world.

590 Secondly, and perhaps more fundamentally, the defendant also criticised the logic and methodology inherent in Professor Robinson's response. The defendant contended that the logic of Professor Robinson's response would lead to the conclusion that, whenever there was an exposure to asbestos at whatever level (albeit non-trivial, in that it had caused pleural plaques), pulmonary fibrosis would always be attributed to the asbestos. As it was put in oral submissions, it is said not to be appropriate to disregard the prevalence of IPF, whatever the level of prevalence is, by attributing all cases where some exposure to whatever levels of asbestos existed, as being asbestosis. The 3 (or 6 or whatever the figure) are actual cases and should not be mathematically consigned to be asbestosis on the basis that 'they are nearly all asbestosis therefore we will treat them all as asbestosis' (ts 1374).

591 At a statistical or general level, I see some force in the submission made by the defendant. However, the question for Professor Robinson (and the question for the court in this case) involves identifying, on the probabilities, the more likely conclusion as to whether the plaintiff's fibrosis is or is not caused by asbestos. In the context of determining that question, I see no flaw in Professor Robinson's logic or methodology in taking account of his views as to the relative probability of IPF and asbestosis in the known circumstances. To the contrary, it seems to me appropriate to take account of those matters.

(a) Professor Robinson and Professor Musk took into account all relevant significant matters in assessing whether the plaintiff had asbestosis or IPF (or, to the extent it was raised, NSIP);

(b) (unlike Associate Professor McKenzie) Professor Robinson and Professor Musk took only relevant matters into account in their opinion as to diagnosis;

(c) Professor Robinson and Professor Musk had regard to their understanding of the work practices and environment leading to the plaintiff's exposure, which was substantially consistent with my findings;

(d) Professor Robinson and Professor Musk gave appropriate consideration to alternative diagnoses, in particular IPF (in Professor Robinson's case that was spelled out in his first report);

(e) Professor Robinson and Professor Musk gave appropriate but not determinative weight to the presence of pleural plaques;

(f) Professor Robinson and Professor Musk gave appropriate consideration to the features of the plaintiff's condition which were atypical for, but not inconsistent with, asbestosis, but concluded that these features did not assist in choosing between asbestosis and IPF;

(g) Professor Robinson and Professor Musk approached the diagnosis in a way which was consistent with the 2004 ATS guidelines;

(h) Associate Professor McKenzie took into account his view that asbestosis would not occur at an exposure level below 25 fibre/ml years, a view which I have not accepted;

(i) Associate Professor McKenzie also took into significant account the radiography, as favouring a diagnosis of IPF/NSIP, whereas I have found that (beyond the common ground) the radiography does not assist in the diagnosis question; and

(j) there were various aspects of Associate Professor McKenzie's evidence which bore adversely upon the weight to be given to it.

593 For the reasons given, in the light of the findings and observations already made, I conclude as follows:

(a) I accept the opinion evidence of Professor Robinson and Professor Musk that the plaintiff suffers from asbestosis;

(b) I do not accept the evidence of Associate Professor McKenzie to the effect that the plaintiff has IPF or NSIP;

(c) on the balance of probabilities, I find that the plaintiff suffers from asbestosis.

Was the plaintiff's asbestosis caused by the defendant's negligence?

594 In the realm of negligence, causation is essentially a question of fact to be resolved as a matter of common sense. In resolving that question, the but-for test has an important role to play but it is not a comprehensive and exclusive test of causation; value judgments and policy considerations intrude: Bennett v Minister of Community Welfare [1992] HCA 27; (1992) 176 CLR 408, 412 - 413; March v E & M H Stramare Pty Ltd [1991] HCA 12; (1991) 171 CLR 506, 515 - 519, 522 - 524; Medlin v State Government Insurance Commission [1995] HCA 5; (1995) 182 CLR 1, 6.

595 Situations where it has been recognised that the 'but-for' test is inadequate as an exclusive test for causation include where there is said to be an intervening cause or an alternative sufficient cause, or where the connection between the defendant's wrong and the plaintiff's damage is insufficient to warrant the attribution of legal responsibility. An example of the last category of case is where the defendant's wrong merely secures the presence of the plaintiff at the time and place of the damage (without thereby having increased the risk of injury). Thus it is not enough that something contributes an essential condition (in the but-for sense) to characterise it as a cause for the purpose of attribution of legal responsibility. However, this case does not raise considerations of any of these characters.

(b) the only asbestos exposure of any significance experienced by the plaintiff occurred during his work as a mechanic;

(c) had the defendant provided the required warning, the protective measures referred to in that warning would have been implemented;

(d) if those protective measures had been implemented, the plaintiff's exposure to asbestos during his work from 1970 to 1987 would have been considerably diminished;

(e) the higher the dose of asbestos, the greater the risk of contracting asbestosis.

597 I find that had the required warning been given, on the balance of probabilities, the plaintiff would not have contracted asbestosis.

598 In so finding, I have taken account of the fact that the plaintiff also worked as a mechanic in a service station not associated with Ford from 1988 to 1994. However, taking into account the evidence as to the extent of exposure during the 1970s at Anderson Ford, and the medical evidence as to the latency of asbestosis, I find that, had the required warnings been given, the plaintiff would not have contracted asbestosis.

599 Thus the question of causation in fact is answered in favour of the plaintiff. That leaves only the question of whether the defendant is in law causally responsible for the damage: Bennett (412 - 413); City of Stirling v Tremeer [2006] WASCA 73; (2006) 32 WAR 155 [73]; Amaca Pty Ltd v Hannell [389].

600 I am satisfied, on the findings just summarised, that the defendant's negligence is properly to be seen as a cause of the plaintiff's asbestosis so as to attribute legal responsibility to the defendant. The defendant had a duty to take steps to reduce the risk of asbestos inhalation injury to a class of persons including the plaintiff. The defendant breached its duty. Had the defendant performed its duty, the plaintiff would not have contracted asbestosis.

601 I find that the defendant's negligence caused the plaintiff's asbestosis. Accordingly, the defendant is liable to the plaintiff for damages for his asbestosis arising from the defendant's negligence.

602 The plaintiff is entitled to judgment for damages in the sum of $840,000.

JURISDICTION : SUPREME COURT OF WESTERN AUSTRALIA

CITATION : LO PRESTI -v- FORD MOTOR COMPANY OF AUSTRALIA LTD [No 2] [2008] WASC 12 (S)

HEARD : ON THE PAPERS (WRITTEN SUBMISSIONS FILED 4 MARCH 2008)

Costs - Indemnity costs - Calderbank offer - Whether gives rise to prima facie entitlement to indemnity costs - Whether rejection of Calderbank offer ground for ordering indemnity costs

Defendant to pay the plaintiff's costs on a party-party basis

1 BEECH J: On 19 February 2008 I delivered reasons for decision after the trial of this action. I concluded that the plaintiff was entitled to judgment for damages in the agreed sum of $840,000. Judgment in that amount was entered on that day.

2 The plaintiff seeks an order that the defendant pay his costs on an indemnity basis, or alternatively on a solicitor and own client basis. No other special costs orders were sought by the plaintiff.

3 The plaintiff relies primarily upon the rejection, by the defendant, of an offer of settlement. On 12 September 2007 the plaintiff offered to settle his claim for $450,000 plus indemnities for certain repayments to Medibank Private and the Health Insurance Commission, plus costs to be taxed if not agreed.

4 The offer was expressed to be without prejudice except as to costs. The letter stated that if the offer was not accepted and the judgment entered after trial was more favourable to the plaintiff than the offer, the plaintiff would apply for costs on a solicitor-own client basis from the date of the letter, in accordance with the principles applied in Calderbank v Calderbank [1976] Fam 93.

7 It is convenient to begin by outlining some general principles relevant to the exercise of the discretion to award costs.

8 The usual costs order is that the successful party in an action is awarded its costs on a party and party basis. An order for indemnity costs will be made only if there is some special or unusual feature in the case to justify departure from the ordinary practice. The court has power to make an indemnity costs order whenever justice requires it: Unioil International Pty Ltd v Deloitte Touche Tohmatsu (No 2) (1997) 18 WAR 190, 191; Flotilla Nominees Pty Ltd v Western Australian Land Authority [2003] WASC 122 (S); (2003) 28 WAR 95 [8].

9 The categories of cases in which the discretion to award indemnity costs may be exercised are not closed: Colgate-Palmolive Company v Cussons Pty Ltd [1993] FCA 536; (1993) 46 FCR 225, 233 - 234; Unioil (191).

10 Most of the situations in which indemnity costs have been awarded have involved an element of improper or unreasonable conduct on the part of the parties or their advisors in the conduct of the case: Flotilla [9]; Colgate-Palmolive (233 - 234).

11 An offer of compromise is capable of being a ground relevant to the award of indemnity costs. However in my opinion, the rejection by a defendant of an offer of compromise which subsequently proves to be more favourable to the defendant than the result of the trial does not necessarily or presumptively lead to an award of indemnity costs for the plaintiff. All the circumstances must be considered in determining whether justice requires the exceptional exercise of the power to award indemnity costs.

12 The plaintiff relies upon the decision of Roberts-Smith J in Alpine Holdings Pty Ltd v Warwick Entertainment Centre Pty Ltd [2003] WASC 53 (S). In that case, his Honour followed the decision of Rolfe J in Multicon Engineering Pty Ltd v Federal Airports Corporation (1996) 138 ALR 425 in holding that an offer of compromise, whether made under the Rules of Court or pursuant to a 'Calderbank letter', gives rise to a prima facie presumption of indemnity costs in the event that the result of the trial was less favourable to the recipient of the offer than was the terms of the original offer [72].

13 The decision in Multicon Engineering was not followed by Lindgren J in MGICA (1992) Pty Ltd v Kenny & Good Pty Ltd (No 2) (1996) 70 FCR 236, 240. Lindgren J pointed to decisions of judges of the Federal Court who had taken an approach different from that stated by Rolfe J. There seems to me to be considerable force in the matters referred to by Lindgren J as supporting the view that non-acceptance of a Calderbank offer does not give rise to a prima facie entitlement to indemnity costs. See also SMEC Testing Services Pty Limited v Campbelltown City Council [2000] NSWCA 323 [37]; Jones v Bradley (No 2) [2003] NSWCA 258 [9]; Gretton v Commonwealth of Australia [2007] NSWSC 149 [10].

14 In any event, in the light of the amendments to O 24A of the Rules of the Supreme Court 1971 (WA) which took effect on 1 March 2007, it does not seem to me to be necessary to decide whether the approach of Roberts-Smith J in Alpine should be followed. That is because his Honour's approach was founded upon the then prima facie entitlement of a plaintiff who had made an offer under O 24A to indemnity costs in the circumstance that the result of the trial was less favourable to the defendant than the terms of the offer. His Honour adopted the view that the same prima facie entitlement to indemnity costs should arise from a Calderbank offer. The amendments to O 24A which took effect on 1 March 2007 mean that there is now no such prima facie entitlement under O 24A. See O 24A r 10(4). Thus the foundation for his Honour's view that rejection of a Calderbank offer can give rise to a presumption in favour of indemnity costs no longer exists.

15 In this regard, I note that in Townsend v Collova [2005] WASC 4 (S), Le Miere J held that rejection by a plaintiff of a Calderbank offer did not give rise to a prima facie entitlement to indemnity costs. In so holding, Le Miere J distinguished Alpine Holdings and Multicon Engineering on the basis that those were cases in which the plaintiff had made a Calderbank offer. In Townsend, the Calderbank offer had been made by the defendant. Under the provisions of O 24A, a defendant had (and has) no prima facie entitlement to indemnity costs in circumstances where a plaintiff has rejected an offer from a defendant that is more favourable to the plaintiff than the outcome of the action.

16 The amendments to O 24A in 2007 have equated the position of a plaintiff offeror under O 24A with the position of a defendant offeror.

17 For these reasons, in my opinion the making of an offer of settlement which is more favourable to the offeree than the outcome of a trial does not give rise to any prima facie entitlement to indemnity costs.

18 The relevance of the rejection of what proves to be a favourable offer of settlement to the award of indemnity costs has been stated in different ways in various decisions. For example, it has been said that rejection of a settlement offer may lead to indemnity costs where the rejection is 'imprudent' (Colgate-Palmolive (233); NMFM Property Pty Ltd v Citibank Ltd (No 11) [2001] FCA 480; (2001) 109 FCR 77 [82]); 'plainly unreasonable' (NMFM [82]); or simply 'unreasonable' (Globaltech Pty Ltd v Pareek [2006] WASC 30 (S) [17]; Fyna Foods Australia Pty Ltd v Cobannah Holdings Pty Ltd (No 2) [2004] FCA 1212 [5]).

19 In Gove v Black [2006] WASC 298 (S) [45] - [46], Templeman J adopted the approach that a failure to accept an offer may give rise to costs on an indemnity basis if the failure to accept the offer was so unreasonable in all the circumstances that an order for costs on a party and party basis would not be just. That is the formulation which I would adopt.

20 In assessing any question of the reasonableness of the rejection of an offer, it is of the first importance that the assessment be made without the benefit of hindsight. See, for example, Gretton [24], [38].

21 In my opinion, in the circumstances of this case the defendant's rejection of the plaintiff's offer of settlement falls well short of being so unreasonable as to mean that it is just to order indemnity costs.

22 The defendant had a case of substance, supported by a substantial body of expert evidence. In some instances (Mr Rogers, Associate Professor McKenzie), the evidence of the defendant's experts conflicted directly with the plaintiff's experts. In other cases, the questions were as to the weight to be given to expert evidence on a subject (for instance, epidemiology), in determining the cause of the plaintiff's fibrosis.

23 The defendant cannot be expected to have been able to predict what my findings would be in determining the various issues regarding the expert evidence. Many of the plaintiff's submissions in support of an award of indemnity costs seem to me to involve, implicitly, expecting the defendant to have been able to do so.

24 The defendant's conduct in deciding to have the court decide the substantial issues arising from the expert evidence was, in my opinion, not unreasonable and certainly not so unreasonable as to make it just to order indemnity costs.

25 The plaintiff submitted that the defendant ought to have recognised that it faced a real risk in the litigation. I accept that that is so, but that fact alone does not provide an adequate basis for the award of indemnity costs.

26 Nor, in my opinion, is the question to be determined (as some of the plaintiff's submissions suggest), by whether the defendant reasonably held the view that it was 'likely' to succeed in its defence. That is a judgment which the court is not well placed to make, in that the views expressed by those who advised the defendant are not available. (The defendant's submissions contain various statements as to what the defendant 'believed' prior to trial, in various respects. As these assertions are not supported by evidence I have not had regard to them.) In any event, a decision to litigate a case of substance which had a reasonable prospect of success (albeit that such prospects were thought to be less than 'even money') in the face of an offer to settle, would not, in the absence of further facts, give rise to a sufficient ground to order indemnity costs.

27 It follows that I do not accept the plaintiff's submission that 'the defendant having chosen to take the risk of litigating, there ought to be a price to pay beyond party/party costs'. The 'price to be paid' by the defendant includes the excess of its liability under the judgment compared to the settlement offer, its own costs after the offer was rejected, as well as its liability for the plaintiff's costs on a party-party basis. In any case, for the reasons I have sought to explain, I do not consider that the plaintiff's submission in this regard reflects a proper basis for the award of indemnity costs.

28 This was not an instance where a party's case was doomed to fail, or suffered from a fatal flaw which was pointed out by the other party in the Calderbank offer; see NMFM [87].

29 The plaintiff emphasised that the defendant rejected his offer within one day of receiving it. In the circumstances of this case I do not consider that that fact affords any support for a conclusion that the rejection was hasty or pre-emptory and so unreasonable in the sense that I have explained.

30 The plaintiff also submitted that the relative ability of the parties to bear the additional costs of the trial is relevant. I do not accept that the differing means of the parties provides any ground for ordering indemnity costs.

31 In my opinion, neither the defendant's rejection of the offer of settlement, nor any other aspect of the defendant's conduct referred to in the plaintiff's submissions provides any sufficient basis to order indemnity costs.

32 The plaintiff seeks, in the alternative, costs on a solicitor-own client basis. No separate submissions were made in support of that application.

33 For the reasons already stated I am not satisfied that it is appropriate in this case to depart from the usual order for costs on a party-party basis.

34 For these reasons I order that the defendant pay the plaintiff's costs of the action, including any reserved costs, such costs to be taxed if not agreed.