AMACA PTY LTD (Formerly James Hardie & Co Pty Ltd) (ACN 000 035 512)

Torts - Negligence - Personal injury arising from exposure to asbestos - Whether duty of care exists - Whether injury foreseeable - Class of persons for purposes of assessing foreseeability is a home handyman - Injury reasonably foreseeable to person in the defendant's position

Torts - Negligence - Personal injury arising from exposure to asbestos - Duty of care - Scope of the duty of care - Duty to take reasonable care to avoid injury being suffered by those using the product as intended or in a normal manner

Torts - Negligence - Personal injury arising from exposure to asbestos - Duty of care - Whether defendant negligently breached duty of care - Whether warnings and cautions were sufficient to discharge duty - Turns on own facts

Torts - Negligence - Personal injury arising from exposure to asbestos - Breach of duty of care - Whether breach caused or materially contributed to plaintiff's injury - Causation in fact - Whether defendant must discharge an evidential onus following plaintiff establishing prima facie case - City of Stirling v Tremeer [2006] WASCA 73 applied

Torts - Negligence - Personal injury arising from exposure to asbestos - Assessment of damages - Assessment of damages for non-pecuniary loss

Civil Liability Act 2002 (WA), s 5B(1), s 10A(1)

Abadon v The Queen [1983] 1 WLR 126

Barker v Corus UK Ltd [2006] UKHL 20

Bennett v Minister for Community Welfare [1992] HCA 27; (1992) 176 CLR 408

Bonnington Castings Ltd v Wardlaw [1956] UKHL 1; [1956] AC 613

Brawski v Quayle [1966] VicRp 54; [1966] VR 382

City of Stirling v Tremeer [2006] WASCA 73

Clyne v State Rail Authority of New South Wales [2005] NSWDDT 4

Cole v South Tweed Heads Rugby League Football Club [2004] HCA 29; (2004) 217 CLR 469

Dovuro Pty Ltd v Wilkins [2003] HCA 51; (2003) 215 CLR 317

Easther v Amaca Pty Ltd [2001] WASC 328

Fairchild v Glenhaven Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32

Gaunt v Amaca Pty Ltd, unreported; Ddt of NSW (Curtis J); Library No 151; 28 August 2003

Hart v Amaca Pty Ltd [2004] NSWDDT 10

Lynch v Amaca Pty Ltd [2004] NSWDDT 1

Makita (Australia) Pty Ltd v Sprowles [2001] NSWCA 305; (2001) 52 NSWLR 705

March v E & MH Stramare Pty Ltd [1991] HCA 12; (1991) 171 CLR 506

McGhee v National Coal Board [1972] UKHL 7; [1972] 3 All ER 1008

McGilvray v Amaca Pty Ltd [2001] WASC 345

Misiani (as Executor of the Will of Misiani (dec)) v Welshpool Engineering Pty Ltd (in liq) [2003] WASC 263

Naxakis v Western General Hospital [1999] HCA 22; (1999) 197 CLR 269

R v Abadon [1983] 1 WLR 364

Rosenberg v Percival [2001] HCA 18; (2001) 205 CLR 434

Seltsam Pty Ltd v McNeill [2006] NSWCA 158

Sharman v Evans [1977] HCA 8; (1977) 138 CLR 563

Skelton v Collins [1966] HCA 14; (1966) 115 CLR 94

Smith v Sydney Water Corporation Ltd [2000] NSWDDT 13

State of New South Wales t/a New South Wales Department of Agriculture v Allen [2000] NSWCA 141

Thompson v Johnson & Johnson Pty Ltd [1991] VicRp 84; [1991] 2 VR 449

Wilsher v Essex Area Health Authority [1987] UKHL 11; [1988] AC 1074

Wyong Shire Council v Shirt [1980] HCA 12; (1980) 146 CLR 40

Adelaide Chemical and Fertiliser Co Ltd v Carlyle [1940] HCA 44; (1940) 64 CLR 514

Amaca v Wallaby Grip [2005] NSWDDT 41

Anderson v Enfield City Corporation (1983) 34 SASR 472

Bale v Seltsam Pty Ltd [1996] QCA 288

Barnes v Irwell Valley Water Board [1939] 1 KB 21

Barrow and Heys v CSR Ltd, unreported; SCt of WA (Rowland J); Library No 7231; 4 August 1988

Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307

Best v Yellow Express Carriers Ltd (in liq) [2004] NSWDDT 46

Birkholz v R J Gilbertson Pty Ltd (1985) 38 SASR 121

Bolton v Stone [1951] UKHL 2; [1951] AC 850

Browne v Cockatoo Dockyard Pty Ltd [1999] NSWDDT 19; (1999) 18 NSWCCR 618

Chance v Alcoa of Australia Ltd (1990) A Tort Rep 81-017

Chapman v Hearse [1961] HCA 46; (1961) 106 CLR 112

Clark v Kramer [1986] WAR 54

Cockatoo Dockyard Pty Ltd v Browne [2001] NSWCA 58; [2001] 21 NSWCCR 544

Cole v South Tweed Heads Rugby League Football Club Ltd [2004] HCA 29; (2004) 217 CLR 469

Cominco Ltd v Westinghouse Canada Ltd (1981) 127 DLR (3d) 544

Commonwealth of Australia v Elliott [2004] NSWCA 360

Commonwealth v McLean (1996) 41 NSWLR 389

Comstock v General Motors (1959) 78 ALR 2d 449

Crimmins v Stevedoring Industry Finance Committee [1999] HCA 59; (1999) 200 CLR 1

CSR Ltd v Wren (1997) 15 NSWCCR 650

CSR Ltd v Young (1998) 16 NSWCCR 56

Drakos v Woolworths (SA) Ltd [1991] 56 SASR 431

E M Baldwin & Son Pty Ltd v Plane (1999) A Tort Rep 81-499

Eaton v Carrier Air Conditioning Pty Ltd [2004] NSWDDT

Flannery v Shire of Leonora [2001] WASCA 47

Graham Barclay Oysters Pty Ltd v Ryan [2002] HCA 54; (2002) 211 CLR 540

Griffiths v Kerkemeyer [1977] HCA 45; (1977) 139 CLR 161

Hall v Tarlinton (1978) 19 ALR 501

Hughes v Lord Advocate [1963] UKHL 1; (1963) AC 837

John Pfeiffer Pty Ltd v Rogerson [2000] HCA 36; (2000) 203 CLR 503

Jones v Dunkel [1959] HCA 8; (1959) 101 CLR 298

Julia Farr Services Inc v Hayes [2003] NSWCA 37; (2003) 25 NSWCCR 138

Kars v Kars [1996] HCA 37; (1996) 187 CLR 354

Kingsgrove RSL v Spasevski [2002] NSWCA 342

Kschammer v R W Piper & Sons Pty Ltd [2003] WASCA 298

Lee Transport Co Ltd v Watson [1940] HCA 27; (1940) 64 CLR 1

Levi v Colgate-Palmolive (1941) 41 SR(NSW) 48

McNeill v Seltsam Pty Ltd [2005] NSWDDT 51

Medlin v State Government Insurance Commission [1995] HCA 5; (1995) 182 CLR 1

Mokta v Metro Meat International Ltd [2005] WASCA 143

Morgan v Tame [2000] NSWCA 121; (2000) 49 NSWLR 21

Mt Isa Mines Ltd v Pusey [1970] HCA 60; (1970) 125 CLR 383

Nagle v Rottnest Island Authority [1993] HCA 76; (1993) 177 CLR 423

National Insurance Co of New Zealand Ltd v Espagne [1961] HCA 15; (1961) 105 CLR 569

Neill v New South Wales Fresh Food and Ice Pty Ltd [1963] HCA 4; (1963) 108 CLR 362

Nicholson v Atlas Steel Foundry & Engineering Co Ltd (1957) 1 All ER 776

Page v Smith [1995] UKHL 7; [1996] 1 AC 155

Paul v Rendell (1981) 55 ALJR 371

Perre v Apand Pty Ltd [1999] HCA 36; (1999) 198 CLR 180

Planet Fisheries Pty Ltd v La Rosa [1968] HCA 62; (1968) 119 CLR 118

Purkess v Crittenden [1965] HCA 34; (1965) 114 CLR 164

Qantas Airways Ltd (No 2) v Cameron (1996) 68 FCR 367

Rentz v Seltsam [2004] NSWDDT 15

Rolls Royce Industrial Power (Pacific) Ltd v James Hardie & Co Pty Ltd [1999] NSWDDT 5

Rolls Royce Industrial Power (Pacific) Ltd v James Hardie & Co Pty Ltd [2001] NSWCA 461

Scanlon v American Cigarette Co (Overseas) Pty Ltd (No 2) [1987] VicRp 23; [1987] VR 281

Seltsam Ltd & Manufacturers Mutual Insurance Ltd v Minahan (1996) 13 NSWCCR 410

Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262

Shire of Brookton v Water Corporation [2003] WASCA 240

Smith v Leech Brain & Co Ltd [1962] 2 QB 405

Stevedoring Industry Finance Committee v Gibson [2000] NSWCA 179; (2000) 20 NSWCCR 417

Sullivan v Moody (2001) 207 CLR 562

Suosaari v Steinhardt [1989] 2 Qd R 477

Sutherland Shire Council v Heyman [1985] HCA 41; (1985) 157 CLR 424

Tame v State of New South Wales [2002] HCA 35; (2002) 211 CLR 317

Todman v Victa Ltd [1982] VicRp 85; (1982) VR 849

Todorovic v Waller [1981] HCA 72; (1981) 150 CLR 402

Van Gervan v Fenton [1992] HCA 54; (1992) 175 CLR 327

Walton & Walton v British Leyland UK Ltd, unreported; HCt of UK; 12 July 1978

Western Australia v Watson [1990] WAR 248

Wintle v Conaust (Vic) Pty Ltd [1989] VicRp 84; [1989] VR 951

Workers' Compensation (Dust Diseases) Board v Kelly [2000] NSWCA 57; (2000) 20 NSWCCR 234

Wren v CSR [1997] NSWDDT 7; (1997) 15 NSWCCR 45

Wright v Dunlop Rubber Co Ltd (1972) 13 KIR 255

1 The plaintiff was born in the United Kingdom on 23 October 1942. He grew up in Islington, London. After leaving school aged 15 years he worked as a gardener and for a short time also drove a black cab part-time around London as well as doing his day job as a gardener.

2 In 1981 the plaintiff emigrated to Western Australia with his family. In or about May 1982 the plaintiff and his wife purchased and moved in to 190 Erindale Road, Hamersley. The plaintiff has lived there ever since.

3 By the end of November 1981 the plaintiff got a job at the Royal Perth Hospital as a gardener. He worked at the rehabilitation annex at Shenton Park until 1987. In 1987 the plaintiff was employed by the Perth Zoo as a horticulturalist.

The plaintiff is diagnosed to be suffering mesothelioma

4 In about October 2005 the plaintiff noticed symptoms of a niggling pain under his right ribs. On 4 November 2005 he saw his general practitioner, Dr Levy. Dr Levy sent the plaintiff for a chest x-ray and subsequently referred him to Sir Charles Gairdner Hospital where he was admitted on 9 November 2005. The plaintiff underwent tests and investigation. On or about 11 November 2005 the plaintiff was informed that he had mesothelioma. The plaintiff subsequently underwent two surgical procedures including a pleuropneumonectomy on 30 December 2005. A pleuropneumonectomy is a surgical procedure involving the removal of the pleura surrounding the lung. Since the operation the plaintiff has completed two cycles of chemotherapy. The plaintiff resigned his employment with the Perth Zoo on 24 March 2006.

5 The plaintiff has malignant mesothelioma. Mesothelioma is an aggressive cancer. The average expectation of survival is about nine months after diagnosis. Following the pleuropneumonectomy and chemotherapy the plaintiff had an expectation for survival of three to four years. The cause of the plaintiff's mesothelioma is asbestos exposure.

6 The only exposure to asbestos that the plaintiff can remember involved working with asbestos cement products at his home at 190 Erindale Road, Hamersley. In 1983 the plaintiff dismantled a Hardiplank woven asbestos fence from the centre of his backyard and relocated it. He

broke and cut asbestos cement sheets using a handsaw and asbestos cutters and used an electric drill. In 1985 he sanded back and repainted the asbestos cement eaves of his house using a wire brush and sandpaper working above his head. In 1990 he painted the corrugated asbestos fence on both sides of his property, brushing down the sheets with a wire brush before painting over them. I will sometimes refer to the plaintiff's work with asbestos cement products at 190 Erindale Road in 1983, 1985 and 1990 as the plaintiff's handyman work and his exposure to asbestos in the course of that work as the plaintiff's handyman asbestos exposure.

7 The defendant was previously named James Hardie & Coy Pty Ltd. It manufactured and sold products containing asbestos, including asbestos cement building products until the 1980s. I will sometimes refer to the defendant as James Hardie.

8 The plaintiff says that each of the asbestos cement products which were the source of his exposure to asbestos were manufactured and supplied to the original constructors of the house and fences by the defendant. The plaintiff's case is that the defendant, as manufacturer and supplier of the products, owes a duty to the class of persons including the plaintiff to take reasonable care to ensure that the plaintiff is not exposed to the risk of injury from exposure to, and the inhalation of, asbestos. The class of persons are handymen who might cut, drill, scrape, brush or otherwise deal with the asbestos cement products manufactured by the defendant. The plaintiff says that the defendant had a duty to warn the plaintiff and other persons dealing with the asbestos cement products of the dangers of dealing with them by affixing suitable warning notices and by advertising the dangers. The plaintiff says that the defendant breached its duty of care to the plaintiff by failing to do so and that that failure caused or contributed to the plaintiff's exposure to asbestos. The plaintiff's case is that his exposure to the defendant's asbestos cement products caused or contributed to him contracting mesothelioma.

Some matters admitted or clearly established

9 In his closing submissions the defendant's senior counsel admitted that the plaintiff suffers pleural mesothelioma. In any event, that was established by the evidence.

10 The plaintiff pleads that the Hardiplank woven fence, the asbestos sheets constituting the eaves of the house and the corrugated asbestos fencing sheets were manufactured and supplied by the defendant to the person who built the house and constructed the fences. In its closing submissions the defendant conceded that the asbestos cement building products to which the plaintiff was exposed were probably manufactured by it. In any event, I find that is established by the totality of the evidence, having particular regard to the evidence of Mr Warwick Gazzard.

11 The defendant's asbestos cement building products were sold through hardware stores and timber yards. I find that the asbestos cement products which were the source of the plaintiff's handyman asbestos exposure were manufactured by the defendant and supplied by the defendant to a person or persons who directly or indirectly supplied those products to the original constructors of the house and fences at 190 Erindale Road.

12 The plaintiff believes the house at Erindale Road was built about five years before he and his family moved in in May 1982. The certificate of title shows that Plunkett Homes, a project home builder, became the registered proprietor of the property in 1980. I find that the house, including the eaves, the woven Hardiplank fence and the corrugated asbestos sheet fences were constructed in the late 1970s.

13 There are two key liability issues, or groups of issues. The first issues concern the duty of care, if any, owed by the defendant to the plaintiff.

14 The plaintiff says that the defendant owed him a duty to minimise or prevent the risk of injury from asbestos exposure by taking all steps reasonably open to communicate the danger and the means of avoiding it, to the class of which the plaintiff was a member. In his counsel's written closing submissions the plaintiff described the class of which he was a member as "end users" of the defendant's products. The plaintiff submits that the defendant breached the duty of care it owed to him.

15 The defendant submits that it did not owe the plaintiff a duty of care with the content postulated by the plaintiff. Secondly, the defendant submits that it discharged the duty of care which it owed to the class of which the plaintiff was a member.

16 The second major issue, or groups of issues, are causation issues. The plaintiff submits that the defendant's breach of duty in fact caused him to contract mesothelioma. That is, the mesothelioma suffered by the plaintiff was caused or contributed to by the asbestos exposures resulting from the plaintiff's handyman activities handling or dealing with the asbestos cement building products manufactured and supplied by the defendant. The plaintiff submits that the defendant's breach of duty of care was a legal cause of the plaintiff suffering mesothelioma.

17 The defendant submits that it did not cause any injury from which the plaintiff suffers. Further, the defendant submits that, in any event, there was no causative breach of any duty of care.

18 A third issue, or group of issues, is the assessment of damages.

19 Before referring to the plaintiff's asbestos exposure in greater detail it is useful to make some brief observations concerning some aspects of the nature and attributes of asbestos.

20 Asbestos is a naturally occurring mineral, exhibiting a fibrous structural property. There are two classes of asbestos, amphibole asbestos and serpentine asbestos. The difference relates to the characteristics and shape of the fibres: amphibole asbestos has fine, straight fibres; serpentine asbestos has curly or feathery fibres.

21 There are two commercially viable types of amphibole asbestos: crocidolite, commonly called blue asbestos, and amosite, commonly called brown asbestos. There is only one type of commercially viable serpentine asbestos: chrysotile, commonly called white asbestos. The asbestos cement building products to which the plaintiff was exposed contained chrysotile and amosite.

22 The asbestos cement building products to which the plaintiff was exposed are a mixture of cement, silica and asbestos. The asbestos comprises in the order of 8 to 15 per cent of the product.

23 An important concept or term is "background exposure". In general, background exposure refers to exposure to asbestos in the general environment. The "background risk" is the risk of contracting mesothelioma as a result of "background exposure".

24 Professor Henderson, an expert in the field of asbestos-related disease, said that background asbestos exposure from the environment at large represents general environmental exposure unrelated to the use of asbestos-containing materials in the workplace or at home, or from significant point sources of asbestos such as factories. Professor Henderson considers that background exposure includes exposures related to the passive weathering of "in place" asbestos-containing materials, including asbestos-roofing materials - with very low or unmeasurably low airborne fibre concentrations - and environmental exposure derived from the brakes of passing automobiles. Professor Henderson excludes from background exposure any exposure arising from active disturbance of any asbestos-containing materials such as asbestos cement building products or insulation materials.

25 The absence of a recalled history of asbestos exposure is not the same thing as an absence of exposure. Many cases of seemingly "background" mesothelioma can be attributed to forgotten or unrecognised asbestos exposures. I will sometimes refer to asbestos exposure from the environment at large excluding exposure arising from the use of asbestos-containing materials in the workplace or at home or from significant point sources of asbestos or any exposure arising from active disturbance of any asbestos-containing materials as ambient environmental exposure. I will sometimes refer to asbestos exposure arising from the use of asbestos-containing materials in the workplace or at home or from significant point sources of asbestos or from the active disturbance of asbestos-containing materials as specific exposure.

26 In general, the other expert witnesses used the terms "background exposure" and "background risk" consistently with the way in which they were used by Professor Henderson.

27 In cross-examination Professor Musk, a respiratory physician and expert in treating asbestos-related diseases, agreed that the members of the background risk group are the group of mesothelioma sufferers who are unable to recall a specific exposure to asbestos. It was put to Professor Musk that repeated studies over the years had demonstrated that between 15 per cent and 30 per cent of mesothelioma sufferers are unable to recall any particular exposure to asbestos. Professor Musk agreed but added: "But that depends on the quality of the questions and the intensity of the questioning process".

28 In cross-examination Professor Musk agreed that he and Dr De Klerk had attempted to calculate a background risk for mesothelioma in Western

Australia and that they had expressed the risk as between two and three persons per million persons per annum or between 140 persons per million per lifetime to 210 persons per million per lifetime, assuming a lifetime of 70 years.

29 I observe that the "background risk" calculated by Professor Musk and Dr De Klerk is not the same thing as the risk of mesothelioma being contracted by persons whose only exposure to asbestos is from ambient environmental exposure. The calculations or estimates of "background risk" by Professor Musk and Dr De Klerk were based on the percentage of recorded mesothelioma sufferers who were unable to recall a specific exposure to asbestos. That cohort includes people who might have suffered specific exposure but who did not recognise or remember the specific exposure or exposures. The risk of mesothelioma caused by ambient exposure is potentially lower than the "background risk" calculated by Professor Musk and Dr De Klerk.

30 The plaintiff suffers pleural mesothelioma. The pleura is a membrane lining the lungs and separating the lungs from other organs of the chest. Mesothelioma was first reported in 1960 in relation to the inhalation of asbestos. Knowledge as to the nature of mesothelioma has accumulated gradually over the years since 1960.

31 In Australia, mesothelioma is associated with the inhalation of asbestos. Generally speaking, there are three major issues relating to the connection between mesothelioma and the inhalation of asbestos: the dose issue, the fibre type issues and the lag time issue.

32 The risk of contracting mesothelioma is related to the dose of the asbestos inhaled. An asbestos fibre must be very small before it can be inhaled and retained in the fine airways of the lung. These tiny fibres are called respirable fibres. A dose may be calculated by counting the concentration of respirable fibres in an atmosphere. This is often expressed in terms of the number of fibres in a millilitre of air and abbreviated to the number of "fibres/ml". Calculations of the cumulative dose of asbestos likely to have been inhaled by an individual may be made by multiplying the concentration of asbestos fibres in an atmosphere by the time that an individual was exposed to that atmosphere. The cumulative dose may then be expressed in terms of the numbers of fibres in a millilitre of air over so many years and abbreviated to the number of "fibres/ml years".

33 The risk of contracting mesothelioma is directly related to the type of asbestos fibre which was inhaled by the individual. Studies have demonstrated that each fibre type has a different propensity to induce mesothelioma. Crocidolite or blue asbestos, is the most potent. Amosite or brown asbestos, is the median in terms of potency. Chrysotile or white asbestos is the least potent.

34 The risk of contracting mesothelioma is greatly increased by the expiry of time since the exposure - the lag time. Mesothelioma has a long latency period. Asbestos inhaled within 10 years of the contraction of mesothelioma is considered by relevant experts to be causally irrelevant to the contraction of the disease.

35 Medical science cannot explain precisely how asbestos causes mesothelioma. There are different theories. Dr James Leigh, an occupational physician, explained one theory, involving multi-stage carcinogenesis through initiation followed by promotion. Professor Bruce Robinson, a chest physician, considered this theory to be unhelpful and outdated. Professor Robinson advanced an alternative theory based upon a prolonged period of irritation and inflammation arising from the inhaled asbestos fibres. Once an asbestos fibre or fibres have initiated the carcinogenesis it is not known whether the inhalation of additional fibres has any role in the development of mesothelioma.

Plaintiff's exposure to asbestos - the detail

36 The plaintiff remembers three activities at his home that involved working with asbestos products.

37 The first was moving a Hardiplank fence located about half way down the backyard or garden of the house. The plaintiff did that work in about April or May 1983.

38 In the course of moving the fence the plaintiff had to take apart the pieces of the fence and cut pieces to fit the new fence line. He did this work over a couple of weekends and a couple of nights after work. He pulled the planks off the post using a claw hammer or screwdriver. Some of the sheets broke in the process. The process of dismantling the fence gave off dust. The plaintiff had to prise the sheets off the posts and handle them by picking them up and placing them towards the side of the property. The process was dusty and the plaintiff got dust on himself and his clothes. He did not wear a mask. He did not try to keep the dust down or avoid the dust. After the sheets came off the plaintiff stacked them up against the fence. He pulled out the fence posts. He dug new holes and

re-used the fence posts. The plaintiff then handled the sheets again by weaving them through the fence posts. He had to cut quite a number because the length had changed. He cut the sheets with a handsaw and used an old pair of tinsnips. Sometimes the plaintiff cut the sheets by scoring the sheets which would give off some dust and once he scored the sheet he would then break the sheet off. He also cut some of the lengths with a handsaw but the handsaw went blunt and he then used tinsnips. He also had to drill through quite a number of sheets to attach the sheets to the post of the fence. The process of cutting and drilling gave off dust. The plaintiff had to drill the holes into the fence posts. This meant drilling new holes through the asbestos sheeting because the fence was a different length and it needed new holes for the sheets. He used an electric drill. Drilling the sheets gave off some dust. When the plaintiff drilled the sheets the drill would usually be fairly close to his face so he breathed in the dust when he drilled through the sheets. After having moved the fence, there were parts of the fence that needed painting. The plaintiff brushed the sheets back with a wire brush and painted over the sheets. This process also gave off dust and he got dust on him again.

39 The second exposure occurred in about February or March 1985 when the plaintiff painted all the underside eaves of the house. Much of the paint was flaking off. The plaintiff did the preparation first by brushing, sanding and then washing the eaves down. He did this above his head. He washed the eaves to get any last dirt or dust off. He used a scaffold board and some steps so he could reach the eaves. The plaintiff had some time off work, about a fortnight, and the first week was taken up with the preparation - sanding and brushing back the eaves and filling holes in timbers. The whole job took about a month. The first two weeks the plaintiff was on holiday and doing the job almost on a fulltime basis. For the next two weeks he finished the job on the weekends and a few nights after work. The initial rubbing down took the first week of the plaintiff's holidays. He did not wear a mask and whilst carrying out this work he sanded and brushed the asbestos sheets above his head. This caused a lot of dust to fall down on him. He got dust on his face and eyes and in his mouth as well as over all his clothes.

40 The third exposure occurred in about February 1990 when the plaintiff painted the corrugated asbestos fence on both sides of his home. The job involved brushing down the fences and the ridge capping. The left fence had lots of bird droppings on it so the plaintiff needed a fairly hard wire brush to get a decent finish on it so it could be ready for painting. Brushing the corrugated fencing gave off a lot of dust. The plaintiff was less than an arm's length away from the fence as he was

brushing and he was often crouching when performing the work. He got dust on his sleeves, hands and clothes and was breathing in dust as he was doing this job. He used a wire brush to brush the entire length of the left fence. On the fence on the right hand side of the property there was hard mould or algae on the corrugated fence which needed to be scrubbed back. The plaintiff used a wire brush to do this. Brushing back this fence gave off dust. The plaintiff got dust on his clothes and breathed it in as he was not wearing a mask. The job took the plaintiff a couple of days.

41 Apart from the exposures to which I have referred the plaintiff does not remember any other exposure to asbestos. The defendant did not plead that the plaintiff had experienced any exposure to asbestos other than the plaintiff's three handyman exposures arising from using or handling the asbestos cement building products to which I have referred.

42 The expert evidence establishes that the plaintiff, like every other person living in London and Perth, has experienced ambient environmental asbestos exposure.

43 Senior counsel for the defendant cross-examined the plaintiff carefully, thoroughly and at times intensely about other domestic or occupational sources of asbestos to which the plaintiff might have been exposed.

44 Senior counsel put to the plaintiff that he was unable to say that he had not been exposed to anything which contained asbestos earlier in his life. The plaintiff agreed but said that as far as he is aware he had never been exposed to asbestos. Senior counsel put to the plaintiff that there may have been asbestos in the houses in which he lived in the United Kingdom but of which he was unaware. The plaintiff said that he did not think there was any asbestos and he was pretty sure he never saw any asbestos. Senior counsel put to the plaintiff that he did not know whether the internal walls at some or all of the places he lived in the United Kingdom were themselves constructed of asbestos-containing material such as fibro. The plaintiff agreed that he would not know and had not looked but said he certainly did not think he ever saw any asbestos. Senior counsel cross-examined the plaintiff about other possible sources of asbestos to which the plaintiff might have been exposed, such as domestic insulation, sheds at his workplace constructed of asbestos and working on car brake linings. The plaintiff did not recall any asbestos insulation in any of the homes in which he lived, was not aware of any of the sheds at his workplace being constructed of asbestos and denied having worked on any car brake linings.

45 I find that the plaintiff experienced ambient environmental exposure to asbestos whilst living in the United Kingdom and Perth. There is no evidence that the plaintiff has experienced any specific exposure other than the exposure in the course of his handyman work. The plaintiff may have experienced exposure related to the passive weathering of "in place" asbestos-containing materials and environmental exposure derived from the brakes of passing automobiles as described by Professor Henderson. Such exposure is part of the ambient environmental exposure.

46 Senior counsel for the defendant cross-examined the plaintiff about the most likely domestic and occupational asbestos exposures that the plaintiff is likely to have experienced if he experienced any specific asbestos exposure. As a result of the plaintiff's response to that questioning I find not only that the plaintiff did not recognise or recall any specific asbestos exposure but on the balance of probabilities the plaintiff did not experience any specific asbestos exposure other than the exposure in the course of his handyman activities.

47 The general principles concerning the existence of a duty of care are reflected in s 5B(1) of the Civil Liability Act 2002 (WA) which provides that a defendant is not liable for harm caused by the defendant's fault in failing to take precautions against a risk of harm unless the risk was foreseeable (that is, it is a risk of which the defendant knew or ought to have known), the risk was not insignificant, and in the circumstances, a reasonable person in the defendant's position would have taken those precautions. In this case, foreseeability is important.

48 The plaintiff submitted that the case comes within an established category of cases where judicial decisions establish the existence of a duty of care. The plaintiff says that the category is that of manufacturer or supplier and consumer.

49 In Dovuro Pty Ltd v Wilkins [2003] HCA 51; (2003) 215 CLR 317 at [29] McHugh J said that it is beyond doubt that a manufacturer of any product owes a duty to a consumer to take reasonable care to prevent the product causing injury or loss to the consumer. In that case the appellant had distributed in Australia canola seed produced in New Zealand. The seed contained a small amount of weed seeds. At the time of the importation no Australian government had declared any of the weeds to be a prohibited weed. The respondent, which conducted a farming business in Western Australia, bought and planted some of the seed which the reseller had bought from the appellant. Shortly after that transaction the Agriculture Department of

Western Australia made declarations which required the eradication of the weed seeds. At trial the appellant conceded that it owed a duty of care but did not elaborate upon the scope of the duty of care. On appeal to the High Court the appellant sought to withdraw its concession. Gummow J at [58] said that it was unnecessary to consider whether the appellant should be permitted to withdraw the concession that, as ultimately formulated by the primary Judge, it owed a duty to the consumers of its canola seed to exercise reasonable care not to expose those consumers to a risk of injury of which the appellants knew or ought to have known. His Honour said that the critical question was whether the primary Judge erred in holding that the appellant breached that duty. Kirby J said at [99] that the concepts of duty, scope and breach represent component parts of a unified notion that must be constantly brought back to the touchstone of reasonableness. His Honour observed that the concession of the existence of a duty of care had been made without much clarity as to the scope of the duty being conceded and that the scope of the duty has significance for the related question of breach. At [159] Hayne and Callinan JJ said that as the respondent's case was presented at trial, the critical question was to identify whether the appellant knew or ought to have known that there was a risk of the sort of injury which it was alleged had been suffered - financial loss occasioned by pursuing a course of action recommended by government authorities to guard against the possible emergence of plants which had been declared to be harmful only after the appellant had distributed the seed and the farmers had acquired it. Their Honours said that only if that sort of loss was reasonably foreseeable by the appellant would the duty asserted by the respondent have been engaged.

50 In Seltsam Pty Ltd v McNeill [2006] NSWCA 158 the plaintiff, a priest, worked with asbestos cement sheeting purchased retail by a relative and manufactured by the defendant and was exposed to asbestos dust and fibres. The work totalled about 12 hours over several days. The plaintiff was diagnosed with mesothelioma. The New South Wales Court of Appeal held that the case was not one of the cases where judicial decisions establish the existence of a duty of care: Bryson J at [33].

51 In Seltsam v McNeill (supra) the plaintiff was not at any time the purchaser or the owner of the asbestos sheeting. In this case the plaintiff did become the owner of the asbestos cement products. However, I do not consider that that fact relevantly distinguishes this case from Seltsam v McNeill. The New South Wales Court of Appeal found that at the time the priest was exposed to asbestos it was not a known or reasonably foreseeable risk that home handymen and other low-intensity, casual end users who worked on asbestos cement products as handymen, not in an

industrial or other controlled situation, not in the course of employment or any like relationship and not for extended periods, exposed to asbestos dust would suffer mesothelioma. The plaintiff was one of an indeterminate class of people who long after the product had been sold by retail might disturb the asbestos in the product by operations such as sawing, drilling or scraping.

52 The plaintiff submits that this case is distinguishable from Seltsam v McNeill because the evidence in this case is that in 1983, 1985 and 1990 the harm which the plaintiff suffered was a reasonably foreseeable consequence of handyman asbestos exposure whereas in Seltsam v McNeill the New South Wales Court of Appeal held that there was no evidence capable of establishing that there was a foreseeable risk of injury in 1961 to a casual user of asbestos cement sheets as distinct from regular users of asbestos cement sheets with prolonged exposure to dust.

53 If, as the defendant submits, this case does not come within an established duty of care category then the next question is: was the harm which the plaintiff suffered a reasonably foreseeable result of the defendant's acts or omissions? Furthermore, if the defendant owed to the plaintiff a relevant duty of care it is necessary to consider questions of reasonable foreseeability of harm to the plaintiff from his handyman asbestos exposure in considering the issue of breach of duty. I turn now to consider whether in 1983, 1985 and 1990 there was a reasonable foreseeability of risk of injury from asbestos exposure to the class of persons to which the plaintiff belonged.

54 As part of the "neighbour" principle for determining a duty of care, reasonable foresight is directed to the identity of the plaintiff. In other words, was the plaintiff, either individually or as a member of a class, someone whom the defendant could reasonably foresee would suffer injury as a result of the defendant's conduct? See Donoghue v Stevenson [1932] AC 562.

55 In Seltsam v McNeill the New South Wales Court of Appeal held that the trial Judge was in error to treat a foreseeable risk of injury to regular users of asbestos cement sheets from prolonged exposure to dust released by cutting, drilling or sawing such sheets, as establishing a foreseeable risk of injury to a casual user exposed to such dust during one or two days work in the open air. In the course of argument in that case the parties distinguished between workers exposed to heavy levels of asbestos in factory situations on the one hand and end users, that is

persons such as carpenters who worked on asbestos cement sheeting on building sites, or other persons who did not work in a factory situation, on the other hand. At [29] Bryson JA said that he did not find end users to be a satisfactory classification because it includes occasional casual users and handymen in the same class as carpenters or other construction workers who work on asbestos cement sheeting, where encounters with the risk of inhalation of dust may take place daily or otherwise very frequently and over extended periods. At [36] Bryson JA said:

"The test of foreseeability is undemanding, but there is no basis for treating it as fictional or nominal, or for equating foreseeability with the limits of the imagination; it must be approached as a test which exists in reality and operates within the limits of the reasonable. It is not real, reasonable or just to adopt one broad class of end users to whom risks of exposure to asbestos were foreseeable. Persons whose exposure to asbestos was reasonably foreseeable include many whose exposure occurred in circumstances altogether different from those of the respondent. Workers who handle asbestos in mining, manufacturing or other industrial operations cannot on a reasonable or just basis be included in the same class as the respondent for purposes of deciding foreseeability. Their exposure was to undiluted asbestos and, as reasonably foreseen, extended to exposure for hours in the course of working days, and to continuous exposure over periods of months or years in a working career. Information which is known or ought to have been known to the appellant with respect to risks to them would be misapplied if it were treated as showing or tending to show some risk of injury relevant to the respondent's position."

56 At [38] Bryson JA approached the test of foreseeability in this way:

"In considering whether a reasonable person in the appellant's position would foresee that carelessness on his part may be likely to cause injury to the respondent, and whether there was a duty of care to the respondent, the position of the respondent must necessarily be considered at a high level of abstraction; the appellant of course could have no actual knowledge of the respondent himself or of the actual circumstances in which his association with the product exposed him to risk. Stepping from actuality into a higher level of abstraction, the person reasonable foreseeability of risk to whom must be considered is and must remain a home handyman who does not encounter the

product in an industrial or commercial continuing situation, who works on the product for a few hours only on one handyman project, not as part of what is otherwise his working life. It would be an error, a legal error to bring to bear considerations relating to the foreseeability of risk of injury to classes of persons with higher degrees of exposure, either in intensity of involvement in working on the product, or in number of occasions and length of time for which the product was worked on, or otherwise with greater intensity. The respondent is not entitled to rely on conduct which was negligent in the sense that there was a breach of a duty of care to some other persons the reasonable foreseeability of risk of injury to whom was different to foreseeability related to the respondent. In my opinion it would be a legal error to treat all end-users of a manufacturer of product uniformly for the purpose of considering the existence of the duty of care to them unless in reasonable foreseeability of risk of injury their circumstances placed them in the same class."

57 In considering what publicly available information should be considered in relation to the issue of foreseeability Bryson JA said at [40]:

"As a class, these home handymen had characteristically far less exposure to risk, for a far shorter time, than building or other industrial workers who handle and shape asbestos cement sheeting in employment situations. Publicly available information should be considered with care before deciding that it has relevance to the reasonable foreseeability of risk to a class of persons to which the respondent belonged."

58 In this case, counsel for the plaintiff submits that the appropriate class may be considered to be the people in this State who have James Hardie products in their home, or alternatively, all end users of the defendant's asbestos cement products. In Seltsam v McNeill the relevant exposure occurred in 1961. The New South Wales Court of Appeal concluded there was no evidence capable of establishing that there was a foreseeable risk of injury in 1961 to a casual, one off, user of asbestos cement sheets as distinct from regular users of asbestos cement sheets from prolonged exposure to dust. Counsel for the plaintiff submits that the evidence in this case establishes that in 1983 there was a foreseeable risk of injury to handymen and other casual end users of asbestos cement building products. That requires an examination of the evidence.

59 In this case, the person against whom reasonable foreseeability of risk must be considered is a home handyman or other casual user of asbestos cement building products who does not encounter the product in an industrial or occupational situation. The court must consider whether it was reasonably foreseeable that there was a risk of injury to a member of that class of persons having regard to the information available to the defendant and publicly available in 1983.

60 The plaintiff relies on the evidence of eminent experts and in particular Professor Musk, Professor Henderson and Dr Leigh and on the evidence of Dr Francis, an occupational hygienist. The plaintiff also relied on the evidence of former employees of the defendant, Mr Peter Russell, Mr Warwick Gazzard, and Mr James Lawless. The defendant further relies upon the defendant's sworn answers to interrogatories, upon a number of documents taken from the defendant's discovery and upon published scientific, medical and other literature.

61 Professor Musk is an eminent respiratory physician. He has many years' experience in treating patients with mesothelioma and other asbestos-related diseases. He has undertaken extensive research and has authored or co-authored numerous publications concerning asbestos-related diseases. In 1992 he was made a Member of the Order of Australia for service to respiratory medicine in the field of asbestos and smoking related diseases.

62 In his written report (Exhibit H14) Professor Musk gave evidence of the development of knowledge in relation to asbestos-related diseases by reference to learned works and other literature commencing with the 1898 annual report of the UK Chief Inspector of Factories and Workshops.

63 Professor Musk referred to J C Wagner (proceedings of the Pneumoconiosis Conference, Johannesburg, February 1959, "Some Pathological Aspects of Asbestosis in the Union of South Africa") and to Wagner, Sleggs and Marchand "Diffuse Pleural Mesothelioma and Asbestos Exposure in the North Western Cape Province" (1960) Br J Ind Med 17:260. Professor Musk said that after the 1959 Johannesburg Conference at which the work of Wagner et al was presented, and after its publication in the British Journal of Industrial Medicine in 1960, knowledge of the effects of exposure to asbestos, even in small amounts was well established. It was by then widely accepted that asbestos could

cause asbestosis, lung cancer and mesothelioma. It was accepted that small doses, particularly of crocidolite could cause mesothelioma. Professor Musk said that mesotheliomas were reported among British shipyard workers who had received only light or intermittent exposure to asbestos dust and Dr Wagner reported on the mesotheliomas he had found in South Africa in people who had not actually worked with asbestos, but merely lived in the vicinity of asbestos mines and mills.

64 By 1965 Dr Newhouse had reported on cases of mesothelioma she had found among the relatives of asbestos workers in London. Professor Musk said that owing to the abundance of literature generated on asbestos, asbestos-related disease and asbestos-related disease prevention from 1965 on it is difficult to single out important individual documents.

65 After reviewing articles, learned works, standards, regulations and legislation Professor Musk concluded:

"In my opinion the above material 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 the time period involved in this case, 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 blue asbestos, without exposure being reduced to a minimum, together with appropriate warnings of the risks to those exposed. The amounts of asbestos to which persons were being exposed can and should have been quantified during the 1960s as a consequence of these serious dangers and risks to health.

By the 1970's 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."

66 Professor Musk was cross-examined about a publication of the Australian National Health and Medical Research Council (NH&MRC) described as being the "Code for the Handling of Asbestos by Small Users" and to a report on the health hazards of asbestos published by the NH&MRC in mid-1981 and other publications. None of the matters put

to Professor Musk, nor his response to them, caused him to qualify his opinions nor did they undermine those opinions. I accept the opinions expressed by Professor Musk.

67 Dr Leigh is an expert consultant occupational physician. He was the head of the Epidemiology and Surveillance Unit and Co-ordinator of the Australian Mesothelioma register from 1988 to 1996. In 1999 he was a consultant to the World Trade Organisation on asbestos issues.

68 In his report (Exhibit H20) Dr Leigh gave evidence about the development of knowledge concerning the hazards of asbestos and the connection between asbestos exposure and diseases including asbestosis and mesothelioma.

69 It is Dr Leigh's evidence that by 1968 the association between asbestos exposure and mesothelioma was well established.

70 Dr Leigh says that in 1969 the well known text Hunter's "The Diseases of Occupations" stated the following, in relation to the then draft UK Asbestos Regulations 1968:

"The new regulations apply to factories, some warehouses, ships under construction or in the course of repair. But the Factories Act cannot protect private users. We [sic] know that inhalation of dust from such activities as sawing or sanding material containing asbestos presents the hazard of malignant mesothelioma outside as well as inside industrial situations. It seems not unreasonable, therefore, to insist that materials containing asbestos should be clearly marked to show this, so that adequate precautions can be taken by the users. For instance, amateur handymen sawing materials containing asbestos could easily wear a lightweight dust mask, and either work out of doors or in a well ventilated room."

"[I]n 1974 the first major report of the UK Mesothelioma Register (relating to cases diagnosed in 1967 - 1968) described several cases of mesothelioma in insulation workers, building workers, dockers, workers handling asbestos cement products and following hobby exposure incurred when sawing asbestos sheets and drew attention to the possibility of mesothelioma

occurring at low dose ... No fibre type distinctions were made. Anderson et al ... drew attention to the risk of asbestos related disease, including mesothelioma, from household contact."

72 Dr Leigh said that in 1976 an authoritative review appeared in American Review of Respiratory Diseases that showed that mesothelioma could be caused by low level exposures. Dr Leigh then concluded that the defendant ought to have foreseen the risks of exposure from 1983 onwards.

73 Dr Leigh said that in 1970 the NH & MRC published the document "Atmospheric Contaminants, Hygiene Standards for Contaminants of the Air of the Workplace" stipulating an occupational standard for asbestos of 4 fibres/ml for chrysotile and amosite asbestos (crocidolite exposure was assumed to be prevented completely). Dr Leigh was cross-examined on that standard or standards and subsequent NH & MRC publications. I note that the NH & MRC report on the health hazards of asbestos of June 1981 recommended that the average fibre concentration of the air breathed by the worker throughout a working shift should not exceed 1 fibre/ml in the case of chrysotile and amosite asbestos. However, that recommendation follows the following statements:

"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 ..."

74 The matters put to Dr Leigh in cross-examination, and his response to them, did not qualify his evidence-in-chief concerning the foreseeability of the risk of injury from occasional or intermittent asbestos exposure. I accept the opinions of Dr Leigh.

75 Professor Henderson is a pathologist. He is a published expert in the field of asbestos-related disease. In 1999 he was appointed as an expert adviser to the World Trade Organisation in relation to issues surrounding measures concerning asbestos and asbestos-containing products.

76 In his report (Exhibit H18) Professor Henderson said:

"The causal relationship between asbestos and mesothelioma had been well established by the late 1980s and early 1990s, and at that time I was aware that no threshold level of asbestos exposure had been delineated below which there is no risk of mesothelioma above background risk: in other words, I and other authorities were aware by that time that mesothelioma could follow exposures to asbestos that were non-occupational in character - brief and transient and low-'dose' - including, for example, the development of mesothelioma from asbestos exposures related to 'handyman' - type work on A-C sheeting material: the development of mesothelioma from bystander, environmental and neighbourhood-type exposures had been recorded even earlier."

Professor Henderson was not cross-examined about those matters. I accept his opinion.

77 Dr Francis is an expert Occupational Hygienist. Dr Francis was initially employed by the Division of Occupational Health with the Health Department of New South Wales and later employed as a Specialist Occupational Hygienist with the New South Wales Workcover Authority. She has over 28 years of practical experience in the field of occupational hygiene, demonstrating a speciality in the area of asbestos from as early as 1971.

78 Dr Francis provided an opinion as to the availability of information as to knowledge in relation to hazards to health associated with exposure to asbestos. She was not cross-examined in relation to that opinion. Her opinion, which I accept, is accurately summarised by the plaintiff as follows:

"(a) From the early 1980s to 1990, and by 1983, asbestos was recognised among occupational health specialists as a carcinogen, with the association of asbestos exposure and lung cancer being reported in medical literature as far back as 1935.

(b) From the early 1980s to 1990, and by 1983, it was recognised among occupational health specialists that there was no threshold of safe exposure to airborne asbestos for mesothelioma induction.

(c) From the early 1980s to 1990, and by 1983, it was recognised among occupational health specialists that each dose of asbestos inhaled by a person increased the risk of that person contracting an asbestos related disease, including mesothelioma."

79 Ms Anne Batt was a medical librarian throughout the relevant period. The effect of her evidence was that there were a large number of available indices at the disposal of a librarian if they were required to obtain information from a particular journal or index and if a particular library did not have a copy of a journal or articles there were extensive co-operating libraries across the world. It may reasonably be concluded that all of the learned works and published studies referred to by Professor Musk, Professor Henderson and Dr Leigh were available to the defendant in the relevant period.

80 Mr Peter Russell worked for James Hardie between 1948 and 1970. His evidence was tendered in the form of a written statement. He was not cross-examined.

81 Mr Russell commenced employment with James Hardie as a laboratory assistant at the Camellia plant in 1948. In approximately 1959 he was promoted to factory superintendent at the insulation factory, where he was in charge of a labour force of approximately 120.

82 In 1961 Mr Russell became safety engineer and fire officer. He stayed in this position until 1964. During and before this period Mr Russell became increasingly aware of the dangers to health associated with asbestos exposure. During his time as safety officer, Mr Russell undertook research into the effects that asbestos had on those who were exposed to it by seeking out publications on the subject. The literature that Mr Russell read said that exposure to asbestos dust had a tendency toward cancer. The literature was starting to mention mesothelioma but the main emphasis was on asbestosis. The literature that Mr Russell read made it clear that some workers were affected with asbestosis after relatively minimal exposure to asbestos dust.

83 In the early 1960s Mr Russell became aware of a conference that was to be held in New York in relation to the dangers of asbestos. Mr Russell obtained a copy of the conference papers. The papers comprehensively

canvassed the asbestos problem, both in the industry and the environment. The gist of what was in the papers was that there was a worldwide serious concern about the dangers of exposure to asbestos and the welfare of people who had already been exposed.

84 Some time, in around 1963 or 1964, Mr Russell attended a production meeting where they were discussing dust problems within the factory. The meeting was chaired by the branch manager. Also present were the chief engineer, the company's chief medical officer Dr McCullagh, the personnel officer, the superintendent of the factory and a representative of the engineering side of the factory. Senior staff officers were present from the Camellia plant. Mr Russell raised the issue of the asbestos dust hazard for end-users of the product. He was concerned that people using asbestos products were relying on James Hardie in relation to their safety.

85 In mid 1963 at a production meeting it was proposed that James Hardie should extend wet processing to include all the treatment of fibre so that the asbestos would be wet from coming to the factory right through to the sheet coming off the machine. Before that, it had been dry treatment of fibre. Mr Russell said that it was necessary to consider that James Hardie did not store a wet product and did not sell a wet product. He said that considerable sawing of the product was done out in the field and that James Hardie should do some labelling of the product or make end-users aware of the problems with it. Mr Russell raised the fact that there were many people other than workers within the factory who were being exposed to asbestos dust from the product because they were selling a dry product that was to be sawed. Mr Russell urged a warning to the effect that James Hardie owed a moral responsibility, not only to the workers at Camellia, but also the end users of the product. Mr Russell urged that a written warning should be put on the product. He was conscious of builders who were using power saws to cut dry products. He had done some research and come to the meeting with a pie chart showing the number of people using the product outside of the factory. The chart indicated that the majority of users of the product were not aware of the problems associated with asbestos. Mr Russell referred to the moral responsibility of James Hardie because the people who were using the product regarded James Hardie as the major user and any approach James Hardie took to the asbestos problem affected the response of the users.

86 On one occasion Mr Russell had discussions with Harry Howorth, who was supervising building demonstration homes. Mr Russell asked Mr Howorth if he was aware of the problem of asbestos dust to end users

of the product. Mr Howorth suggested there was no problem because James Hardie sold special hand guillotines that did not produce a lot of dust. These guillotines, however, could only cut flat sheets.

87 Mr Russell did not see any studies done by anyone else at James Hardie. He was told that it was not a company problem, that it was the end users' problem, not James Hardie's. The company did not want to deal with it.

88 By 1964 Mr Russell had become distressed by his impotence to do anything about the asbestos problem at the Camellia plant. He decided to take leave to assess his situation. Before taking leave he prepared a detailed memorandum for distribution amongst senior company staff on a confidential basis. The memorandum outlined the development of knowledge concerning the health hazard of asbestos dust exposure. Mr Russell concluded with the observation that asbestos dust was one of the most dangerous of all industrial poisons and that his aim was not to cause alarm but to ensure that James Hardie fully appreciated the possibilities and gave the necessary priority to dust control work.

89 When Mr Russell returned from leave he took up a position as quality controller in the brake lining division. At some stage in the second half of the 1960s Mr Russell recalls reading papers published in various medical journals on the relationship between asbestos exposure and mesothelioma. One such paper was by Newhouse and Thompson published in the British Journal of Industrial Medicine in 1965. At about the same time Mr Russell became aware that it had been established in America that there was a clear link between asbestos exposure and mesothelioma.

90 Mr Russell resigned from his employment with James Hardie in 1970.

91 Mr Lawless was employed by James Hardie from 1973 to 1988 as an assistant occupational hygienist based at the defendant's factory in Welshpool, Western Australia. He was called by the defendant. Mr Lawless gave evidence that warnings went onto the defendant's products in the 1970s and that it ceased using asbestos in its products in the 1980s.

92 In cross-examination Mr Lawless gave evidence that there were a lot of asbestos cement products manufactured by James Hardie in the

community. They included products manufactured using crocidolite between 1955 and 1966. And between 1966 and 1984 amosite was used in the products. There were no warnings on the defendant's asbestos cement products until 1979.

93 Mr Lawless was aware of concerns expressed about the risk to end users of the product that was out in the community but without warning labels. Those concerns were that people would in an uncontrolled manner take to the James Hardie products to cut them in various ways, or to demolish them or to brush and sand them and that in doing those things they would release asbestos fibres into the breathing space.

94 There were discussions within James Hardie about how to communicate the risks of the use of the unlabelled product that was out in the community to the users or owners of those products. There were various discussions as to how James Hardie could get this information to people. There was a road show put together where they visited hardware stores and invited hardware store owners in to demonstrate the safe methods. There were all sorts of brochures distributed advising how to use the correct tools and equipment.

95 Before 1988 James Hardie used brochures to communicate the risks of using asbestos cement building materials in the home in such ways as cutting, demolishing or brushing and sanding. The brochures were displayed in hardware stores advertising the products and giving instructions as to how they were to be safely handled and used. Those advertisements did not appear in daily newspapers. James Hardie advertised their products for sale in daily newspapers.

96 The senior management of James Hardie was aware of concerns such as those expressed in a letter of 6 September 1983 from Alco Hardware Store operator to Dr McNulty, Commissioner of Public Health in Western Australia. The letter is Exhibit H82. The letter says that Alco had for many years distributed a range of asbestos products manufactured by James Hardie and referred to a recent television programme on Channel 2 that argued a direct connection between asbestos products and various forms of cancer contracted by people who were exposed either to the raw material or the end product for varying periods of time. The letter said that Alco was "concerned with any present or potential health risk to either our customers or staff" and sought advice:

"(a) Whether the range of asbestos products manufactured by James Hardie is in your opinion a health hazzard [sic] either to those handling or the end user.

(b) If in your opinion, they do constitute a health hazzard [sic], what action we should take with regard to the handling, warehousing and sale to the public."

97 Mr Lawless said that there was concern within James Hardie about the possibility of persons cutting, demolishing, brushing and sanding asbestos cement building products out in the community. The concerns were that they would use inappropriate methods to demolish a house or a wall. The standard practice in those days was to take a sledge hammer to it. The standard practice for trimming the top off a Super Six fence was to take a brush grinder to it. James Hardie believed at that time that using a brush grinder was totally inappropriate and if the safe working methods that James Hardie proposed were used the exposure to people would be minimal. The concern was that the cutting or demolishing or the brushing and sanding would release asbestos fibres and be inhaled and that could cause mesothelioma or some asbestos-related disease, particularly in tradesmen who were doing it all the time.

98 Answers to interrogatories of the plaintiff for the examination of the defendant are in evidence as Exhibit H117. In its answers to interrogatories 3, 4, 5, 6 and 7 the defendant says that throughout the period from 1978 to approximately September 1990 the defendant was aware that home handymen might use its asbestos cement products and that cutting asbestos cement products could release asbestos fibres or dust into the atmosphere which could be inhaled. In answer to interrogatory 11 the defendant said that it first became alerted during the mid-1940s to the suggestion that the inhalation of asbestos fibres could cause asbestosis but only in circumstances involving the inhalation over a sufficiently lengthy period of time of considerable quantities of asbestos fibres in visible clouds of dust emanating from the handling of raw asbestos in a factory manufacturing asbestos-containing products. The defendant says that it first became aware in the mid-1960s that the inhalation of asbestos fibres could cause mesothelioma but only in circumstances involving the inhalation over a period of time of quantities of asbestos fibres contained in visible clouds of dust emanating from the handling of raw asbestos in a factory manufacturing asbestos-containing products.

99 In answer to interrogatory 73 the defendant admitted that it probably saw extracts from a book entitled "Asbestos Work as a Health Hazard" published by the ABC at about the time it was published in 1978. Chapter 5 of the book is entitled "Asbestos and the Consumer". At p 95 the Executive Officer of the Australian Consumers Association, Mr Ettinger, was asked:

"How serious a problem do you think it is, though? Something like an asbestos stove mat or asbestos cement sheets for building? How much of a risk do you think there is?"

"Well, they're not dangerous unless the fibres are released, so that in a stove mat they might not be for quite some time - but why wait till they are? In using building materials there are many more dangers and of course a lot of people do handyman work around the home and they don't know, for example, that they shouldn't use power tools on them. They don't know that it should be damp. They don't necessarily know that they should vacuum up all the dust before they keep going."

Mr Ettinger was then asked what he suggested were practical precautions to be taken with things like asbestos cement sheets or brake linings. He said:

"They probably are necessary in some applications and they are probably cheaper than other substitute products so in using them we feel that asbestos should be kept damp, that people should work outside and up-wind where possible. They should use hand tools instead of power tools and that definitely they should clear up the dust very quickly if they have any around when they're cutting them."

Available literature and constructive knowledge of dangers to health consequential upon exposure to asbestos

100 The plaintiff submits that if the defendant wanted to find out more about the likely hazards posed by exposure to its products, the evidence provided by expert witnesses demonstrate that an extremely large amount of literature concerning the occupational and environmental health hazards of exposure to asbestos dust was available upon enquiry in Australia up to and including the early 1980s and there was a massive amount of literature available upon enquiry concerning the occupational and environmental health hazards of exposure to asbestos dust by 1990.

101 In the course of the trial the plaintiff tendered a vast amount of material which counsel submitted showed what the defendant knew and could have known about the risk from asbestos exposure to persons in the class to which the plaintiff belonged. The material includes seven lever arch files of documents from the defendant's discovery and a further five lever arch files of available literature and other literature references.

102 It is not practicable to review all of that material in these reasons for decision. In appendices to the plaintiff's written closing submissions the plaintiff summarised documents from the defendant's discovery demonstrating actual knowledge or awareness of asbestos-related disease, relevant media publications contained within the defendant's discovery and extracts from medical or scientific literature available to the defendant upon enquiry. I have considered those materials but once again it is not practicable to review all of them in these reasons for decision. The medical experts I have referred to summarised the effect of medical or scientific literature and I will not refer to any particular publications. I will refer to some of the material from the defendant's discovery that is of particular significance.

103 The plaintiff submits that documents contained within the defendant's discovery demonstrate that the defendant knew that asbestosis, lung cancer and mesothelioma could result from brief and transient and low dose asbestos exposure that was non-occupational in character such as exposures related to handyman work on asbestos cement building products. I will refer to some of those materials that are of particular significance or which were identified by the plaintiff as being of particular significance.

104 Exhibit P148 is a James Hardie inter-house letter of 15 February 1966 from J B Reid, the chairman of James Hardie, to Mr Pysden, the personnel manager. The letter attaches a copy of an article given to Mr Reid by Mr Walker, managing director of Goliath Portland Cement Ltd, Tasmania. Mr Reid says that Mr Walker, "is concerned about this sort of information getting around Australia". The article is written by Dr Alfred Byrne who is described as the newspaper's medical correspondent. The author writes:

"A disquieting 'new' occupational disease capable of killing not only the exposed workman but also perhaps his womenfolk and even people living near his place of work is the subject of intensive behind-the-scenes activity by British scientists,

experts on industrial health and representatives of at least two Government Ministries."

The disease referred to is mesothelioma. Mr Reid concluded his letter by stating that he had promised to let Mr Walker have information on the recommended treatment against asbestosis and asked Mr Pysden for whatever information was available on this.

105 Exhibit P149 is a letter from Mr Pysden, personnel manager, to Mr Reid of 16 February 1966 and appears to be in response to Mr Reid's inter-house letter that is Exhibit P148. In his letter Mr Pysden says:

"The mining and processing of nearly all minerals creates a dust hazard and a health problem. The article is not new - it is merely one of many reports on world studies which have been conducted since 1935 when the association between exposure to dust and carcinoma of the lung, mesothelioma of the pleura, tumour of the bladder and uterus and other fatal complaints, was first recognised. The nucleus is dust particles - fibre. Four types of asbestos - chrysotile, amosite, crocidolite and anthophylite - have similar effects on the body and it has not been possible to establish that one is more pathogenic than the others. There is no cure for Asbestosis."

Mr Pysden went on to say that the only preventive action is to eliminate the presence of dust. Mr Pysden warned that moving employees around between "dusty" and "clean" jobs was not necessarily effective because some people seem to be affected more readily than others although the reason had not yet been discovered.

106 Exhibit P152 is a document dated 29 March 1966 signed by Dr S F McCullagh, and entitled "Notes and Comment, Biological Effects of Asbestosis, Annals of the New York Academy of Sciences, Volume 132, pages 1 - 766, 31 December 65". Dr McCullagh's letter head describes his practice as industrial and preventive medicine. He later became James Hardie's chief medical officer and was titled the company's Federal Medical Officer. Dr McCullagh writes that in the US the accepted safe upper limit is 5 million particles per cubic foot while the British adopt a rather lower level expressed as 4 fibres per millilitre. However, in both the US and the UK it is said that there is no safe upper limit, that all fibre and any fibre is dangerous. In the UK there is reason to believe that in some plants dust is now so well controlled that it no longer is any danger - though it would be years before it can be established that this is so. Dr McCullagh noted that it seems that once a

sufficient exposure has occurred it is simply a matter of time before asbestosis develops, one is concerned with time from first exposure rather than with the duration of the exposure, but he could find no certain information as to what is a sufficient exposure. Dr McCullagh said it was fair to say that asbestos fibre is generally held to be associated with and probably the cause of two forms of cancer, bronchogenic carcinoma and mesothelioma. Dr McCullagh noted that it was suggested that even a brief and slight exposure may result in mesothelioma. Dr McCullagh noted that it was suggested that the increasing use of asbestos products, with their slow disintegration and the release of "indestructible" asbestos fibres, was leading to a dangerous pollution of the urban atmosphere throughout the world.

107 Exhibit P555 is a James Hardie inter-house letter of 21 April 1966 from F A Page, to Mr N E Gilbert. Mr Page was chief engineer and a director of James Hardie. Mr Gilbert was the manager of Camellia, James Hardie's largest plant. Mr Page says: "It is not possible nor is it, I feel desirable, to try and define a safe concentration. All dust is harmful so that we must regard the best we can do as still inadequate". It can be seen from the letter that Mr Page is concerned with the conditions at the defendant's factory at Camellia.

108 Exhibit P162 is a memorandum of 22 June 1966 from Mr Pysden, to H C Sadgrove of the defendant's Penrose factory in New Zealand. Mr Pysden stated the company's belief that the only way to control dust is to engineer it out of existence. In the meantime, Mr Pysden said, all potential sources of dust should be spotted and suitable action taken to get the dust out of the atmosphere. Mr Pysden referred to the classical case of an English woman whose only contact with dust was brushing her husband's clothes when he came home from work.

109 Exhibit P2619 is a letter of 14 September 1966 from E M Rathus, director of industrial medicine, to the works manager of James Hardie. The author says: "It is quite invidious to say more than that the asbestos industry has posed a great problem in all countries for many years and that only absolute enclosure of dusty processes would be really effective". This letter is about employees of James Hardie working in dusty situations who had abnormal appearances on X-rays.

110 Exhibit P2622 is a letter of 31 May 1967 from E M Rathus to the James Hardie factory manager. The author states: "My reading of modern literature suggests that the obstacles can be overcome, and I hope your firm is successful in its design problems ... it is indeed a great pity

that men will not heed the advice to use the masks provided". Again, the author is referring to employees at the defendant's factory.

111 Exhibit P74 is an extract from notes taken from the factory managers' conference 19 - 23 June 1967 p 35. The notes are concerned with dust control in factories and medical supervision of employees. It is noted that recent research has established a relationship between contact with asbestos and mesothelioma and lung cancer. It is noted: "Incidence of mesothelioma is very low but newspaper publicity can build it up to such an extent that it could cause the imposition of very severe regulations by the various State Health Departments and resistance to use of products containing asbestos".

112 Exhibit P1255 is a letter of 18 December 1967 from the branch works manager of the Brisbane office of Wunderlich Ltd to the finance director. The author states that there is apparently growing evidence to suggest that the hazard presented by asbestos is not confined to employees only, but may possibly be present for employees' families, local residents and even for the user of the product. Three articles in the British Medical Journal are cited as authority for that proposition.

113 Exhibit P598 is a copy of a publication entitled "Hygiene Standards for Chrysotile Asbestos Dust" from the Committee on Hygiene Standards of the British Occupational Hygiene Society published in 1968. It was a publication received by the defendant. The publication commences with the following summary and recommendations:

"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."

The committee stated that as long as there is an appreciable amount of dust in the air, it recognised that there may be some risk to health. On p 11, under the heading "Cancer" it is stated that it is generally recognised that there is significant risk of lung cancer associated with asbestosis and

a risk of mesothelioma exists in connection with the inhalation of crocidolite dust in particular. The committee states:

"There can be little doubt that these risks will be least in the lowest concentration ... 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."

114 Exhibit P893 is a letter of 12 September 1968 from an English asbestos cement company, Turners Asbestos Cement Co Ltd, to Mr Page. The letter attached two tables analysing the results of dust count tests on building sites and in customers' workshops. The letter states: "The tests show the seriousness of the handling and cutting problem with low density high fibre content materials in comparison with the position of corrugated sheeting. The cutting of fully compressed materials with abrasive wheels can also present problems".

115 Mr Page replied by letter of 2 October 1968 (Exhibit P230). Mr Page remarked that he was perturbed at the practice in Australia of mitring the corners of corrugated sheeting with an abrasive cut wheel disc rather than a handsaw. That must be a reference to the practice of end-users of the product, whether by people doing so in the course of their occupation, such as carpenters, or home handymen.

116 Exhibit P1873 is a memorandum of 28 October 1968 from Mr Page attaching a draft reply to the acting engineering chief at the General Post Office, Wellington. In the memorandum Mr Page commented: "This is one of those ticklish queries where one can't deny that a hazard exists so that the problem becomes one of keeping it in perspective". In the draft letter Mr Page stated that the inhalation of finely divided asbestos dust over a period of time can cause asbestosis. The letter refers to post office conduit and similar articles manufactured from asbestos cement and states that whether the dust liberated during the cutting and machining of asbestos cement products is clinically harmful is not proven but it certainly cannot be beneficial. The draft letter states that the industry point of view is that it should be regarded as harmful and that control measures should be adopted. Mr Page comments that "our experience has been that respirators are useful only for intermittent work and should only be regarded as temporary expedients".

117 Exhibit P1864 is a James Hardie inter-house letter of 28 January 1969 from P G Elley to head office at Camellia. Attached to the memorandum is a letter from Mr Elley to the manager of Channel 9 in preparation for a news interview. The letter states:

"... the inhalation of substantial quantities of asbestos dust does present a serious health risk. This has been recognised for some years as an occupational hazard to people handling asbestos fibre in the mining and manufacturing industries. The handling and use of asbestos containing products does not expose the general public to it. Only in extremely rare cases has there been any suggestion that incidental exposure to asbestos dust has been harmful."

"Despite intensive general investigations into the health hazard of exposure to asbestos dust there is no known risk to the general public for example, from asbestos containing materials in buildings, or asbestos in domestic appliances such as stove mats or ironing boards or from dust produced by the wear of brake linings."

118 Exhibit P262 is a letter of 18 June 1969 from Dr McCullagh to Mr Palfreyman. Dr McCullagh says that asbestosis is a condition that develops very slowly and hence the older a man is when he enters the industry the less likely he is to develop asbestosis and it is therefore desirable where practicable for older men to be employed in areas where dust occurs to any degree.

119 A similar point is made in Exhibit P277, a letter of 1 December 1969 from Dr McCullagh to James Hardie head office.

120 Exhibit P899 is a James Hardie inter-house letter of 9 December 1971 from N Wildsmith to Dr McCullagh. The author states:

"We agree with your suggestion concerning the time a Roof Fixer would spend cutting Mitres i.e., approximately 7 hours per week. However, it is not considered to be a major hazard because the handsaw cut into the edge of the sheet is very small and the longer mitre cut is made with Asbestos Cement Cutters. Dust from the drilling of holes is a greater hazard because of the fine deposit left on the surface of the sheet. It is necessary either to brush or blow the dust to remove it. However, because

of the location of the work i.e., out in the open air usually well off the ground so giving almost continuous airflow, the dust is very quickly removed from the work area. ... On repairs to old Asbestos Cement Sheets it is often necessary to use one or other of [fibrelog and diamond wheels] because of the age of the sheets and this causes a dust problem. Another hazard is created when trimming of Bullnose Sheets is necessary after erection. This is required to eliminate a stepped effect from one sheet to another. (Action is being taken to correct this fault by modifications to the method of moulding). When trimming these sheets the machine is held close to the operator's face and because of the fine dust it is compulsory for an operator to wear a respirator. However, it is known that when the supervisor is not present there is a tendency not to use the respirator. It is very difficult to get a reliable estimate of the time and employees exposed to a dust hazard because weather conditions, the type of job, what tools the Fixer uses etc., all combine to vary the conditions from job to job."

121 Exhibit P898 is a letter of 29 March 1972 from Dr McCullagh about the exposure of roof fixers. Dr McCullagh says that any exposure of roof fixers should be minimised. He recommends rotating the job of cutting among the members of the roof fixing teams. Dr McCullagh said that independent roof fixing contractors should also be advised to adopt this practice, though they should be reassured that even where it is not adopted it is believed that the time weighted average exposure does not exceed the 4 fcm3 recommended both by James Hardie and the Australian National Health and Medical Research Council.

122 Exhibit P2135 is a James Hardie inter-house letter of 19 July 1972 from Dr McCullagh to the factory manager. Dr McCullagh said that it was not then the company's intention to issue advisory literature or to place warning labels on the cartons of its products but rather to await the Model Regulations of the National Health and Medical Research Council.

123 Exhibit P916 is a confidential report of 15 September 1972 by Dr McCullagh to Mr Palfreyman, who was then the personnel director, on the present position of medical and hygiene services at James Hardie. The report is primarily concerned with asbestos exposure in the workplace. However, at p 6 Dr McCullagh says:

"Attention is increasingly turning from mining, milling and manufacture to the exposures encountered by those who use

asbestos products ... Both the Royal Navy and Australian Navy are progressively eliminating asbestos from their ships ... As to the use of products such as are made by James Hardie it is to be noted that the U.S. Federal Register of 07 June 72 now requires that all 'power operated and hand held tools' have exhaust ventilation and dust collection equipment fitted to them. Such provisions could well make the use of asbestos building products so cumbersome and expensive as to incline the users to turn to alternative materials. The precautions required seem grossly excessive when it is considered that there is no established case of asbestosis of the lung among men who have spent their lives in their trade working with asbestos building products. The introduction of power tools has undoubtedly increased the exposures of these men over recent years but since these were commonly in use in the United States 20 years ago and in the U.K. and Australia some 15 years ago and since there are still no reports of pulmonary asbestosis occurring among carpenters and others it begins to seem unlikely that they have, in fact, materially altered the situation. While it remains true that no case of pulmonary asbestosis in such a man has yet been established and only one case reported and that very unsatisfactorily, there has been a recent report that there is an incidence of pleural change among such people attributable to asbestos exposure. Until recently one would have said that this was of no consequence but there have also been recent reports that such pleural changes are related to an increase of malignant disease attributable to asbestos exposure - this latter claim it should be noted, is not yet proven and faces a considerable body of evidence which argues that there is no such association."

124 Exhibit P642 is a James Hardie inter-house letter of 5 July 1974 from Mr Palfreyman to State managers circulating observations and comments on an article entitled "Blue Asbestos: Is this Killer in Your House?" written by Tim Hall and published in the Bulletin on 6 July 1974. The observations and comments include:

"5. Mr Hall's allegation that the danger may be in the building industry to those engaged in demolition of houses and flats is irresponsible in its implication so far as the use of asbestos cement building materials is concerned. Since the first use of asbestos cement sheets in Australia early this century many millions of sheets have been used in all types of buildings throughout the

Commonwealth: there is no evidence that the public, including handymen and those engaged in the building trade, have been affected by the handling of these products. It has pointed out that in asbestos cement the fibres are 'locked in' the final product by the cement bond. There is admittedly danger in demolition work where asbestos has been used in the form of limpet spraying. James Hardie and Coy. Pty. Ltd. is not engaged in this business."

125 Exhibit P2230 includes a letter of 12 September 1974 from F Heyworth, a physician with the Occupational Health Division of the Western Australian Department of Public Health, to fencing contractors. The letter says:

"Concern has been expressed about the health of people handling asbestos at work. Normal handling of asbestos cement products is not a health hazard but cutting operations, as in cutting asbestos cement sheets, gives rise to dust which may be a health hazard. The Department has tried to get into touch with fencing contractors at work to assess the degree of health hazard and to advise how it may be minimised but has not, so far, been successful."

126 Exhibit B2310 is an inter-house letter of 1 October 1974 from Dr McCullagh to Head Office, Personnel Director, in relation to proposed asbestos regulations in New Zealand. Dr McCullagh says that the defendant "must consider not only the factory situation but the construction site situation with which I am much less well acquainted".

127 Exhibit P1764 is a James Hardie inter-house letter of 12 November 1974 from R V Bolton, manager community relations, to Mr Page, who was then deputy chairman of James Hardie, concerning a forthcoming Four Corners programme dealing with asbestos dust. In the letter Mr Bolton says that Dr McCullagh appears on the programme and "reassures the interviewer that the householder is not at risk by having asbestos cement sheets in or around his home". It is said that other items likely to be touched upon in the programme include "the special risks found in demolition and insulation work and shipyards".

128 Exhibit P1265 is a James Hardie inter-house letter of 26 July 1976 from Mr Palfreyman who was then general manager, growth and development, to the general manager, research and engineering. The

subject of the letter is "Construction Site Use of Power Tools - Asbestos Cement Products". The letter starts by referring to recent publicity in New Zealand "given to health risks associated with asbestos in the call by the Carpenters' Union for a ban on its use". The letter then refers to:

"... the immediate serious situation which arose to disrupt the use of Fibrolight Building Products was the action taken by the Auckland Branch of the Carpenters' Union in banning power cutting on three major jobs because of the dust created. Respirator protection was claimed to be inadequate and in any case uncomfortable to use, not always available, and not maintained properly. It is stated that the main problem areas are when cutting corrugated, thick sheets, and, to some degree panels. About 25% to 30% of sales fall in these categories."

129 The letter goes on to refer to experiments carried out by James Hardie using power cutting machines with attachments to produce and control the flow of water over the cutting blade and to recommend methods for cutting various products. The letter says that "there is an urgent need to provide answers to the dust problem associated with the power cutting, drilling and shaping of our products by the end user field".

130 Exhibit P2366 is a memorandum of 26 May 1976 from A A Parts to Mr P A Elkington about asbestos cement sheet cutting dust. The memorandum says that:

"... yesterday three short A.C. [Asbestos Cement] Sheet cutting trials had been carried out. Breathing zone samples were taken during three cutting periods ... These tests were carried out in the open air ... the exposure to airborne asbestos is specified in terms of 8 hour time weighted average and is then a maximum of 4 fibres/ml in N.S.W."

"These results show that about a quarter of an hour of sawing A.C. sheet is all that could be allowed in a day in well ventilated surroundings, such as were used in these trials."

Counsel for the plaintiff submitted that this shows that at the time the defendant realised that the permissible standard, that is permitting someone to be exposed at 4 fibres/ml over an eight hour time weighted average, could be exceeded by as little as 15 minutes of cutting.

131 Exhibit B2307 is a confidential James Hardie inter-house letter of 14 October 1976 from Dr McCullagh to the New Zealand general manager concerning New Zealand asbestos regulations. Dr McCullagh says that James Hardie should not seek to have Hardiflex removed from the ambit of the regulations and that the authorities will quite properly be concerned with the airborne asbestos levels to which people are exposed. Dr McCullagh says that reg 3 would appear to apply the regulations not only to the tradesmen but also to the home handyman and reg 5(3) requires "suitable warning" to be given. Dr McCullagh says that as "far as the home handyman is concerned exposures, in the absence of crocidolite, one would expect to be such as to render any warning unnecessary". Dr McCullagh went on to say that if we are to label potentially dangerous substances then "we will label every bottle of grog with a warning as to alcoholism and chirrosis [sic] of the liver and every packet of sugar and most dairy products with a warning of the dangers of coronary heart disease". Dr McCullagh said that a company committee was then studying the saws that will generate least dust in cutting James Hardie product and, particularly, the problem of cutting super six across the ridges. Dr McCullagh indicates that caution should be advanced in relation to issuing warnings on asbestos products and says: "I would resist any attempt to have our products labelled with any warning".

132 Exhibit P2175 is a report by Mr Palfreyman of a visit by he and Mr Winters to Canberra on 22 August 1977 to discuss the safe use of asbestos with the Master Builders Association, ACT Health Department and discussions on an ACT building site on which union representatives had insisted that men working with asbestos cement material, irrespective of the type of tools being used and whether or not dust was being created, be provided with safety equipment and be paid an allowance for doing so. The report refers to a Technical Directive issued by the Commonwealth Department of Construction in March 1977 setting out work procedures for the safe use of asbestos. The report refers to a clause in the Directive which said that asbestos cement boards, sheets and pipes can be handled without producing hazardous dust, but dust will arise when the materials are cut or drilled. The Directive refers to safety devices being fitted on power tools and says that the use of power tools without such exhaust ventilation will produce harmful concentrations of dust and in those cases respiratory protection equipment shall be used and the work area shall be isolated. The Directive says that the cutting or drilling of asbestos cement by hand-operated saws or drills for short periods, say after 15 minutes, will not generally produce harmful dust concentrations in well-ventilated areas.

133 Exhibit P1103 is an internal Hardie's memorandum of 24 May 1978 entitled "Standard Wording Proposed for Use in all Hardie's Building Products Publications which include Instructions for Working and Fixing". The wording includes under the heading "Caution": " ... Asbestos dust can damage health but this is unlikely when cutting or fixing asbestos cement sheets since only a small percentage of dust is asbestos. As a precaution, however, you should keep dust levels down by following these simple safety rules". The document then sets out rules including working in a well ventilated space, using hand tools designed for cutting asbestos cement sheets or an old handsaw, if cutting by power saw use one which has a dust suppression attachment, avoid drilling overhead and damp down dust.

134 Exhibit P439 is an exchange of correspondence between Dr McCullagh and Dr Vianna and Adele Polan who had published an article in the Lancet of 2 September 1978. In their reply to Dr McCullagh, Vianna and Polan say that there have been 37 case reports suggesting an association between non-occupational asbestos exposure and malignant mesothelioma.

135 Exhibit 1166 is a revised health booklet of 16 October 1978 published by James Hardie. At p 13 is a section entitled "What about Tradesmen and Handymen?" The booklet says:

"Most of the asbestos used in Australia is for the manufacture of asbestos cement building products and these present practically no risk to tradesmen or handymen if simple precautions are taken to keep dust down. ... When dry-cutting asbestos cement sheets, tradesmen or handymen are advised to work in the open air or in well ventilated spaces. Hand tools such as a fibro cutter, score and snap knife or saw should be used wherever possible. Dust extraction or wet cutting equipment is available for power tools such as circular saws and should be used where exposure to high dust levels would be involved."

136 Exhibit P1148 is a James Hardie memorandum of 19 October 1979 concerning "agitation" by various groups for the abolition of the use of asbestos in any form. The report refers to a number of unions and the Workers' Health Resources group and says that these groups "have the attitude that there is no safe level of exposure to Asbestos dust".

137 Exhibit P1483 is a handwritten note indicating that the attached report entitled "Criteria Document for Swedish Occupational Standards:

Asbestos and Inorganic Fibers" by William J Nicholson had been circulated at James Hardie in or about April 1982. The report is a lengthy one. Four conclusions are set out on p 75. The first is to the effect that three studies indicated that "excess mortality" may result from exposures as low as 0.5 f/ml for a working lifetime which was below the then current national standards. The second conclusion is that no data existed in any study that would indicate a threshold below which there is no risk for asbestos cancers. The third conclusion is that all fibre types carry significant cancer risk, although differences in exposure may result in variations in the distribution of types of neoplasms. The fourth conclusion is that exposure control to the lowest level possible is required not only for the usual asbestos worker trades, but for the vastly larger number of exposure circumstances associated with the use of asbestos products or their maintenance and repair.

138 In his written submissions counsel for the plaintiff submitted, and I accept, that the defendant had known from the 1950s that asbestos inhalation was dangerous and that fibre released from its products could cause respiratory illness. The defendant knew that product purchasers should be warned of such risks by the mid-1970s. That submission is established by the evidence.

139 The evidence of Mr Russell and Mr Lawless shows that senior managers within the defendant were aware of medical and scientific literature to the effect that small doses of asbestos could lead to mesothelioma and respirable fibres could be released from the sort of handyman activities the plaintiff engaged in. That conclusion is confirmed by the documents discovered by the defendant to which I have referred. Senior managers within the defendant were aware of medical and scientific literature as well as popular literature that said that even low-dose exposure could lead to mesothelioma or other lung diseases and that handymen or non-occupational users of the asbestos cement products might inhale respirable asbestos fibres in the course of activities such as cutting or drilling the products.

140 The defendant knew that a brief and slight exposure to asbestos dust might result in mesothelioma. There was no known safe level of exposure below which there was no risk of mesothelioma. The defendant knew that there was concern amongst various people, including public health authorities, and unions, about the hazards of asbestos to people cutting or drilling asbestos in the course of using asbestos products. The defendant

knew that even sawing asbestos cement products for a quarter of an hour could reach or exceed the permitted standard for asbestos exposure in a day. The defendant knew that handymen drilling or cutting asbestos should take precautions to keep dust levels down.

141 The defendant knew that asbestos exposure could cause mesothelioma. The defendant knew that cutting or demolishing or brushing or sanding asbestos cement products would release asbestos fibres into the air and be inhaled and could cause mesothelioma. The defendant knew that handymen used asbestos cement products and that cutting them releases fibres into the atmosphere that could be inhaled. The defendant knew that many of the users of asbestos cement products were not aware of the risk of mesothelioma or cancer from inhaling asbestos dust as a result of using asbestos cement products.

What the defendant would have learnt upon enquiry

142 In his written submissions counsel for the plaintiff submitted that upon inquiry in the early 1980s a product manufacturer should have ascertained the following information:

1. Asbestos dust is dangerous to health and may cause asbestosis, lung cancer or mesothelioma;

3. The health risks associated with asbestos are extremely serious, and in the case of mesothelioma, invariably fatal.

4. There is a dose-response relationship between asbestos and likelihood of injury.

5. Cutting, sanding, drilling and demolishing its products released respirable asbestos fibre.

I accept that submission. It is established by the evidence.

143 I find that in 1983 it was reasonably foreseeable to a person in the position of the defendant that a home handyman or other casual user of asbestos cement building products would suffer mesothelioma as a result of inhaling asbestos dust released from the asbestos cement products by the home handyman or casual user cutting, sanding, drilling or demolishing the asbestos cement products.

144 Dr Leigh referred to the well known 1969 text, Hunter's "The Diseases of Occupations" in which it was said that it was known that inhalation of dust from such activities as sawing or sanding material containing asbestos presents the hazard of malignant mesothelioma outside as well inside industrial situations. Dr Leigh said that in 1974 the first major report of the UK mesothelioma register described several cases of mesothelioma following hobby exposure incurred when sawing asbestos sheets and drew attention to the possibility of mesothelioma occurring at low dose and that Anderson and others had drawn attention to the risk of asbestos-related disease including mesothelioma from household contact. Dr Leigh opined that the defendant ought to have foreseen the risks of handyman exposure from 1983 onwards.

145 Professor Henderson said in his report, that the risk to health from inhalation of asbestos fibres - including non-occupational "handyman-type" domestic, neighbourhood and environmental exposures to asbestos - and especially in relation to the induction of malignant mesothelioma, had been well established in the scientific literature well before the late 1980s and early 1990s and that by that time it was well recognised that mesothelioma could follow asbestos exposures that were apparently brief, transient and low-dose (minimal). The defendant did not cross-examine Professor Henderson about those opinions, which I accept. Professor Henderson referred to "well before the late 1980s and early 1990s". In my opinion, Professor Henderson was specifically addressing the dates on which he had been informed the plaintiff had experienced the "handyman" exposure, that is 1983, 1985 and 1990, and was referring to the state of knowledge "well before" those times.

146 Professor Musk said that 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.

147 I accept the opinion of Professor Musk that well before 1983 a reasonable product supplier had means of being aware of the necessity to minimise the risk of inhalation of asbestos and to warn of the potential dangers.

148 I find that in 1983 it was reasonably foreseeable to a person in the position of the defendant that if the plaintiff, or a person who casually, intermittently or from time to time cut, sawed, sanded or drilled the defendant's asbestos cement products, was not warned of the dangers of doing so and of the preventive measures that should be taken in

undertaking such activities, then that person would suffer mesothelioma or some asbestos-related disease.

149 The harm which the plaintiff suffered, that is mesothelioma, was a reasonably foreseeable result of the defendant's failure to take reasonable care to avoid injury being suffered by the plaintiff, or the class of persons to which he belonged, from using the defendant's asbestos cement building products by cutting, sawing, drilling, brushing and scraping them.

150 Manufacturers owe a duty of care to take reasonable care to prevent foreseeable injury being caused to the ultimate recipients or users of products: Donoghue v Stevenson (supra) per Lord Atkin at 599.

151 The asbestos cement products manufactured and supplied by the defendant were sawed, sanded and drilled by the plaintiff. That was a normal use of the products that should have been, and was, contemplated by the defendant.

152 I find that the defendant owed a duty of care to the plaintiff as a member of the class of persons who cut, saw, sand or drill the defendant's asbestos cement products occasionally, intermittently or from time to time. The important question is to determine the scope of the duty of care owed by the defendant to the plaintiff as one of the class of persons who could be reasonably foreseen to use the product in the manner I have described.

153 In Thompson v Johnson & Johnson Pty Ltd [1991] VicRp 84; [1991] 2 VR 449 the plaintiff sued the defendants who were manufacturers and distributors of a particular brand of tampon manufactured in New Zealand and purchased by the plaintiff in Australia and used by her soon thereafter alleging negligence resulting in personal injuries to her in the form of toxic shock syndrome. The Appeal Division of the Supreme Court of Victoria constituted by Murphy, O'Bryan and McDonald JJ said at 488:

"The threshold question in considering the matter is to determine the scope of the duty of care owed by the respondents as distributors and manufacturers of Carefree Super tampons used by the appellant being one of the class of persons who could be reasonably foreseen to be purchasers and users of that product.

That a duty of care was owed by the respondents to the appellant was not disputed by the respondents. The tampons used by the appellant and manufactured by the second respondent and distributed by it to the first respondent and by it in turn to the public for purchase by that section of them using the same was of a nature, kind and composition as designed and intended. It was not part of the appellant's case that it suffered from any defect or fault brought about in its preparation or distribution as to give rise to consideration of that type of duty of care as was considered, for example, in Donoghue v. Stevenson [1932] A.C. 562 and Grant v. Australian Knitting Mills Ltd [1936] A.C. 85.

However, where the manufacturer and/or distributor of the product ought reasonably to have foreseen that there was a risk of injury, which was not far-fetched, in the sense referred to by Lord Reid in The Wagon Mound (No 2) [1966] UKPC 1; [1967] A.C. 617 at pp. 643-4 and by Mason J., as he then was, in Wyong Shire Council v. Shirt [1980] HCA 12; (1980) 146 C.L.R. 40 at pp. 46-7, there exists a relationship between the respondents and the appellant as a member of the class of persons likely to purchase and use the products so manufactured and distributed which gave rise to a duty of care by the respondents to the appellant.

The question is 'what is the scope of that duty of care?' Is it to take reasonable care to avoid injury to the appellant from her use or continued use of the product? If such is the duty then in determining whether the respondents were in breach of that duty it is necessary to evaluate the magnitude of that risk and all other relevant circumstances and matters in order to determine whether the respondents' response to the risk was reasonable or whether it was such as to constitute a breach of the duty owed: See Wyong Shire Council v. Shirt, at p. 47. If, however, as was contended for on behalf of the appellant the scope of the duty was to warn the appellant as being a member of the class of persons to whom the duty was owed, of the risk involved in using or continuing to use Carefree Super tampons then, putting aside any question of causation in the event of a breach of that duty, the appellant would be entitled to succeed."

154 The Full Court then reviewed a number of cases concerning the question of the duty of care owed by the manufacturer and distributor of a product, the content of that duty and what was required to discharge it.

The Court concluded that it was a question of fact in each case whether the duty owed had been breached. The manufacturer must act reasonably in placing its product on the market and the almost infinite variety of circumstances forbade any categorical exegesis of the manner of performance of the relevant duty of reasonable care. At 490 - 491 their Honours said:

"Accordingly the duty of care cannot be categorised in the circumstances of such a case as this as being merely a duty to warn or alternatively to withdraw the product from the market. A duty is a duty to take reasonable care in the Donoghue v. Stevenson sense to avoid injury or harm being suffered by those using the product as intended. In some circumstances a discharge of such duty of care might require and demand that the product be withdrawn from the market so as to prevent it being used. In other circumstances in order to discharge the duty it might be necessary to give adequate warning as to the risks involved in its use. It does not follow that the failure to warn with respect to those risks will necessarily constitute a breach of duty. In each case it will be necessary for the tribunal of fact to determine whether in all the circumstances those marketing the goods failed to take reasonable care and whether that failure was a cause of injury suffered by the user."

155 Their Honours held that in determining the existence and nature of any duty of care on the part of the defendants, regard must be had, amongst other things, to the knowledge possessed and the circumstances which existed in Australia and New Zealand in 1980 of the nature and extent of risk then thought to have arisen, the economic and other costs involved in addressing that risk as well as the practical difficulties in doing so, and the seriousness of the potential circumstances. The Court concluded that the evidence did not allow a finding to be made that the defendants were, in failing to warn by placing notices on packaging or by advertising, in breach of the duty of care owed by them to consumers of their products. The evidence did not allow a finding that if such steps were taken the plaintiff might have become aware of the existence of the possible risk.

156 In determining the scope of the duty of care owed by the defendant in this case it is necessary to consider what a reasonable person in the position of the defendant would have done to respond to the foreseeable risk of injury to the class of persons to which the plaintiff belonged between the late 1970s and 1990. The duty is a duty to take reasonable

care to avoid injury being suffered by those using the product as intended or in a normal or usual way. That includes cutting, sawing, drilling, brushing and scraping the asbestos cement building products.

157 I have found that the defendant owed a duty of care to the plaintiff. The duty is a duty to take reasonable care to avoid injury being suffered by those using the product as intended or in a way in which the product was normally used. The Court must determine as a matter of fact whether in all the circumstances the defendant failed to take reasonable care and whether that failure was a cause of injury suffered by the user: Thompson v Johnson & Johnson (supra).

158 The asbestos cement products of the defendant which gave rise to the plaintiff's exposure to asbestos dust were supplied, and it is to be inferred, supplied by the defendant in the late 1970s.

159 By that time the defendant knew that the inhalation of a small amount of asbestos dust could cause mesothelioma. The defendant knew that tradesmen or handymen cutting, sawing, sanding or drilling asbestos cement products should take precautions to keep dust down and minimise the chance of suffering mesothelioma as a result of asbestos dust inhalation. The defendant knew that the consequences of contracting mesothelioma are extreme - a painful death is the inevitable outcome. The defendant knew that a handyman or other casual end user might not know any of those things or even that the asbestos cement products they were cutting, sawing, sanding or drilling contained asbestos. Alternatively, I find that the defendant ought to have known each of those things and would have learnt those things upon making enquiry because they were known to relevant experts and could be ascertained from consulting relevant experts or relevant literature and publications available to the defendant.

160 In those circumstances the defendant's duty to take reasonable care to avoid injury being suffered by handymen and other end users of its products involved taking reasonable steps to warn those persons that the products contained asbestos, of the potential health hazards of asbestos exposure and of preventive steps to minimise the risk of injury when cutting, sawing, sanding or drilling asbestos.

161 The defendant says that it discharged its duty of care by the provision of warnings and cautions.

162 Mr James Lawless, a former James Hardie employee, gave evidence about warning labels. Mr Lawless gave evidence of his recollection of when warning labels were placed on James Hardie asbestos cement building products. As might be expected, he was not able to say precisely when warning labels commenced to be placed on the products. In cross-examination, having been referred to a letter from the South Pacific Asbestos Association, he agreed that it was about 1979 that warning labels first went on James Hardie products. Warning labels did not go on all of the products initially. Mr Lawless said that it commenced in 1979 and then progressively over the years other products received warning labels. That occurred over a period of maybe one year and probably not more than two so by 1981 all products were labelled. Mr Lawless did not recall any labels being placed on products manufactured at James Hardie's Rivervale factory.

163 The labels were put on the back of the sheet so that they did not appear on the front face. Once an eave lining was put in place you would not see the sticker. On corrugated fence sheeting they were put on the last overlap so once the corrugated fence was in place you could not see them.

164 The early warning labels included "Caution. This product contains asbestos. Breathing asbestos dust can damage health. Keep dust down". The label said to follow four simple safety rules:

"1. When sawing, drilling, etc. work in a well ventilated space, preferably outdoors.

2. Use hand tools designed for cutting asbestos-cement sheets such as fibro cutters or a score and snap knife - or use an old hand saw. If cutting by power saw use one which has a dust suppression attachment.

3. Avoid drilling overhead where possible by pre-drilling before fixing.

4. Damp down waste dust and dispose of it in a sealed bag."

165 The label contained a note: When fixed in position asbestos cement sheets present no known risk to health.

166 Later labels contained the caution that breathing asbestos dust may cause serious damage to health including cancer and that smoking greatly increases the risk in accordance with NH & MRC recommendations. The safety rules recommended were preceded by the words "when cutting or drilling follow the simple safety rules". There then followed the same safety rules as on the earlier caution except that rule 4 was "dispose of any waste and dust in a safe manner".

167 Mr Warwick Gazzard is a former James Hardie employee. He gave evidence that in the 1970s James Hardie included warnings in literature which was placed in literature racks in hardware and other outlets. He said that there was very little literature relating to a flat sheet and that most of the literature related to moulded products and Hardiplanks and roofing. He agreed that some warning labels were placed on the products but not all. Most of the labels were applied by hand by workers. In some cases the labels were not applied. Some products did not have labels on them at all. Mr Gazzard never saw a warning label attached to a flat sheet. He did not see any warning labels placed on any Hardiplank before he left in 1981. He never saw any labels attached to corrugated sheets.

168 There was also evidence about a "road show" in which safe handling methods were demonstrated. Mr Lawless said that James Hardie put a road show together where people would visit hardware stores and demonstrate to hardware store owners the safe methods. There were all sorts of brochures that went out advising them how to use the correct tools and equipment. The defendant communicated risks of cutting, demolishing, brushing and sanding asbestos cement materials by placing information in brochures displayed in hardware stores.

169 The plaintiff did not see any warnings on any of the asbestos cement products around the house at 190 Erindale Road. Of course, he would not have been able to see any labels on the flat sheets constituting the eaves, nor on that part of the corrugated fencing sheets that overlapped other sheets. Also, it is possible that any warning labels may have been covered with paint.

170 I make the following findings. The process of placing warning labels on the defendant's asbestos cement products occurred progressively commencing in 1979 and the process of placing warning labels on all products was only in place by 1981. The process involved warning labels being stuck on individual sheets by workers at various plants and factories. There was no process in place to ensure that warning labels were placed on all sheets. The flat sheets and corrugated sheets were not

amongst the first products to have warning labels placed on them. There were no warning labels placed on the asbestos cement products on which the plaintiff worked. That is because those products were probably manufactured before 1979 or in any event at a time prior to the labels being placed on flat sheets or corrugated sheets.

171 Where a product supplier seeks to discharge its duty to take reasonable care to avoid injury being suffered by users of its products by providing warnings and cautions then the warnings must put the user of the product in a position to make an informed decision about whether or not to use the product by telling the person about material risks inherent in the use of the product and by providing other relevant information. The product supplier must exercise reasonable care to give the person such information as a reasonable person in that person's position would, in the circumstances, want to be given before making a decision whether or not to use the product. In this case the relevant information that a reasonable person would want would include the nature and probability of inherent risks in using the product and measures that the person might take to minimise those risks. The relevant information that a reasonable person would want and which a reasonable product supplier in the position of the defendant would provide includes precautions that could and should be taken by the user to minimise the risk of contracting mesothelioma or some other asbestos-related disease.

172 The first labels placed on the defendant's asbestos cement products were inadequate. Those labels cautioned the reader only that breathing asbestos dust can damage health. That caution fails to bring to the reader's attention the seriousness of the injury that might result from breathing asbestos dust. The subsequent labels did inform the reader that breathing asbestos dust may cause serious damage to health including cancer but still failed to inform the reader that cancer, or mesothelioma, might result from inhaling a small amount of asbestos dust and that there is no known threshold dose below which no risk of mesothelioma exists.

173 I find that the defendant failed to take reasonable steps to bring to the attention of the class of people to which the plaintiff belonged the risk of injury that might result from cutting, sawing, drilling or brushing the defendant's asbestos cement products and the preventive measures that should be taken when undertaking those activities.

174 Where, as here, the risk of injury is serious, resulting in death, then the steps that a reasonable person would take to avoid injury are greater than if the risk of injury was less serious. The defendant could have and

should have placed more effective warning labels on all of its asbestos cement products at an earlier time. The defendant could have taken other, and more effective, steps to bring those matters to the attention of the class to which the plaintiff belongs.

175 In this case the defendant could not identify individual users of the asbestos cement building products it had manufactured and sold. In the late 1970s and the 1980s there was a vast amount of asbestos cement building products manufactured and distributed by the defendant in places throughout Western Australia, and elsewhere in Australia. It was reasonably foreseeable that if the asbestos fibres in those products were disturbed by activities such as cutting, sawing, drilling, brushing or scraping, the fibres might be released into the air and inhaled by the person carrying out those activities. There were no warning labels on most of the products and where labels had been attached to the product those labels would in most cases have not been visible because they had been covered up, painted over or otherwise ceased to be visible.

176 The risk of contracting mesothelioma from cutting, sawing, drilling or scraping asbestos cement products was not obvious. The defendant ought to have known that the people carrying out such activities on the products, or many of them, did not know of the dangers inherent in such activities and the need to take preventive measures to minimise those dangers. In those circumstances it must be considered whether a reasonable person in the position of the defendant would have used the public media as a means to convey appropriate warnings to users of its products. It may also have issued public announcements.

177 Whether a post-sale warning to users is effective depends in part on its cost. As the group to whom warnings might be provided increases in size, the cost of communicating warnings may increase and their effectiveness may decrease. This is a factor to be considered. If a product supplier may cost-effectively communicate to the users of its products then the post-sale warning language must be reasonably calculated to impress upon users the gravity of the risk. Vague warnings indicating neither the potential problem nor the possible risk of harm are inadequate.

178 A warning must be effectively communicated. To justify the potentially high cost of providing a warning by mass media advertising, those to whom such warnings are provided must be in a position to reduce or prevent the risk of harm resulting from the intended or normal or usual use of the product. Such recipients of warnings need not be the original

purchasers of the product so long as they are able to avoid or reduce the risk of harm effectively. A reasonable person would give a warning when the risk of harm is sufficiently great to justify the burden of providing a warning.

179 Requiring the defendant to provide a warning by mass media advertising imposes a heavy burden upon the defendant. The defendant may have to expend large sums of money to effectively convey the warning. Those costs must be balanced against the risk of harm, the severity of the potential harm and the number of product users affected. A product supplier can satisfy its duty to take reasonable care by taking reasonable steps to warn foreseeable users. Such reasonable steps may include a variety of measures including adequate warning labels, notices to distributors, public announcements and mass media advertising.

180 In this case the factors to consider include the nature of the harm that may result from use without notice of its risks, the likelihood that harm will occur, how many persons are affected, the economic burden on the product supplier of warning users, and the amount of the product manufactured or sold. It is important that these matters be considered by reference to the time at which the decision whether or not to advertise warnings was or should have been made and not with the benefit of hindsight.

181 In this case the harm that may have resulted from use of the asbestos cement products without taking appropriate preventive measures was very serious; it may have resulted in death. The likelihood that harm would occur is small but not fanciful or farfetched. A large number of persons were affected. There was a great quantity of asbestos cement building products manufactured or supplied by the defendant in homes and other places throughout Western Australia and elsewhere in Australia.

182 The economic burden on the defendant of conducting a mass media advertising campaign was considerable. However, the defendant conducted advertising campaigns for the sale of its products. There is evidence before the Court of the defendant's financial position. There is also evidence of the cost of some forms of advertising. It was within the economic capacity of the defendant to undertake an extensive mass media advertising campaign to draw attention to users of its product of the potential risks and preventive measures that should be taken in its use. The defendant could have made public announcements of the risk to handymen or other casual users of its asbestos cement building products from disturbing the asbestos fibres in the product by cutting, sawing,

drilling, brushing or scraping and of the preventive measures that should be taken to avoid or minimise the risk. Having regard to the public and media attention given to the dangers of asbestos exposure in the 1970s and 1980s evidenced by the numerous newspaper clippings and other media publications in evidence I infer that it is likely that such announcements would have received widespread publicity.

183 I find that the defendant breached the duty of care it owed to the plaintiff by failing to take reasonable steps to bring home to end users of its products the risk involved in using the products and preventive steps that should be taken in their use.

184 The defendant submits that if there was a duty that advertisements had to be placed in newspapers, there was no breach of duty. It would be necessary, the defendant submits, in accordance with Wyong Shire Council v Shirt [1980] HCA 12; (1980) 146 CLR 40, to weigh considerations including practicability and cost. It would be wrong to look only at the practicability and cost of advertising only in one newspaper, and only in Perth. If such a duty exists, then it would be necessary for advertisements to be placed in newspapers all over Western Australia, penetrating all cities, country centres and hamlets, and not just Western Australia - it would need to extend over Australia. The defendant asks: "how often should these advertisements appear? And for how long? And why would the advertisements only appear in English? And why just newspapers? Think of the cost and logistics of such a campaign. And such a campaign might not even work".

185 The answer to these questions is that the duty of care is not a duty to warn the appellant, as a member of the class of persons to whom the duty was owed, of the risk involved in using the defendant's products. The duty is a duty to take reasonable care to avoid injury to the class of persons to which the plaintiff belongs from use of the defendant's products. In the circumstances of this case discharge of that duty required the defendant to take a range of measures including the placing of adequate warning labels on its products and undertaking a public advertising campaign to bring home to handymen or casual users the risk of harm from using the products and the preventive steps that should be taken to avoid or minimise that harm. The extent of that advertising campaign, including the newspapers or other media to be used, the size or prominence of advertisements and the duration of the campaign or campaigns are to be considered in the light of the defendant's financial capacity to undertake such campaigns. In this case the evidence establishes that the defendant had the capacity to undertake substantial

campaigns over a period of time. The defendant had the financial capacity to place an advertisement in a Perth daily or weekly newspaper at least once a month during the late 1970s and early 1980s. The defendant could have made public announcements and issued media releases to the same effect at no cost. The defendant could, and should, have undertaken a media advertising campaign at least in Perth and other Australian capital cities in which the defendant's product had been widely distributed. The defendant took no such steps. The defendant breached its duty to take reasonable care to avoid injury to the class of persons to which the plaintiff belongs from the use of the defendant's products.

186 Causation is a central issue in this case. The defendant submits that it did not cause the plaintiff's injury.

187 It will be necessary to discuss the principles of law in relation to causation in fact and the application of those principles to the facts of this case. Before doing so, I will refer to medico-scientific knowledge concerning the development of mesothelioma.

188 A number of eminent experts in the field of mesothelioma and asbestos-related diseases gave evidence. The evidence shows that there has been a relatively recent growth in medical and scientific knowledge concerning the development of mesothelioma but severe limitations as to this knowledge continue to exist.

189 In his report of 12 March 2006 Dr James Leigh referred to recent literature that concluded that asbestos fibres can have effects at both the initiation and promotion/proliferation phases of tumour development and said that the concept of asbestos as an initiator and promoter for mesothelioma is accepted in recent standard textbooks. In his oral evidence Dr Leigh explained the concept of asbestos as an initiator and promoter of mesothelioma:

"The current accepted theories of carcinogenesis in general, not just with asbestos but with many other agents, is that cancer is initially a genetic change in the cell. In other words, the genetic material that normally regulates cell division so that ... when one mesothelioma cell divides it becomes two more normal mesothelioma cells and that's regulated by the genes on the chromosomes in the cell. All cancer is thought to be due to a

disordered cell division. A cancerous cell is an abnormal cell, that when a cell divides into two, one or both of them is not a normal cell and then that abnormal cell will divide again and again and again and will become a tumour, as long as other things happen as well. That's what is [meant] by initiation initial genetic damage to the cell and asbestos can do that to cells. ... Once this abnormal cell has been produced by a genetic alteration and some of these abnormal cells are starting to grow that does not necessarily mean that the little clone of abnormal cells will become a clinical tumour because the body will have defence mechanisms to mop up these funny-looking cells. There will be immune mechanisms and there will be tumours, oppressor genes will come into action and not all genetically initiated cell damage will turn into a tumour, however other factors then act on the promotion of growth of these abnormal cells. What makes the abnormal cell that has been initiated become yet more abnormal cells. This is due to the action of promoters. They promote the proliferation of abnormal cells and asbestos can act in that way as well, so it can act both on the initial genetic damage and it can act to promote the growth of already initiated cells."

"In view of the capacity of asbestos fibres to be involved at several stages of tumour development, all cumulative exposure to asbestos in an individual case must be considered to play some part in causation."

"That's because the later exposures may be involved in promotion rather than initiation. They may also be involved in and get more initiation than new cells because some of these things are happening simultaneously. They are all happening at different times and, as I say, different processes are occurring at cells. You have got a dose of carcinogen, a number of fibres if you like, acting on a number of cells in a probabilistic way. Not every fibre acts on every cell and at different points in time some cells are suffering genetic damage, some cells that have already suffered genetic damage are being promoted into clones of abnormal cells and becoming tumours. At the same time you've got repair processes going on with suppressogenes (sic) being activated and you've got pathological defence

mechanisms like antibodies to the cells that are recognised as abnormal and destroying them. Some cells are just dying anyway, necrosis, and some are dying by so called program cell deaths or apoptosis, where the genetic mechanism in the cell actually programmes it to die. At the same time you've got fibres are being cleared, some of the fibres are being cleared at different rates, depending on the type of fibre and if further exposure is occurring more fibres are being deposited and these are potentially acting either in an initiating or a promoting fashion, so you've got all these processes going on simultaneously so that, as I say in the report, ... "

"All these processes at cellular level are stochastic in that probabilities of fibre/cell interaction depend on the number of fibres and number of cells present at any point in time. Hence, simplistically, the more fibres, the more free radicals and greater probability of initiated, promoted or proliferated cells at any given time point."

191 In his oral evidence Dr Leigh further explained:

"A free radical is an active - a very reactive molecule with a free electron around an oxygen that has a potential to damage chemically the DNA which is the chemical basis of the genetic process, so that a free radical is the actual intermediate mechanism between the fibre and the damage to the DNA. The free radicals can be produced by the fibre directly reacting with tissue or by the fibre being phagocytosed by a macrophagic cell which is a cell that tries to gobble up the fibre in the first place because it's a foreign body, but in the case of asbestos these fibres cannot always be fully gobbled up by macrophages and this frustrated phagocytosis, as we call it, also produces free radicals, so free radicals can be produced sort of directly or indirectly but it's the free radical that ultimately does the chemical damage to the DNA, which produces the genetic change. ... it's like sperm and ova. I mean, only one sperm actually fertilises the ova but there's millions sent out to do the deed, so the more there are the more chance of one being hit. ... Ultimately one fibre does initiate the change in the cell but it's because it's been given a big chance by being one of a huge force."

192 In his oral evidence Professor Robinson was asked and gave the following opinion on how mesothelioma tumours develop:

"Whilst it's not absolutely certain, I can tell you, ... current concepts of what is most likely. The types of asbestos that cause mesothelioma or are most likely to cause it are shaped like a spear, are long and narrow, and when they're inhaled they work their way through the lungs and find themselves on the outside of the lungs where they irritate the sac in which the lung sits known as the pleura ... It is thought that over a period of time the damage caused by that fibre, which is probably made worse by breathing - if you can imagine the lung rubbing up against the pleura every time you take a breath and you've got fibres sticking out, it's always scratching the pleura causing damage and it's those repeated cycles over many years of damage and repair, damage and repair and production of molecules like oxidants that damage the DNA that allow pleura mesothelial cells to accumulate DNA damage. Now, most of the time damage does not cause mesothelioma but it is thought that in everybody that has been exposed to asbestos there is probably some DNA damage. How much DNA damage do you need to get mesothelioma? Well, the answer is every cancer cell probably has tens of thousands of mutations but most of them occur in non-dangerous genes. It's when you get a set, may be two, three, four, five, six genes, that cause cancer in that, let's say 15,000 or 11,000 mutations - call it 11,000. You need 11,000 and you get six maybe that are the dangerous ones. They are the ones that unfortunately trigger the mesothelioma but it takes a long time to accumulate that much DNA damage. When the cancer is finally triggered, it has disordered growth. Cells of course normally grow. That's how we grow from childhood to adulthood and that's how when we have a wound the skin will grow and cover it over. So growth is normal but cancer is when that growth has lost its controls. I guess like a mob out of control. That happens because of a number of reasons but the simplest way to think about it is that the cell growth is driven by an accelerator, which are growth factors and by brakes which stop growth, so that when your skin has healed from a wound the body realises that and the skin stops growing. So there's an accelerator and a brake and cancer is when there's too much accelerator and no brake. The things that are accelerators are ... things called oncogenes and the things that

are the brakes are things called tumour suppressor genes and mesothelioma clearly has disorders in both of those two things. So it grows. It takes a while to kick off but once it has kicked off it grows relentlessly unfortunately ..."

193 Professor Robinson was asked what is meant by the terms initiation and promotion with respect to asbestos and mesothelioma. The Professor replied:

"I'm not sure they're actually that helpful those sorts of terms, because initiation is something that will cause initial DNA damage and promotion is something that takes the cells from that point to becoming a cancer. In the case of asbestos which probably does the whole lot, causing DNA damage right through to - I mean, it doesn't need help from anything else. It can get help, for example, in lung cancer, from smoking, but it doesn't need help, if you like. So I don't actually find those terms - those terms are a little bit outdated I think in science. It's better to think of cancer and exactly what is going on in terms of DNA. So, for example, you can get DNA damage and then you can get a disorder of growth that causes those cells to then become more dominant in that pool of cells."

Professor Robinson then further referred to initiation and promotion in this context:

" ... there's initiation which by itself won't cause cancer and they you get subsequent molecular events that take the cancer from its damaged state to a ... growth advantage state."

194 Professor Robinson was asked whether, after asbestos fibres have caused initial DNA damage, it required further asbestos fibres to cause the subsequent development of the tumour. Professor Robinson replied:

" ... it's impossible to answer because the asbestos stays there. ... the asbestos stays in the lung. But why it's interesting is that the other thing that asbestos does is to cause chronic inflammation and chronic inflammation is thought to promote cancer, not only in the lung but also, for example, in the gut, so that anti-inflammatory drugs can marginally reduce the risk of cancer, bowel cancer. So the capacity of asbestos to induce inflammation is another reason why it takes such a long time. So no-one knows whether it's ongoing damage from DNA or

the inflammation that's associated with it over that period of incubation or both."

195 I make the following findings based on the expert evidence:

1. Mesotheliomas are, by definition, tumours that arise from mesothelial cells.

2. The development of mesothelioma tumours are preceded by the inhalation of asbestos fibres.

3. The inhalation of asbestos fibres does not necessarily lead to the development of mesothelioma. Everyone living in urban areas will inhale asbestos fibres in their lifetime but few develop mesothelioma.

4. The precise process by which the inhalation of asbestos fibres leads to mesothelioma is unknown but it involves damage to the DNA. Not all DNA damage causes mesothelioma. Some cancer cell mutations occur in genes that trigger the mesothelioma. The mesothelioma then grows relentlessly.

5. It is not known whether, after asbestos fibres have caused initial DNA damage, further asbestos fibres are required to cause, or increase the risk of, the subsequent development of the mesothelioma tumour, but they may increase the risk of the development of the mesothelioma tumour.

196 The relationship between the inhalation of asbestos fibres, the risk of developing mesothelioma and the inhalation of asbestos fibres contributing to the development of mesothelioma was the subject of considerable evidence.

197 All of the expert witnesses agreed that there is a positive dose-response relationship between asbestos exposure and mesothelioma - the heavier the exposure to asbestos, the greater the risk of developing mesothelioma. There is no established threshold - that is a minimal lower limit below which asbestos fibres cannot cause the tumour - and thus it is plausible that even very low exposure can cause mesothelioma, even if the risk is very low.

198 Once a person has developed mesothelioma it is not possible to identify the asbestos fibre or fibres that caused or facilitated the DNA damage and the subsequent growth of the tumour. Professor Musk agreed with senior counsel for the defendant that medical science does not permit

us to know, at least yet, by looking at an individual patient, which exposure caused the mesothelioma.

199 In this case the plaintiff's exposures to asbestos consisted of the three exposures arising from his handyman activities in relation to the defendant's asbestos cement building products in 1983, 1985 and 1990 and the so called "background exposure" that is exposure from the environment at large unrelated to the use of asbestos-containing materials in the workplace or at home, or from significant point sources of asbestos or from active disturbance of materials containing asbestos.

200 The evidence of the expert witnesses is to the effect that the handyman exposures in 1983, 1985 and 1990 contributed to the risk of the plaintiff developing mesothelioma. The "background exposure" also contributed to the risk of the plaintiff developing mesothelioma.

201 Some of the witnesses attempted to assess the extent of the increase in risk of suffering mesothelioma over the background risk created by a specific exposure. The means of mathematically expressing an increase in risk is by reference to the "Relative Risk". There are three steps in that exercise.

202 The first step is to work out an annual risk of contracting mesothelioma due to background exposure. An annual risk in the "background group" is the number of persons, per million persons, who will contract mesothelioma in a year in the absence of any specific exposure to asbestos. The number of persons in the "background group" who will contract mesothelioma in a year is measured by the number of persons in a population who have contracted mesothelioma in the absence of any recalled specific exposure to asbestos.

203 Professor Berry, a biostatistician and epidemiologist called by the defendant, said in his report of 21 March 2006 that not all mesotheliomas can be attributed to established asbestos exposure and between 1986 and 1995 for one-sixth of the mesotheliomas in Australia there was no apparent asbestos exposure. In his report of 12 March 2006 Dr Leigh gave a figure of 18 per cent. Professor Berry says that these cases are generally referred to as "background cases". Professor Berry said that it cannot be concluded that these mesotheliomas were not due to asbestos exposure, but only that they were not due to any specific exposure that was extracted from an occupational and environmental history. This annual risk in the background group of contracting mesothelioma can be

converted into a lifetime risk by assuming a lifetime of 70 years, so the risks are the number of persons, per million persons, per lifetime.

204 Professor Musk, in collaboration with Dr De Klerk, has calculated that the background risk for mesothelioma is an annual risk of two to three persons, per million, per annum. This translates into a lifetime risk of 140 to 210 persons, per million, per lifetime.

205 The second step in calculating the relative risk is to calculate the increase in the risk of contracting mesothelioma created by any specific exposure by taking into account the factors of dose, fibre type and lag time. The increase can be expressed as a percentage.

206 The third step is to convert the risks into a concept known as "Relative Risk" ("RR"). In making a conversion it is appropriate to treat the "background group" as having an RR of 1. When an RR has increased by a specific exposure to asbestos, the extent of the increase is shown by an increase in a RR. If the risk was doubled or increased by 100 per cent then RR equals 2.

207 Dr Francis, who was called by the plaintiff, and Mr Rodgers, who was called by the defendant, each calculated the approximate dose of asbestos likely to have been inhaled by the plaintiff from his handyman exposures.

208 Professor Berry was provided with a report from Mr Rodgers which estimated that the plaintiff's cumulative exposure to asbestos was about 0.001 fibres/ml/years for the dismantling and re-erection of the fence, between 0.000004 and 0.0001 fibres/ml/years for the sanding and repainting of the eaves and 0.00002 fibres/ml/years for the sanding and repainting of the fence. Professor Berry then used a table published by J T Hodgson and A Darnton in 2000 in which they estimated the lifetime risks per 100,000 persons exposed to different exposures to amosite asbestos specified in fibres/ml years. The table provides a "best estimate", "lowest arguable" and "highest arguable" estimate of lifetime risks per 100,000 persons exposed for each level of cumulative exposure to amosite in fibres/ml years.

209 Professor Berry says that some adjustment has to be made in order to apply the information in the Hodgson and Darnton table to the plaintiff because the plaintiff's first exposure in 1983 was at aged 40 years whilst Hodgson and Darnton standardised the risks to exposure at aged 30 years. Using another table prepared by Hodgson and Darnton, Professor Berry assesses that the risk associated with exposure at aged 40 is 0.4 times the

risk associated with exposure at age 30. Incorporating that factor, for an estimated cumulative exposure of 0.001 fibres/ml/years of which half was amosite, Professor Berry calculates that the best estimate of lifetime mesothelioma risk is about one per 100,000 persons if all the amphibole asbestos was crocidolite, and if half were amosite and not crocidolite the risk would have been lower.

210 Professor Berry then says that since the background risk is about 70 to 140 per million, that is seven to 14 per 100,000 it follows from his previous calculations that the risk due to the plaintiff's exposure would have been less than the background risk. For example, Professor Berry says that taking the background risk as seven per 100,000 (the lowest figure) and the risk due to specific exposure as one per 100,000 (the highest estimate) the total risk would be eight per 100,000, corresponding to a relative risk of 1.14 or an attributable fraction of about 12 per cent.

211 My brief discussion of Professor Berry's assessment and calculations shows that there a number of variables and assumptions made in arriving at his conclusion. The assumptions are based on research data, including the lifetime risks per 100,000 persons exposed to various cumulative exposure levels of amosite. There is a substantial difference between the "lowest arguable" and "highest arguable" figures. Another assumption, based on published research, is that the risk associated with exposure at age 40 is 0.4 times the risk associated with exposure at age 30.

212 One of the most important variables in the calculation is the cumulative exposure measured in fibres/ml/years of the plaintiff's specific exposure, that is the plaintiff's handyman exposures. The figures used by Professor Berry in his report of 21 March 2006 were taken from an assessment by Mr Rodgers. Another assessment of the plaintiff's exposure was made by Dr Francis.

213 In his oral evidence-in-chief Professor Berry was asked to calculate the increase of the plaintiff's risk of contracting mesothelioma due to the home handyman exposure basing his calculation on the "worst case scenario" for the defendant - that is Dr Francis' assessment. Dr Francis calculated the cumulative exposure to be 0.2 fibre/ml/years. Professor Berry applied that exposure level to the figures in the tables in his report, adjusted the risk in a factor of 0.4 to take into account that the plaintiff's exposure was at aged 40 years not aged 30 years, and calculated that the risk due to that exposure would be six per 100,000. Compared to a background risk of 14 to 21 per 100,000 this calculation produces a range of elevation of risk from RR equals 1.3 to RR equals 1.4.

214 To consider what reliance should be placed on these calculations, and Professor Berry's opinion based on them, it is necessary to examine the calculation of cumulative exposure from the plaintiff's handyman activities as assessed by Mr Rodgers or Dr Francis.

Estimates of plaintiff's handyman exposures

215 Mr Rodgers is an occupational hygienist. Occupational hygiene is the applied science concerned with the recognition, evaluation and control of chemical, physical and biological factors arising in or from the workplace which may affect the health or well-being of those at work or in the community.

216 In measuring exposure to asbestos dust occupational hygienists refer to a time weighted average. A time weighted average exposure concentration is calculated over a normal eight hour working day, or a five day working week and is the fundamental premise of exposure standard setting. In his report of 20 March 2006, Mr Rodgers says that an asbestos "dose" is expressed as a working life cumulative exposure obtained by multiplying the long-term average daily exposure of the workforce by the proportion of time they are exposed in the week or year and also by the number of years that they are so exposed. The resultant value is expressed in fibres/ml years. 100 fibres/ml years is the cumulative dose that would result from, for example, exposure to a constant dust concentration of 10 fibres per ml over 10 years, or two fibres per ml over 50 years for eight hours a day five days a week.

217 Mr Rodgers assessed the plaintiff's cumulative exposure to chrysotile and amosite from his handyman activities in fibre/ml years. First, Mr Rodgers assumed that the plaintiff had undertaken each of the handyman activities described by the plaintiff for the durations and over the periods described by the plaintiff. Mr Rodgers then undertook a review of the peak and time weighted average exposures for working with the products described by the plaintiff. In cross-examination counsel for the plaintiff referred Mr Rodgers to p 5 of his report where he set out his assessment or estimate of the daily time weighted average exposure of workers carrying out each of the handyman activities described by the plaintiff. It can be seen from p 5 of Mr Rodgers' report that he arrived at those estimates by adopting or adjusting an exposure reported for activities Mr Rodgers considered to be similar to the activities undertaken by the plaintiff reported in the documents or literature referred to by Mr Rodgers on p 5 of his report. Counsel then asked Mr Rodgers to confirm that on p 5 of his report he had assigned exposure values to the

particular types of work that he understood the plaintiff had done. Mr Rodgers replied: "Yes, as best as the literature provided that information". That answer causes me to be wary of the reliability or accuracy of the assigned exposure values used by Mr Rodgers to estimate the plaintiff's cumulative exposure from his handyman activities.

218 The literature referred to by Mr Rodgers was varied. Some of the publications were little more than hearsay of unknown or doubtful provenance. For example, Mr Rodgers assessed the asbestos exposure from fence construction using Super Six to be 0.8 fibres/ml. The source of that figure or value was a letter of 7 November 1974 from James Hardie to Dr Heyworth of the Western Australian Department of Public Health.

219 Mr Rodgers calculated that the plaintiff's cumulative exposure from work on the Hardiplank fence is 0.001, and for the work on the asbestos cement flat sheet eaves was 0.0001 fibre/ml years or less and for the work wire brushing and painting the super six fence is 0.00002 fibre/ml years.

By reference to published tables based on research Mr Rodgers then estimated that the lifetime risk for the period on the Hardiplank fence is 0.2 per million, the lifetime risk for the period when scraping and sanding the eaves is 0.008 per million and the lifetime risk for the period when wire brushing and painting the super six fence is 0.004 per million.

220 Mr Rodgers said that he had calculated those lifetime risks assuming mainly amosite exposure which he said was not correct. Mr Rodgers said that the asbestos in Hardiplank was 100 per cent chrysotile, the flat sheets contained some chrysotile and some amosite and the super six 80 per cent chrysotile and 20 per cent amosite.

221 Mr Rodgers then adjusted the lifetime risk due to the relative periods of exposure and asbestos types and concluded that the plaintiff's exposure to asbestos cement products during Hardiplank fence reconstruction, preparation and painting, the preparation and painting of the eaves and the preparation and painting of the super six fence amounted to a theoretical lifetime risk of 0.002 per million or less.

222 Mr Rodgers said that in addition to the risk from the handyman exposures referred to, the plaintiff would have experienced the same lifetime background risk of mesothelioma as does the remainder of the Australian population. Mr Rodgers assumed that this background risk is due to natural or artificial low level asbestos contamination in the environment, other environmental agents or due to genetic factors.

Mr Rodgers then refers to the estimated lifetime background risk based on research of the National Occupational Health and Safety Commission that he was responsible for, published research in the United States and the Western Australian Advisory Committee on Hazardous Substances, Asbestos Cement Products publication of August 1990 and to a background risk based on Canadian studies in the 1980s.

223 I pause to observe that there is a problem with that approach. The "background" risk as measured by the Western Australian Advisory Committee on Hazardous Substances and other bodies, arises not only from natural or artificial low level asbestos contamination in the environment or other environmental agents but also from specific asbestos exposure which the mesothelioma sufferer has forgotten. It seems likely that the other sources of background risk calculations or estimates also include the risk from specific exposures not identified or recalled by the sufferer. I have found that the only specific asbestos exposures to which the plaintiff was exposed were those arising from his handyman work involving the defendant's asbestos cement products. Accordingly, the "background risk" applicable to the plaintiff is not the same as that measured in the studies to which Mr Rodgers referred. I will return to this issue later in these reasons.

224 Mr Rodgers then calculated the percentage increase in lifetime risk likely to be caused by the handyman exposure above that of the natural background risk and found that it varied from 0.0008 per cent to 0.0029 per cent according to which study the background risk rate was taken from. Mr Rodgers concluded that:

"Using the Australian population data or even the most recent overseas data on the background rate used by international occupational health authorities, there is around a 99.999% probability that the mesothelioma experienced by the plaintiff is a naturally occurring mesothelioma and Mr Hannell would have experienced it regardless of his claimed exposure to asbestos."

225 Similar observations may be made about the reports and evidence of Dr Francis as I have made in relation to the evidence of Mr Rodgers. Senior Counsel for the defendant says that Dr Francis' calculations and conclusions represent the "worst case scenario" for the defendant. That is true in as much as Dr Francis' quantitative estimates are the least favourable to the defendant in evidence. However, that does not mean

that Dr Francis' estimates represent the highest possible cumulative exposure that the plaintiff was exposed to by his handyman activities.

226 It is necessary to refer to the legal principles relating to causation before making conclusions about causation arising from the evidence.

227 The causation issue in this case arises from a situation of scientific uncertainty. Asbestos may have caused the plaintiff's mesothelioma through either a single fibre or through multiple fibres, but there is no way of identifying the source of the fibre or fibres which initiated or promoted the genetic process or processes which culminated in the malignant tumour.

228 In McGhee v National Coal Board [1972] UKHL 7; [1972] 3 All ER 1008, the pursuer, a workman employed to empty brick kilns, contracted dermatitis. The dermatitis was attributable to his work in the brick kilns. The employer was found not to have breached its duty of care in exposing the pursuer to the dust but admitted a breach in failing to provide showers to remove the dust at the end of the working day. The employer contended that its breach of duty had not caused the pursuer to contract dermatitis. The medical evidence did not establish that, had the pursuer been able to wash immediately in showers provided by his employer, he would not have contracted the disease. The medical evidence established that the fact that the pursuer had to cycle home caked with dust added materially to the risk that he might develop the disease but did not and could not explain just why that was so. The House of Lords held that, in the absence of complete medical knowledge of all the material factors relating to the disease, there was no substantial difference between materially increasing the risk of injury and making a material contribution to the injury and accordingly the pursuer was entitled to recover damages from his employer in respect of its admitted breach of duty for an injury within the risk which it had created.

229 In Wilsher v Essex Area Health Authority [1987] UKHL 11; [1988] AC 1074 Lord Bridge said at 1090 that McGhee laid down no new principle of law but merely affirmed the principle that the onus of proving causation lies on the pursuer or plaintiff. His Lordship said that adopting a robust and pragmatic approach to the undisputed primary facts of the case, the majority concluded that it was a legitimate inference of fact that the defendant's negligence had materially contributed to the pursuer's injury. That view of McGhee was rejected by a majority of the Law Lords in Fairchild v Glenhaven Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32 at [21] -

[22] per Lord Bingham, at [70] per Lord Hoffmann, at [144] and [154] per Lord Rodger.

230 In Fairchild three appeals were heard together. They related to employees who had developed mesothelioma caused by exposure at work to asbestos dust. All the employees had been exposed to asbestos dust during periods of employment with more than one employer. In each case the plaintiff sought damages against defendants who, in breach of their duty to protect the employee from the risk of contracting the disease, had exposed him to substantial inhalation of asbestos dust or fibres. It was common ground that the mechanism initiating the genetic process which culminated in mesothelioma was unknown, that the trigger might equally probably be a single, a few or many fibres, that once caused the condition was not aggravated by further exposure but the greater the quantity of fibres inhaled the greater the risk of developing the disease. The Court of Appeal held that since mesothelioma was an indivisible disease triggered on a single unidentifiable occasion by one or more fibres it could not be proved on a balance of probabilities, where the plaintiff had been exposed to asbestos fibres by several potential tortfeasors, which period of exposure had caused the disease and hence that each plaintiff had failed to establish causation against any of the defendants. The House of Lords allowed the appeals against this decision.

231 At [21] Lord Bingham took McGhee as authority for the proposition that, on the facts of that case, no distinction was to be drawn between making a material contribution to causing the disease that the employee had contracted and materially increasing the risk of his contracting it. At [34] Lord Bingham concluded that it was:

" ... just and in accordance with commonsense to treat the conduct of A and B in exposing C to a risk to which he should not have been exposed as making a material contribution to the contracting by C of a condition against which it was the duty of A and B to protect him."

232 The other members of the House of Lords all reached the same conclusion and, with the exception of Lord Hutton, for essentially the same reasons. Lord Hutton took the view that an inference of actual causation should be drawn where it could be shown that the breach of duty had materially increased the risk of the victim contracting the disease that he had eventually contracted (see [108]). But the other members of the House were prepared to impose liability not on the basis of an

inference of actual causation but on the basis that the causing of a material increase in risk would suffice.

233 In Fairchild each employer in breach of its duty of care was jointly and severally liable for the whole of the plaintiff's damages. In Barker v Corus UK Ltd [2006] UKHL 20, the House of Lords ruled that, where more than one employer has negligently exposed a claimant to asbestos and the claimant goes on to develop mesothelioma, each employer should only be held liable to the extent that their breach of duty increased the risk of the plaintiff contracting the disease. Mr Barker died of mesothelioma in June 1966. During his working life, he had three material exposures to asbestos. The first was for six weeks in 1958 while working for a company that subsequently became insolvent without any identified insurer. The second was between April and October 1962 while he was working for a predecessor of Corus. The third was for at least three short periods between 1968 and 1975 while working as a self-employed plasterer. The circumstances were different from Fairchild in that although the first two exposures were the consequences of breaches of duty by employers, the last involved a failure by Mr Barker to take reasonable care for his own safety. The House of Lords agreed that the McGhee-Fairchild principle applied but concluded that liability should be apportioned according to the relative degree of contribution each defendant had made to the risk of the disease being contracted.

234 The "material contribution to risk" principle allows negligent conduct to be treated as a factual cause of harm even though it cannot be proved on the balance of probabilities that there was in fact a causal link between the conduct and the harm. The Fairchild principle accepts that it is appropriate in certain circumstances to bridge the evidentiary gap by allowing proof that negligent conduct materially contributed to the risk of harm to satisfy the requirement of proof of factual causation. The plaintiff did not submit that the Fairchild principle is the law in Australia.

235 Another way in which the problem of evidentiary gaps might be dealt with is by shifting the evidential onus of proof on the issue of factual causation from the plaintiff to the defendant once the plaintiff has established that the defendant's failure to take reasonable care to avoid the risk in question materially contributed to the risk that the plaintiff would contract mesothelioma.

236 In Bennett v Minister for Community Welfare [1992] HCA 27; (1992) 176 CLR 408 at 420 - 421, Gaudron J said:

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

237 In Chappel v Hart (1998) 195 CLR 232 at 273, Kirby J said:

"One means of alleviating the burden cast by law on a plaintiff to establish a causal relationship between the breach and the damage concerns the evidentiary onus. Australian law has not embraced the theory that the legal onus of proof shifts during a trial. Nevertheless, the realistic appreciation of the imprecision and uncertainty of causation in many cases - including those involving alleged medical negligence - has driven courts in this country, as in England, to accept that the evidentiary onus may shift during the hearing. Once a plaintiff demonstrates that a breach of duty has occurred which is closely followed by damage, a prima facie causal connection will have been established. It is then for the defendant to show, by evidence and argument, that the patient should not recover damages. In McGhee v National Coal Board, a Scottish appeal, Lord Wilberforce explained why this was so. Although Lord Wilberforce's statement in McGhee has proved controversial in England, it has received support in this Court. Its principle has also been accepted by international experts such as Professor Giesen. I find Lord Wilberforce's exposition compelling ..."

238 In Naxakis v Western General Hospital [1999] HCA 22; (1999) 197 CLR 269, a school boy sued a hospital and a surgeon for negligence. He had been struck on the head by another boy and upon admission to hospital was diagnosed as having suffered a subarachnoid haemorrhage caused by the blow to the head. He was kept in hospital for nine days. Two days after he was discharged he collapsed. He was then found to have suffered a major intracranial bleed from a burst aneurysm. It was contended for him at the trial that an angiogram should have been performed when he was first admitted to hospital which would have disclosed the aneurysm. At the close of the evidence the defendant's counsel submitted that there was no case to go to the jury. None of the medical witnesses gave evidence that an angiogram should have been ordered or that the failure to order an angiogram was in the circumstances open to criticism. The Judge held that in the absence of such evidence it would not be open to the jury to

find that the defendants were in breach of their duty and directed the jury to find for all the defendants. The High Court held that the jury should not in the circumstances have been directed to return a verdict for the defendants and ordered a new trial.

"It has been suggested that to allow compensation for the loss of chance would alleviate problems associated with proof of causation. There is, in my view, a tendency to exaggerate the difficulties associated with proof of causation, even in medical negligence cases. For the purposes of the allocation of legal responsibility, 'if a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contributed to that injury occurring'. [Chappell v Hart (1998) 195 CLR 232 at 244-45 per McHugh J]. And in that situation, the trier of fact - in this case, a jury - is entitled to conclude that the act or omission caused the injury in question unless the defendant establishes that the conduct had no effect at all or that the risk would have eventuated and resulted in the damage in question in any event. [See Bennett v Minister for Community Welfare [1992] HCA 27; (1992) 176 CLR 408 at 420-21 and the cases there cited. See also Chappel v Hart (1998) 195 CLR 232 at 237-38 per Gaudron J; at 247-48 per McHugh J; at 257-59 per Gummow J; at 272-73 per Kirby J]."

"Once the jury took the first step, and concluded that Mr Jensen did not, as he should have, consider aneurysm and the need for an angiogram, it would have been a small step for them to conclude that the failure to consider this alternative diagnosis was a cause of the second haemorrhage suffered by the appellant with its grave results [March v Stramare [1991] HCA 12; (1991) 171 CLR 506; Chappel v Hart (1998) 195 CLR 232 at 272-73; McGhee v National Coal Board [1972] UKHL 7; [1973] 1 WLR 1 at 6]. Where, as here, a plaintiff demonstrates that it was open to a jury to conclude that the respondents were in breach of their duty of care to him and this breach was closely followed by his damage, a prima facie causal link is established. It may be displaced and

it may be rejected; but it cannot be ignored in considering a motion for judgment for the defendant for want of evidence."

"In Chappel v Hart McHugh J was one of two dissentients in a Court of five members of this Court, but I do not take his Honour's observations that I am about to quote and adopt as being in any way affected by that dissent:

'Before the defendant will be held responsible for the plaintiff's injury, the plaintiff must prove that the defendant's conduct materially contributed to the plaintiff suffering that injury. In the absence of a statute or undertaking to the contrary, therefore, it would seem logical to hold a person causally liable for a wrongful act or omission only when it increases the risk of injury to another person. If a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contributed to that injury occurring.'"

242 In Rosenberg v Percival [2001] HCA 18; (2001) 205 CLR 434 at [88] Gummow J cited the statement of McHugh J in Chappel v Hart at [34]:

"The onus of proving that the failure to warn was causally connected with the plaintiff's harm lies on the plaintiff. However, once the plaintiff proves that the defendant breached a duty to warn of a risk and that risk eventuated and caused harm to the plaintiff, the plaintiff has made out a prima facie case of causal connection. An evidentiary onus then rests on the defendant to point to other evidence suggesting that no causal connection exists. Examples of such evidence are: evidence which indicates that the plaintiff would not have acted on the warning because of lack of choice or personal inclination ... Once the defendant points to such evidence, the onus lies on the plaintiff to prove that in all the circumstances a causal connection existed between the failure to warn and the injury suffered by the plaintiff."

243 The principles of causation were recently addressed by the Court of Appeal in City of Stirling v Tremeer [2006] WASCA 73. The respondent was rendered quadriplegic as a result of falling from a track ride in a

children's playground in a public park in the municipality controlled by the City. The trial Judge found that the respondent's injuries occasioned by the fall were caused by the City's negligence in failing to have sufficient soft sand underneath the playground equipment from which the respondent fell. At the time of the accident there was patchy grass at the sides of the track ride and yellow sand in a shallow depression immediately underneath it. The trial Judge found that the respondent fell from a height of more than 970 millimetres in an upside down position head first onto the ground under momentum generated by a partial somersault. The City argued that its negligence in failing to provide in the order of 300 millimetres of sand was not the cause of, nor did it materially contribute to, the respondent's injuries as a result of him falling from the track ride.

244 The trial Judge found that the City was negligent in failing to provide sufficient sand. Her Honour found that if there was a foot or more of loose beach sand that probably would have been sufficient to prevent the injury. Her Honour found that the breach of duty caused the respondent's injuries and certainly materially contributed to them.

245 In the Court of Appeal, McLure JA (with whom Steytler P and Roberts-Smith JA agreed) discussed the legal causation principles. Her Honour stated that the legal onus of proof of causation is, and remains, on the plaintiff. At [74] her Honour said that generally a plaintiff will fail if he cannot satisfy the "but for" test but that there are some situations where causation can be established without satisfying the "but for" test. For example, where there are multiple sufficient causes resulting in indivisible damage. Her Honour then said that in the United Kingdom the failure to satisfy the "but for" test for causation is not determinative where there is an evidential gap that occurs where there is positive evidence that on the current state of knowledge in the relevant area, experts are unable to say whether the damage would or would not have been suffered but for the negligent act or omission. Her Honour referred to McGhee as such a case. Her Honour quoted a passage from the judgment of Lord Wilberforce in McGhee which her Honour noted as having been relied upon by the High Court. Her Honour then referred to Fairchild.

246 Her Honour then turned to consider the law in Australia. Her Honour said that a number of members of the High Court, relying on the judgment of Lord Wilberforce in McGhee, support a rule that on its face applies to proof of causation generally (it not being confined to evidential gaps that cannot be filled by either side) and said the approach is reflected in the oft cited statement of Gaudron J in Bennett v Minister for

Community Welfare (supra) at 420 - 421 that I have set out earlier in these reasons. Her Honour noted that Gaudron J's statement has been cited with approval in Chappel v Hart (supra) at 239 per Gaudron J; at 247 per McHugh J (cf at 244); at 257 per Gummow J and at 273 per Kirby J; in Rosenberg v Percival at 461 per Gummow J and in Naxarkis v Western General Hospital (supra) at 279 per Gaudron J. Her Honour noted that any suggestion that Gaudron J's statement contemplates the legal burden shifting to the defendant is rejected by McHugh and Kirby JJ in Chappel v Hart at [68] and [93]. Her Honour then said at [80]:

"As I understand the law in Australia, once a plaintiff demonstrates that a breach of duty has occurred followed by injury within the area of the foreseeable risk, a prima facie causal connection will be established and the defendant has an evidential burden to show that the breach had no effect. However, once there is evidence sufficient to displace the plaintiff's prima facie case, it remains for the plaintiff upon the whole of the evidence to satisfy the tribunal of fact of the extent of the injury caused by the defendant's negligence: Purkess v Crittenden [1965] HCA 34; (1965) 114 CLR 164 at 168."

247 Her Honour then turned to consider the evidence and found that it established that soft sand reduces the risk of severe injuries from a fall from playground equipment. There was expert evidence that there is an inverse relationship between the impact force and the absorption capacity of the surface. Her Honour found that the respondent had established a prima facie case that the City's omission caused or materially contributed to the respondent's quadriplegia. The next question was whether the City discharged its evidentiary onus of adducing evidence that the injury would have occurred even if soft sand had been provided. Her Honour found that the evidence of Mr Scull and the ETRS Pty Ltd reports satisfied the evidentiary burden and accordingly the issue was whether the respondent, on the whole of the evidence, established that the omission to provide soft sand caused or materially contributed to his quadriplegia. Her Honour concluded that the expert evidence established, on the balance of probabilities, that the respondent would have suffered injuries resulting in quadriplegia even if he had fallen onto soft sand and hence that the trial Judge erred in concluding that the City's failure to provide soft sand caused or materially contributed to the respondent's quadriplegia.

248 It is informative to consider the evidence which her Honour found to have discharged the evidential burden on the City. The first ETRS report concluded that, from the height the respondent was considered to have

fallen, the same injury would have been inflicted whether there was soft sand or a grassy surface under the track ride. The calculations in the first ETRS report were carried out on the assumption that there was purely compressive axial impact to the neck. The second ETRS report evaluated the response of the human head and neck to impact on grass and soft sand with a neck inflexion or an extension. ETRS concluded in its second report that the substitution of sand for grass under the track ride would not have substantially reduced the injuries to the respondent's neck. Both reports were based on the results of experimental work.

249 Mr Scull was a biomechanical engineer. Mr Scull concluded that the predominant force that produced the injury to the respondent was an axial compression force but that did not exclude the possibility of flexion or extension moments superimposed over and above the axial force depending on the posture of the body. Mr Scull reviewed the experimental work of ETRS. His conclusion appears at [60]:

"Because of the complex dynamics involved, I cannot exclude the possibility that [the respondent] would have been spared the severe injuries incurred by the impact on a grass surface had he sustained a similar fall onto sand. One cannot exclude the possibility that a different fall under similar conditions onto sand could have produced a different complex of injuries with a worse prognosis.

It is my opinion however that, because of the severe nature of the impact and the predisposition of the cervical spine to trauma under such an impact it is highly unlikely that an identical impact on sand would not have caused a significant injury. In the event that the shock attenuation offered by sand, as evidenced by the reduction in peak deceleration at impact when compared with that for the grass surface, was sufficient to ameliorate the primary injury attributed to the burst fracture of the body of C5, it is still probable that the secondary injuries associated with axial compression - flexion loading of the spine and lateral bending - rotation would have caused injuries sufficient to compromise the spinal cord (eg. injuries such as fracture dislocation, vertebral subluxation and ligamentous tears, etc.) resulting in quadriplegia."

250 Mr Scull concluded that there was a high probability that there would have been a similar injury to the spinal cord resulting in quadriplegia even if the respondent had fallen onto soft sand.

251 The above review of Australian law concerning causation principles demonstrates that the following principles should be applied:

1. Establishing a connection between the plaintiff's injury and the defendant's negligent act or omission is a prerequisite to the recovery of damages.

2. The standard of proof is the balance of probabilities.

3. The legal burden of establishing that the defendant's negligent act or omission caused or contributed to the plaintiff's injury rests on the plaintiff at all times.

4. The evidentiary onus may shift in the sense that where the plaintiff has proved a breach of duty by the defendant and that the breach increased the risk of injury and that risk eventuated then, in the absence of evidence that the breach has no effect or that the injury would have occurred even if the duty had been performed, it will be taken that the breach of the common law duty of care caused or materially contributed to the injury.

252 If, as a matter of fact or law, there is no evidential onus on the defendant to adduce evidence that the defendant's breach of duty had no effect or that the injury sustained by the plaintiff would have occurred even if the duty had been performed, or if the defendant has discharged such an evidential onus, the plaintiff must establish on the balance of probabilities that the defendant's negligent act or omission caused or contributed to the plaintiff's injury. In this case, if, as a matter of law, or in the factual circumstances of the case, there is no evidential onus on the defendant to adduce evidence that the defendant's breach of duty had no effect or that the plaintiff would have contracted mesothelioma even if the defendant had performed its duty, or if the defendant has discharged such an evidential onus then the plaintiff must establish on the whole of the evidence and on the balance of probabilities that his exposure to asbestos by the defendant caused or materially contributed to him contracting mesothelioma.

253 The High Court has held that a commonsense approach should be taken to causation: March v E & MH Stramare Pty Ltd [1991] HCA 12; (1991) 171 CLR 506 at 509.

254 In Fairchild Lord Hutton joined in allowing the appeals but did not consider that the House of Lords had laid down any new principle of law in McGhee. Lord Hutton took the view that an inference of actual causative effect should be drawn where it could be shown that the breach of duty had materially increased the risk of the victim contracting the disease that he had eventually contracted. Lord Hutton considered that the decision of the House of Lords in McGhee was based on an inference from the facts. At [109] of his speech, Lord Hutton said:

"Whilst there is very little practical difference between the two views I prefer, with respect, to take the view that the McGhee approach is based on the drawing of a factual or legal inference leading to the conclusion that the breach of duty was a cause of the disease rather than that the decision in McGhee laid down a new principle that, in cases where medical evidence as to the precise nature of the causation cannot be adduced, the material increase in the risk is taken in law to be a cause of the disease without reliance on a factual or legal inference."

Lord Hutton said in Fairchild at [104] of his speech that courts in Australia have also taken the view that the decision in McGhee was arrived at on the basis of an inference.

255 I have found that the plaintiff has proved a breach of duty by the defendant. The next question is whether the plaintiff has proved that the breach increased the risk of injury, that is of the plaintiff contracting mesothelioma.

256 It is common ground, and established by the evidence, that inhaling asbestos dust increases the risk of contracting mesothelioma. The risk of contracting mesothelioma is related to the dose of asbestos inhaled. Each inhaled fibre of asbestos increases the risk of the disease.

257 The plaintiff must prove that the defendant's negligent act or omission materially increased the risk of the plaintiff contracting mesothelioma. In McGhee their Lordships equated materially increasing the risk that the disease will occur and making a material contribution to its occurrence. In Bonnington Castings Ltd v Wardlaw [1956] UKHL 1; [1956] AC 613 at 621 Lord Reid observed:

"A contribution which comes within the exception de minimis non curat lex is not material, but I think that any contribution

which does not fall within that exception must be material. I do not see how there can be something too large to come within the de minimis principle but yet too small to be material."

258 The evidence establishes that the plaintiff's asbestos exposure resulting from his handyman activities materially contributed to the risk of him contracting mesothelioma. I will refer briefly to some of the relevant evidence.

259 In his report of 20 March 2006 Professor Musk stated his opinion that the cause of the plaintiff's mesothelioma was asbestos exposure "as described" that is, the plaintiff's handyman activities in 1983, 1985 and 1990.

260 Professor Robinson said in his report of 13 February 2006 that the plaintiff's mesothelioma is likely to be due to his asbestos exposure about 20 years ago whilst working on fences where he was cutting and drilling asbestos fences.

261 Professor Henderson said in his report of 17 April 2006 that the plaintiff's "handyman" exposures were significant for induction of his mesothelioma in that they represented exposures in excess of any background exposure derived from the environment at large for a control/reference urban or rural population with no identifiable occupational, domestic or environmental exposure to asbestos. Professor Henderson concluded therefore that the plaintiff's handyman exposure was significant for causation of his mesothelioma.

262 Dr Alvares, the cardiothoracic surgeon who performed the pleuropneumonectomy on the plaintiff, said that the plaintiff's exposure to the asbestos fibres of Hardiplank in 1982, 1983 and the early 1990s and the method of exposure, are powerful aetiological factors in causing the plaintiff's mesothelioma.

263 In his report of 12 March 2006 Dr Leigh stated his opinion that the plaintiff's total cumulative asbestos exposure during the period 1983 - 1990 was significantly greater than background exposure from the environment at large and the plaintiff's exposure to asbestos in 1983 - 1990 made a material contribution to causation of the plaintiff's mesothelioma.

264 The plaintiff's asbestos exposure resulting from his handyman activities materially contributed to the risk of the plaintiff contracting mesothelioma and the risk eventuated, that is the plaintiff did contract

mesothelioma. Accordingly, it will be taken that the defendant's breach of its duty of care caused or materially contributed to the plaintiff contracting mesothelioma unless the defendant discharges the evidential onus that its breach had no effect or that the plaintiff would have contracted mesothelioma even if its breach of duty had not occurred.

265 It is not sufficient for the defendant to lead evidence that the plaintiff might have contracted mesothelioma in the absence of the asbestos exposures from his handyman activities. In Tremeer McLure JA described the evidential burden as a burden to "show that the breach had no effect". In the statement of Gaudron J in Bennett v Minister for Community Welfare cited by McLure JA, Gaudron J said that "in the absence of evidence that the breach had no effect, or that the injury would have occurred even if the duty had been performed, it will be taken that the breach of the common law duty caused or materially contributed to the injury". In Tremeer McLure JA at [86] said that the "question is whether the appellant discharged its evidentiary onus of adducing evidence that the injury would have occurred even if soft sand had been provided". That is, to discharge the evidential burden upon it the appellant had to adduce evidence that the injury would have occurred even if soft sand had been provided not merely that the injury might have occurred even if soft sand had been provided. Her Honour found that the evidence of Mr Scull and the ETRS reports discharged that evidentiary burden. The ETRS reports concluded that the respondent would have suffered the same injury whether there was soft sand or a grass surface under the track line. Mr Scull concluded that it was highly unlikely that an identical impact on sand would not have caused a significant injury, that is that the respondent would not have been injured if he had fallen onto sand.

266 The defendant relies upon the evidence of Professor Berry, Mr Rodgers, Professor Breslin, and evidence adduced in chief or in cross-examination from Dr Francis, Professor Musk, Professor Robinson, Professor Henderson and Dr Leigh. I have already referred to the evidence of Professors Musk, Robinson and Henderson and Dr Leigh.

267 I will first consider the evidence of Mr Rodgers. As I have said, Mr Rodgers estimated the plaintiff's cumulative asbestos exposure from handyman activities and concluded that "there is around a 99.999% probability that the mesothelioma experienced by the plaintiff is a naturally occurring mesothelioma and the plaintiff would have experienced it regardless of his claimed exposure to asbestos".

268 Of fundamental importance to Mr Rodgers' calculations and his conclusion is his assessment or estimate of the plaintiff's cumulative asbestos exposure from his handyman activities. Mr Rodgers made that assessment or estimate by adopting or adjusting cumulative exposures for activities that Mr Rodgers considered to be similar to the plaintiff's handyman activities and that were recorded in documents or literature that Mr Rodgers referred to. The cumulative exposures recorded in those documents or literature were based upon tests of which Mr Rodgers has no personal knowledge or upon estimates made by other people. That raises the question of whether or not such assumed or accepted exposure estimates are admissible or may form a proper foundation for Mr Rodgers' opinions.

Admissibility and weight of expert evidence

269 If evidence tendered as expert opinion is based on assumed or accepted facts then for the opinion to be admissible the assumed or accepted facts must be identified and proved. It must be established that the facts on which the opinions are based form a proper foundation for the opinion and the opinion requires demonstration or examination of the scientific or other intellectual basis of the conclusions reached. If the court cannot be sure of those matters then the evidence is strictly speaking not admissible, and, so far as it is admissible, is of diminished weight: Makita (Australia) Pty Ltd v Sprowles [2001] NSWCA 305; (2001) 52 NSWLR 705 at [85] per Heydon JA.

270 Proof means either that the facts upon which the opinion is based must be established by direct evidence from people who have perceived them. If the facts on which the opinion is based are not facts which the expert has perceived personally, they are hearsay and thus prima facie inadmissible. However, an expert may express an opinion based upon the research and writings of others, including unpublished statistical material: Brawski v Quayle [1966] VicRp 54; [1966] VR 382; R v Abadon [1983] 1 WLR 364. The court must be able to test, or at least assess the reliability, of the material assumed by the expert as the basis for his opinion. If that material is numerical data collected by others, the expert may still be able to express an opinion. In Abadon v The Queen [1983] 1 WLR 126 at 129 the English Court of Appeal said:

"In the context of evidence given by experts it is no more than a statement of the obvious that, in reaching their conclusion, they must be entitled to draw upon material produced by others in the field in which their expertise lies. Indeed, it is part of their

duty to consider any material which may be available in their field, and not to draw conclusion merely on the basis of their own experience, which is inevitably likely to be more limited than the general body of information which may be available to them. Further, when an expert has to consider the likelihood or unlikelihood of some occurrence of factual association in reaching his conclusion, as must often be necessary, the statistical results of the work of others in the same field must inevitably form an important ingredient in the cogency or probative value of his own conclusion in the particular case. Relative probabilities or improbabilities must frequently be an important factor in the evaluation of any expert opinion and, when any reliable statistical material is available which bears upon this question, it must be part of the function and duty of the expert to take this into account."

271 Of course, the information on which Mr Rodgers drew was not statistical information. It was the outcome of tests done by other people to ascertain the amount of asbestos released in the air when conducting particular activities in particular situations.

272 I am not satisfied that the information on which Mr Rodgers drew was sufficiently reliable for any weight to be given to the conclusions which Mr Rodgers drew.

273 Mr Rodgers prefaced his estimate or calculation of the plaintiff's cumulative exposure from work on the Hardiplank fence and other handyman work with the following assumptions:

"Mr Hannell alleges that it took him four days @ five hours each day to complete the work. I will assume for the purpose of this report that the handling and occasional cutting of previously painted Hardiplank fence would amount to 10% of the 1 fibre/ml or less exposure experienced by tradesman working with asbestos cement products ie 0.1 fibre/ml or less."

274 The exposure of 1 fibre/ml or less experienced by tradesmen working with asbestos cement products is an estimate explained by Mr Rodgers elsewhere in his report. It is based upon published airborne fibre concentrations generated by types of work in other situations that Mr Rodgers considered to be similar to the plaintiff's handyman activities.

275 In s 4 of his report Mr Rodgers sets out the cumulative exposure applicable to various activities working on asbestos cement products. In relation to "handling, drilling, rasping and cutting flat or moulded products" Mr Rodgers said:

"Based on my review of the available data specifically that reported by German and Australian studies conducted on actual building sites, I conclude that the daily time weighted average exposure of workers cutting, handling and fixing asbestos cement products in the building industry is around 1.25 fibres/ml or less. The proportion of time spent in the working week doing such work and the number of years of such activities is subject to information obtained directly or indirectly from the working history of the individual."

276 Elsewhere in s 4.1 of his report, Mr Rodgers refers to a number of "Australian studies". The first is a letter of 7 November 1974 from James Hardie to Dr Heyworth of the Western Australian Department of Public Health. Another is the James Hardie Asbestos-Cement Cutting Tools Study, February 1980. A third is the James Hardie inter-house letter of 20 May 1977 from John Winters, industrial hygiene engineer. In appendix A1 Mr Rodgers refers to the same sources. Mr Rodgers also refers to "exposure of 0.1 fibre/ml or less while doing the specific cleanup of asbestos cement", based on 1984 results provided to the Victorian government authority for shovelling and sweeping up asbestos cement waste during demolition work. In cross-examination Mr Rodgers said that the information was provided in answer to a request by the Victorian Government to consultants involved in monitoring asbestos removal to provide all their results and put them into various categories, one of which was cleaning up the site.

277 In s 4.1 of his report Mr Rodgers refers to a German report "Faser Jahre BK Report HVBG 1/97".

278 One of Mr Rodgers' sources was a letter of 7 November 1974 from James Hardie to Dr Heyworth of the Western Australian Department of Public Health. In that letter Mr Seares, the State Manager in Western Australia of James Hardie, said that the company's industrial hygiene engineer had collected "two long term samples from men engaged in the erection of asbestos cement fences" and said that the results had been advised to him in a letter from Dr McCullagh. The results were that one contractor had recorded airborne asbestos level of 0.8 fibres/ml over a two and a half hour period and the other contractor had an airborne asbestos

level of 0.4 fibres/ml over a period of almost five hours. In his letter Mr Seares referred to his understanding that the Department of Public Health had conducted some tests some seven months earlier that "collected some ten minute operator breathing zone samples during the actual cutting operation". Mr Seares said that "[t]hese will naturally give a far higher count that the time-weighted average on which the N.H.&M.R.C. standard is based".

279 Mr Rodgers said that the James Hardie letter was the only source material for determining the value for exposure to cutting asbestos corrugate. There was, of course, no evidence of the accuracy or reliability of the two tests referred to in Mr Seares' letter. Mr Rodgers was referred to some subsequent correspondence from James Hardie in which the chief industrial hygiene engineer expressed some reservations about using the membrane filter method for measuring airborne asbestos outside their factories. That appears to be the method used in the tests referred to in Mr Sears' letter. Mr Rodgers agreed that there were problems in using that method outside the factory. Mr Rodgers said that he was not aware of any results done from testing in domestic settings such as that in which the plaintiff undertook his activities.

280 The small sample of two tests, and the widely divergent results of those two tests, is sufficient itself to cast doubt on the reliability of the data. Furthermore, nothing is known of the circumstances in which the tests were carried out and there is no basis for any degree of satisfaction that the measurements were accurate or reliable. The form in which the material was available to Mr Rodgers is at least third hand hearsay. Finally, the tests were conducted and the information assessed and conveyed by James Hardie at a time when it had an interest to minimise the concern about the amount of asbestos dust generated by such activities.

281 Mr Rodgers relied upon the James Hardie asbestos-cement cutting tool study of February 1980 to state that "field tests at North Ryde NSW, on re-cutting of a cottage, (unpainted Hardiplank) indicated for a total of 19 linear metres cut, with 3.3 per cent of the working day spent cutting, resulted in an exposure of 0.4 fibres/ml". The relevant s 5.2.4 of the study states that "only one fibre count has been obtained from field testing so far" and then refers to the field test at North Ryde. Once again, the limited information available to Mr Rodgers and to the court about the way in which the test was conducted and the measurements made, together with the small sample and the circumstances in which it was conducted make it such that I am not satisfied that the test forms a reliable

basis for an expression of Mr Rodgers' opinion as to the asbestos exposure that the plaintiff experienced in carrying out the handyman activity or activities.

282 The third James Hardie data Mr Rodgers relied upon was the James Hardie inter-house letter of 20 May 1974 from John Winters, industrial hygiene engineer. Again, the source of the information, the limited information available and the circumstances of the data do not satisfy me that it is sufficiently reliable to form a proper foundation for Mr Rodgers' opinion concerning the asbestos exposure of the plaintiff from the relevant activity.

283 Mr Rodgers placed considerable weight upon the German material referred to. Having considered Mr Rodgers' evidence about this matter and in particular his cross-examination I am left with a lack of confidence that the materials and activity the subject of the German study are sufficiently similar to that of the activity undertaken by the plaintiff in the circumstances in which he undertook those activities for the German data to be a sufficiently reliable basis for Mr Rodgers' opinion.

284 In the end, I am not satisfied that the material which Mr Rodgers used to form his opinion as to the cumulative asbestos exposure of the plaintiff arising from his handyman activities is sufficiently reliable to form a proper foundation for his opinion. Mr Rodgers' calculations are based upon unpublished results of tests where there is no evidence of the scientific reliability of those tests. Mr Rodgers has done the best he can to compare the handyman activities undertaken by the plaintiff with results he has found in a variety of sources. But they are simply not sufficiently reliable or scientifically based to form a proper foundation for the assumptions and estimates made by Mr Rodgers.

285 There is a second and independent reason why I place no weight upon Mr Rodgers' conclusion concerning the plaintiff's cumulative exposure from his handyman activities and Mr Rodgers' opinion concerning the probability that the plaintiff's mesothelioma "is a naturally occurring mesothelioma that the plaintiff would have experienced regardless of his claimed exposure to asbestos".

286 I have referred to only parts of the evidence of Mr Rodgers concerning how he assessed and calculated the cumulative exposure of the plaintiff in the course of carrying out the handyman activities he described. On considering the whole of the Mr Rodgers' evidence I am not satisfied that his calculation or assessment of the cumulative exposure

of the plaintiff from the handyman activities is sufficiently reliable or accurate to provide a proper basis for calculating the relative risk of contracting mesothelioma from the handyman activities compared to "background exposure". There are simply too many assumptions, estimates and variables involved in Mr Rodgers' calculations.

287 There is a third, separate and independent reason why I do not accept Mr Rodgers' conclusion that "there is around a 99.999% probability that the mesothelioma experienced by the plaintiff is a naturally occurring mesothelioma". Mr Rodgers bases his opinion on the "background risk" of mesothelioma. Mr Rodgers says this "background risk" is due to natural or artificial low level asbestos contamination in the environment, other environmental agents or due to genetic factors.

288 One of the background risk rates that Mr Rodgers relies upon is the Western Australian Advisory Committee on Hazardous Substances, Asbestos Cement Products, August 1980 which estimated the background rate of mesothelioma in Western Australia as 2-3 per million adults per year, a lifetime risk of 140 to 210 per million. Professor Musk was a member of that Committee. Professor Musk agreed with senior counsel for the defendant that the group who are generally described as members of the background risk are that group who present and are unable to recall a particular exposure to asbestos. Professor Musk earlier said in relation to the group who are unable to recall a particular exposure to asbestos that the number of mesothelioma sufferers who are unable to recall any particular exposure to asbestos depends on the quality of the questions and the intensity of the questioning process. Professor Musk, and indeed Professor Robinson and Professor Henderson, did not equate the "background risk" as being due to natural or artificial low level asbestos contamination in the environment, other than environmental agents or genetic factors. They included in the "background risk" specific exposures to asbestos that the sufferer had been unable to recall.

289 In this case the plaintiff was subject to careful, thorough and at times intense cross-examination as to other specific exposures to asbestos he may have experienced. I have found that the only specific exposures to asbestos experienced by the plaintiff were those arising from his handyman activities in 1983, 1985 and 1990.

290 Mr Rodgers' conclusion is based upon the number of persons in the Australian, or Western Australian, population contracting mesothelioma without any recalled significant exposure to asbestos. The Western Australian Advisory Committee on Hazardous Substances, Asbestos

Cement Products, August 1990 estimated that 2 to 3 per million adults in Western Australia per year contract mesothelioma without any recalled significant exposure to asbestos. What differentiates the plaintiff from the "background risk" group is that the "background risk" group includes people who experienced a significant exposure to asbestos, other than low level environmental exposure, but who did not recall it. The plaintiff has been subjected to careful and intensive cross-examination to determine whether he experienced asbestos exposure, other than that arising from his handyman activities and low level environmental exposure. I have found that the plaintiff did not experience any material asbestos exposure other than that from his handyman activities and low level environmental exposure. Thus, the probability of the plaintiff contracting mesothelioma from exposures other than the handyman exposures is not equivalent to that of the "background risk" group.

291 The defendant relied in the alternative on the evidence of Dr Francis of the plaintiff's cumulative asbestos exposure from his handyman activities to establish that the background risk of contracting mesothelioma is greater than the risk of the plaintiff contracting mesothelioma from his handyman activities. I find Dr Francis' calculations and quantitative conclusions to be no more reliable than those of Mr Rodgers.

292 Dr Francis' evidence-in-chief was principally contained in a report of 2 May 2006. At par 6.1 Dr Francis opined that the likely exposure to asbestos of the plaintiff when he carried out home maintenance would have been substantially greater than background exposure derived from the environment at large. Dr Francis goes on to say that when the plaintiff cut the Hardiplank fence with a handsaw she estimates that he would have been exposed for about 10 per cent of the time to airborne asbestos levels of about 3 fibres per millilitre or about 300 times general environmental background levels. Dr Francis assigns the latter at 0.01 f/ml "from my extensive personal experience with air sampling in such environments, although I have just as often found environmental background levels of "It is unknown what proportion of these really had an incident of exposure that was not detected by the survey techniques."

299 Further, after referring to the general background risk rate of 2 per million per year Professor Berry then says that:

"... it is possible that this rate includes some people whose mesothelioma was caused by some unknown specific exposure, and a rate of about 1 per million may be appropriate, corresponding to a lifetime risk of 70 per million."

300 Importantly, Professor Berry concludes his discussion of background risk with this statement:

"Thus for the 18% of mesothelioma cases in Australia for whom no evidence of even slight exposure was found, it cannot

necessarily be concluded that these mesotheliomas were not due to asbestos exposure, but only that they were not due to any specific exposure that was extracted from an occupational and environmental history."

301 The background risk rate of suffering mesothelioma which Professor Berry compares with the risk of suffering mesothelioma as a result of the plaintiff's handyman exposures is not the risk of suffering mesothelioma without any specific asbestos exposure. Professor Berry does not have a background risk rate derived from mesothelioma sufferers whose mesothelioma is not due to any specific exposure. The background risk rates from which Professor Berry makes his calculations are based upon mesothelioma sufferers who are unable to recall any specific asbestos exposure but who may have experienced a specific asbestos exposure. I have found that the plaintiff has not experienced any specific asbestos exposure other than the handyman exposures. Accordingly, the background risk rates used by Professor Berry do not apply to the plaintiff.

302 Professor Breslin is a thoracic physician. Professor Breslin has not examined the plaintiff but provided an opinion based upon materials provided to him including Mr Rodgers' detailed report of 20 March 2006. Professor Breslin referred to "background mesotheliomas" and said:

"There is a background incidence of mesothelioma that is seen in people who have no history of occupational or obvious environmental exposure to asbestos other than the background exposure which we all encounter. Up to 20% of patients with mesothelioma have no identifiable history of definite exposure. This background incidence has been calculated by a number of authors including Mr Rodgers and he estimates that the lifetime background risk for the Australian population where there is no history of asbestos exposure is 260 per million. This means that there is a definite incidence of mesothelioma in the population where no history of asbestos exposure could be encountered and the assumption is made that such individuals either cannot remember or have forgotten the particular time of exposure or that the environmental exposure to which all of us are exposed is sufficient in them to induce the development of mesothelioma." (Emphasis added.)

303 In forming his opinion Professor Breslin relies upon a number of assumptions including: "The cumulative exposure to asbestos that he claims has been calculated by Mr Rodgers as 0.002 fibres/ml years ...". Professor Breslin also says that the plaintiff's history is incomplete and he does not have details of whether the plaintiff may have encountered asbestos through his father's occupation or some other domestic exposure or even in his own work. The plaintiff was carefully and at times intensively cross-examined about those matters and I have found that the plaintiff had not encountered asbestos in those ways.

" ... it is unlikely that the claimed asbestos exposure made a significant contribution to the development of his mesothelioma and that it is more probable than not that he has either forgotten some earlier asbestos exposure of more significance or that his mesothelioma was due to background environmental exposure."

305 That opinion was expressly based on, amongst other things, "the very very low total asbestos exposure". I do not accept the total asbestos exposure estimated or calculated by Mr Rodgers. For that reason I do not accept Professor Breslin's opinion. Furthermore, I find that the plaintiff has not forgotten some earlier asbestos exposure of more significance.

306 Professor Breslin goes on to express the same opinion in a different way by saying that it is more probable than not that the claimed exposure made no significant contribution to the development of his mesothelioma or put another way, his contribution was de minimis. I do not accept that opinion for the reasons I have stated.

Defendant has not discharged evidential onus

307 The defendant has not discharged the evidential onus upon it to show that its breach of duty had no effect or that the plaintiff would have contracted mesothelioma even if its duty had been performed. I find that the defendant's breach of duty caused, or materially contributed to, the plaintiff developing mesothelioma.

308 If, as a matter of law or fact, and contrary to my findings, there is no evidential onus on the defendant of adducing evidence that its breach of duty had no effect or that the plaintiff would have contracted mesothelioma even if its duty had been performed or if, contrary to my findings, the defendant has discharged that onus then it is necessary to

determine whether the plaintiff has in those circumstances discharged the legal onus of establishing on the balance of probabilities that the defendant's breach of duty caused or materially contributed to the plaintiff developing mesothelioma. That is, should an inference be drawn leading to the conclusion that the defendant's breach of duty was a cause of the plaintiff's mesothelioma or materially contributed to it?

309 The evidence of the medical experts is to the effect that the plaintiff's handyman exposure increased the risk of contracting mesothelioma but it was not possible to say that the plaintiff's handyman activities caused him to contract mesothelioma because once a person has the disease medical science is not able to detect which asbestos exposure caused it. That is because, as Dr Leigh expressed it, there is no way of knowing which fibre did what to which cell at which time.

310 The concepts of proof and probability in the legal sense are different from the scientific concepts. If a person had worked at the Wittenoom asbestos mine, mining blue asbestos for 20 years, it would not be possible to prove, according to scientific concepts of proof, that the person's mesothelioma was caused by inhaling asbestos fibres in the course of his employment. That is because it is not possible to identify the particular asbestos fibre or fibres that started or progressed the process leading to the growth of the tumour. It is possible that the Wittenoom miner may have inhaled an asbestos fibre as part of background exposure that led to the development of the mesothelioma. However, legal proof is different from scientific proof. In State of New South Wales t/a New South Wales Department of Agriculture v Allen [2000] NSWCA 141 at [2] Priestley JA said that there is a major cleavage between proof of fact in a non-criminal court case to the satisfaction of the fact-finding tribunal on the balance of probabilities and proof of a fact for scientific purposes to the satisfaction of those expert in the particular field of science. His Honour said that the latter kind of proof is much more rigorous and demanding than the former. The law does not require scientific proof but rather proof on the balance of probabilities on the whole of the evidence, both scientific and lay.

311 It is common ground, and established by the expert medical opinion, that inhalation of asbestos fibres caused, or materially contributed to, the plaintiff's mesothelioma. Three possible sources of asbestos inhalation had been identified. The plaintiff's handyman activities, some specific exposure or exposures that the plaintiff did not recognise or has forgotten and the background exposure in the sense of ambient environmental exposure as I have earlier described it.

312 I have already referred to the evidence of the principal expert witnesses. Professor Musk opined that the cause of the plaintiff's mesothelioma was asbestos exposure as a result of his handyman activities in 1983, 1985 and 1990. Professor Robinson considered that the plaintiff's mesothelioma is likely to be due to his asbestos exposure in the course of those handyman activities. Professor Henderson said that the plaintiff's handyman exposures were significant for induction of his mesothelioma in that they represented exposures in excess of any background exposure derived from the environment at large. Professor Henderson concluded that the plaintiff's exposure was significant for causation of his mesothelioma. Dr Alvares said that the plaintiff's handyman exposures are clearly powerful etiological factors in causing the plaintiff's mesothelioma. Dr Leigh stated his opinion that the plaintiff's total cumulative asbestos exposure from his handyman activities was significantly greater than background exposure from the environment at large and the plaintiff's handyman exposure made a material contribution to causation of his mesothelioma.

313 Contrary views were expressed by Professor Berry and Professor Breslin. However, for the reasons I have given, I attach no weight to their opinions that the plaintiff's handyman exposures did not contribute to the plaintiff contracting mesothelioma, or at least that the background risk of suffering mesothelioma was greater or much greater than the risk of the plaintiff contracting mesothelioma from his handyman exposures.

314 I prefer the evidence of the medical experts - Professor Musk, Professor Robinson, Professor Henderson, Dr Alvares and Dr Leigh - to that of the industrial hygienists - Mr Rodgers and Dr Francis - on the issue of the contribution of the plaintiff's handyman asbestos exposures to the plaintiff contracting mesothelioma and the risk of the plaintiff contracting mesothelioma from his handyman exposures compared with the background risk.

315 Having regard to my findings based on the evidence of the plaintiff and the opinions of the medical experts and industrial hygienists I draw the inference that the plaintiff's handyman exposures caused or materially contributed to him contracting mesothelioma.

1. The defendant breached the duty of care it owed to the plaintiff.

2. That breach of duty increased the risk of the plaintiff contracting mesothelioma.

3. That risk eventuated in that the plaintiff did contract mesothelioma.

4. There is no evidence, or evidence that I accept, that the defendant's breach of duty had no effect or that the plaintiff would have contracted mesothelioma even if the defendant had performed its duty.

317 Having regard to the legal principles of causation I have discussed earlier I conclude that having made those findings it is to be taken that the defendant's breach of duty caused or materially contributed to the plaintiff contracting mesothelioma.

318 Alternatively, if the proper approach to causation as a matter of law or in the factual circumstances of this case is to determine whether it should be concluded as a matter of inference and on the balance of probabilities that the defendant's breach of duty was a cause, or materially contributed to, the plaintiff contracting mesothelioma, then I find that the inference should be drawn in this case.

319 For those reasons, I conclude that the defendant's breach of duty of care caused, or materially contributed to, the plaintiff contracting mesothelioma.

320 The defendant submits that if there was a duty to advertise, a breach was not causal, that is the negligence of the defendant was not a cause of the plaintiff's injuries.

321 In Cole v South Tweed Heads Rugby League Football Club [2004] HCA 29; (2004) 217 CLR 469 at [82] Gummow and Hayne JJ said that the critical question in that case was whether the negligence of the defendant was a cause of the plaintiff's injuries. Their Honours said that the duty that must be found to have been broken is a duty to take reasonable care to avoid what did happen, not to avoid "damage" in some abstract and unformed sense.

322 The defendant says that the plaintiff would not have seen or responded to advertisements.

323 In his witness statement the plaintiff said that there were no warning labels on any of the products he handled and he was never made aware

that the products were dangerous. He was never advised about any risk or danger in doing any of the work that he did on the asbestos cement products. The plaintiff said that if he had known that exposure to asbestos could cause cancer he would have either worn effective respiratory protective equipment or not done the work at all and got someone in to do all of the work.

324 The plaintiff described himself as someone who is very careful to follow instructions on equipment. He said that if he had been provided with instructions on how to properly handle asbestos he would have followed the instructions.

325 The plaintiff said that he is not an avid news watcher but he watches the news if it is on. The only newspaper he gets is the Sunday paper. Most of the time he listens to the radio at work but mainly Classic FM. In cross-examination the plaintiff said that he used to get a paper on Wednesday but that was some years ago.

326 In cross-examination the plaintiff was shown a number of articles relating to asbestos risks published in newspapers from 1983. The plaintiff did not recall having seen any of them. The defendant submits that it should be inferred that the plaintiff would not have seen public announcements or advertisements placed in the newspaper by the defendant concerning asbestos risks even if they had been published in newspapers circulating in the Perth area in 1983. I do not accept that argument. There is a significant difference between an announcement or advertisement by the manufacturer of a product that there is a risk of cancer from using the product and that the risk may be avoided or minimised by following certain preventive steps on the one hand and on the other hand information or opinions concerning asbestos risks emanating from some other person.

327 It may be inferred, and I do infer, that if in or before 1983 the defendant had made public announcements or placed advertisements in a Perth daily or weekly newspaper monthly or more frequently saying that a handyman or casual user of asbestos cement building products ran a risk of contracting mesothelioma and that the risk could be minimised by the taking of certain steps then that information is likely to have come to the attention of a person such as the plaintiff who watched the news, listened to the radio and regularly read a newspaper, even if only weekly. It may be inferred, and I do infer, that it is likely that the information would have come to the attention of the plaintiff either directly or through

republication or repetition by other media sources or family, friends, work colleagues or other acquaintances.

328 All that the defendant did to bring the risk of using the asbestos cement products and preventive steps to minimise the risk to the attention of the public was to place inadequate labels on its products, distribute some literature in hardware stores and conduct a "road show" for store retailers. The steps taken by the defendant were wholly inadequate to bring the risks home to the class of persons to which the plaintiff belonged. The defendant's failure to take those steps was a failure to take reasonable care to avoid what did happen to the plaintiff, that is the exposure to asbestos that the plaintiff experienced in 1983, 1985 and 1990 when working on the defendant's asbestos cement building products as described in his evidence and his resulting contracting of mesothelioma.

329 I find that the defendant's breach of duty was relevantly causal to what did happen to the plaintiff, that is the exposure to asbestos in the course of his handyman activities, which I have found in fact caused or contributed to him suffering mesothelioma.

330 The plaintiff is entitled to recover from the defendant damages for the defendant's breach of duty that caused, or materially contributed to, the plaintiff contracting mesothelioma.

331 The plaintiff claims damages under a number of headings. The plaintiff and the defendant agree on the quantum of some heads of damages but not on others. The heads of damages which have not been agreed are:

332 The parties have agreed the following heads of damages in the following amounts:

Interest on past out of pocket expenses (on non-Medicare and non-Medibank items only)

333 Non-pecuniary damages include damages for pain and suffering, loss of amenities of life, loss of enjoyment of life and loss or curtailment of expectation of life. The parties dealt with non-pecuniary damages under the heads of loss of expectation of life and general damages including pain and suffering, loss of amenities of life and loss of enjoyment of life. I will do the same.

334 In "Assessment of Damages for Personal Injury and Death", 4th ed Harold Luntz says at [7.1.5] that justice requires treating like cases alike and that, though it is sometimes denied that any two cases of personal injury are really alike, consistency of treatment necessarily involves a notional tariff as the starting point for the ascertainment of the damages for non-pecuniary loss in any particular case. Section 10A(1) of the Civil Liability Act 2002 (WA) provides that in determining damages for non-pecuniary loss, a court may refer to earlier decisions of that or other courts for the purpose of establishing the appropriate award in the proceedings and that for that purpose the parties to the proceedings or their counsel may bring the court's attention to awards of damages for non-pecuniary loss in those earlier decisions.

335 Senior counsel for the defendant submitted in his written outline of closing submissions that decided cases establish a range of damages between $110,000 and $180,000. Counsel for the plaintiff in his closing written submissions submitted that that is not correct. Counsel submitted that there have been a number of awards delivered in mesothelioma cases in recent years for general damages in excess of $180,000. They include:

• Hart v Amaca Pty Ltd [2004] NSWDDT 10 - an award of $200,000;

• Lynch v Amaca Pty Ltd [2004] NSWDDT 1 - award of $200,000;

• Clyne v State Rail Authority of New South Wales [2005] NSWDDT 4 - award of $190,000;

• Smith v Sydney Water Corporation Ltd [2000] NSWDDT 13 - award of $200,000;

• Gaunt v Amaca Pty Ltd, unreported; Ddt of NSW (Curtis J); Library No 151; 28 August 2003 - award of $220,000.

336 Counsel for the plaintiff referred the Court to the following recent awards in this Court to a plaintiff with mesothelioma:

• Misiani (as Executor of the Will of Misiani (dec)) v Welshpool Engineering Pty Ltd (in liq) [2003] WASC 263 - award of $150,000 (in a claim assessed after the death of the sufferer;

• McGilvray v Amaca Pty Ltd [2001] WASC 345 - award of $160,000;

• Easther v Amaca Pty Ltd [2001] WASC 328 - award of $130,000.

337 I must have regard to the fall in the value of money even in relatively low inflationary years but as Luntz points out at [7.1.5] the High Court has warned of the need to be alert to the danger of carrying over the familiar complaint that prices and wages are too high into the immediate response to any amount of damages: "The compensatory nature of an award of damages requires that it should be wholly unaffected by any instinctive time lag in one's adjustment to new levels of prices and wages".

338 The plaintiff is aged 63. The plaintiff was shocked to be informed by Professor Robinson on 17 November 2005 that he had a life expectancy of six to 12 months. The plaintiff has undergone two surgical procedures.

The procedures were very painful. Since the pneumonectomy the plaintiff has undergone three cycles of chemotherapy that have made him feel sick and caused some constipation, diarrhoea and an upset stomach. The plaintiff has an awful amount of trouble breathing and gets pain in his chest. At the time of giving evidence the plaintiff said that he spent most of his day at home, which is extremely frustrating but if he goes out he can only walk short distances and must have breaks which he finds frustrating and he gets nervous and anxious when in public places.

339 The plaintiff submits, and I accept, that the pain and suffering of the plaintiff is immense. I also have regard to the evidence of Professor Robinson as to the horrific nature of this disease and the pain and suffering associated with it.

340 It is relevant to consider the plaintiff's life expectancy and hence the duration of his suffering.

341 Professor Musk examined the plaintiff on 20 March 2006. After examining the plaintiff Professor Musk provided an opinion that the plaintiff had an expectation of survival of three to four years.

342 Mr John Alvarez is the plaintiff's treating cardiothoracic surgeon who conducted surgery on the plaintiff. Mr Alvarez provided a report on 14 February 2006 in which he said:

"The patients we have selected as suitable for tri modality therapy (plueropneumonectomy, combination chemotherapy and radiotherapy) we expect/hope to confer a better diagnosis. Data from North America (Dana-Faber Cancer Institute, Boston, US) has yielded 5-year survival in these select group of 48%."

343 Mr Alvarez said that it remains to be seen whether this result can be replicated in Australia. Counsel for the plaintiff submitted that in giving evidence the plaintiff indicated that he had only just given up driving, he rises himself and gets in and out of bed himself, dresses himself (except for doing his shoes up) and at the time of giving evidence was walking unaided. Having regard to all those matters I find that the plaintiff has an expectation for survival of approximately three and a half years.

344 The plaintiff had had some health problems associated with his heart and some high blood pressure. However, he said that before the onset of the mesothelioma symptoms he was healthy. I accept that prior to the onset of the mesothelioma symptoms the plaintiff was in generally good

health in that he was not incapacitated or inconvenienced by any heart or blood pressure problems.

345 The plaintiff said in his statement that he is extremely sad that he and his wife will not be able to retire together because they had had a long and happy marriage and looked forward to relaxing and spending time together.

346 I assess general damages in the sum of $180,000.

347 Counsel for the plaintiff says that the plaintiff's loss of expectation of life is a loss of 21.78 years of life having regard to the Life Tables, Life Expectancies Australia, 2005.

348 A conventional sum is awarded for this loss: Skelton v Collins [1966] HCA 14; (1966) 115 CLR 94; Sharman v Evans [1977] HCA 8; (1977) 138 CLR 563. The defendant says that the conventional sum is $15,000. The plaintiff says that an award of $20,000 should be made.

349 At [3.4.4] Luntz says that the Tables of Quantum of Damages in Australian current law in the 1990s reveal that, where a separate amount was specified for this head, awards ranged from $500 to $8,000, though in one reported case in New South Wales counsel's suggestion that the range was $5,000 to $20,000 was not challenged.

350 In McGilvray v Amaca (supra) Pullin J noted that the plaintiff could have expected to live for another 28.7 years and that the award of damages under this head is a conventional sum. His Honour allowed $15,000. In Easther v Amaca (supra) Scott J allowed $15,000 in circumstances where the plaintiff was almost 67 years of age. In Misiani (supra) Barker J also allowed $15,000 under this head of damage.

351 I award $15,000 for loss of expectation of life.

352 Before the onset of his mesothelioma symptoms the plaintiff was employed by the Perth Zoo as a gardener. If he remained in that employment he would presently be earning $555 net per week.

353 The plaintiff gave evidence that his intention was to continue to work for as long as he could at the Perth Zoo and had no plans on retiring before 70 years. He was not cross-examined on those matters. His

employer provided a letter that the Perth Zoo does not have a mandatory retirement age and places no age restriction on employment and that if the plaintiff was otherwise well, there is nothing that will prevent him from continuing his employment at Perth Zoo until aged 70 or beyond. But for his now expected premature death from mesothelioma the plaintiff would have obtained aged 70 in six years five months' time from the date of trial. I have found that the plaintiff has a life expectancy of approximately three and a half years at the time of trial.

354 For a further three and a half years from the date of trial at $555 net per week using 6 per cent multiplier (of 167) for three and a half years the loss is $92,685. From that some deduction must be made for the balance of adverse contingencies over favourable contingencies. The plaintiff suffered a myocardialinfarct about three years ago. At the same time he was found to suffer high blood pressure and elevated cholesterol. On the other hand, the plaintiff was not incapacitated or inconvenienced at the time of trial and said that he was in good health. Three and a half years after trial the plaintiff would have been in his 68th year. I find that the plaintiff's loss of earning capacity for the three and a half years after trial should be discounted by 15 per cent. That makes a loss of $78,782.

355 But for his now expected premature death from mesothelioma the plaintiff would have obtained age 70 in six years five months time. However, the plaintiff now has a life expectancy of approximately three and a half years from the date of trial, that is to about November 2009. During those "lost years" expenses that would necessarily have been incurred by the plaintiff in producing the earnings, but that are now saved, must be deducted from the earnings that are used as the basis for the calculation of damages for lost earning capacity: see Luntz at [5.4.3]. I deduct an amount of $100 per week on that account. To work out the plaintiff's loss of earning capacity from November 2009 to October 2012 (ie the lost years) the 6 per cent multiplier for three and a half years, that is 167, is subtracted from the 6 per cent multiplier for six years five months, that is 282, that is a multiplier of 115. Applying a multiplier of 115 to a loss of $455 per week gives a loss of $52,235. I apply a slightly higher discount rate for adverse contingencies for working years between the age of 68 and 70 than for younger years. I apply a discount rate of 18 per cent. That gives a loss of $42,832.70 for the "lost years".

356 I assess future loss of earning capacity at $78,782.00 plus $42,832.70, that is $121,614.70.

357 The plaintiff's employer would have contributed superannuation at 9 per cent of his gross pay of $36,463.00, that is $3,281.67 per annum or $63.11 per week. For a further six years five months from the date of trial at $63.11 per week using 6 per cent multiplier for six years five months [282] gives $17,797.02. Deducting 16 per cent for contingencies gives $14,949.50.

358 The plaintiff's wife gave evidence that she estimates the plaintiff needs approximately three hours of care per day for meal preparation and tasks that the plaintiff is unable to do himself. The plaintiff's daughter gave evidence that she estimates the amount of care the plaintiff requires presently is approximately three hours per day shared between her mother, her sister and herself. She referred to transporting the plaintiff to and from medical appointments and the plaintiff's severely restricted mobility.

359 Ms Raylene Nestler is a qualified registered nurse experienced in providing assessments for the future care of complex cases for clients with disabilities. Ms Nestler gave evidence of the costs of care that the plaintiff is likely to require in the end stages of his disease, a period of nine months.

360 I accept that in the two years and nine months from the date of trial the plaintiff will require assistance of the sort that his wife and daughter gave evidence. I allow damages for future assistance on the basis of two hours per day at a rate of $28.35 per hour, the commercial rate advanced by the plaintiff. The allowance for the next two years and nine months should be calculated as $28.35 per hour multiplied by two hours per day multiplied by seven days per week, that is $396.90 per week. The multiplier for two years and nine months is 133. Accordingly, the allowance for the next two years and nine months is $396.90 multiplied by 133, that is $52,787.70. I deduct 10 per cent for adverse contingencies and allow $47,508.93 for that period.

361 Ms Nestler has calculated the likely costs of the plaintiff's final nine months care to be $26,822.90 for six months, $49,950.40 for the next three months and $5963.80 for the last week. I am not satisfied that all of the allowances claimed and calculated are appropriate. It is difficult to calculate an appropriate allowance having regard to every item referred to by Ms Nestler. That is because the duration of the end stages of the plaintiff's care cannot be predicted with any accuracy and the particular

care that he will need is not certain. In the course of cross-examination Ms Nestler properly conceded that the precise care and services that the plaintiff will require cannot be predicted with certainty. As Ms Nestler said things can change quite quickly with this type of disease with the plaintiff's breathlessness and ability to help himself and the plaintiff may or may not be able to do certain things for himself in the final nine months of his life. I allow an amount of $50,000 in respect of the final or end stage of the plaintiff's care. Thus, I allow an amount of $97,508.93 for future care and services.

362 The plaintiff claims $47,984.62 for future out of pocket expenses. That is based upon an estimate of future care by Professor Robinson in the amount of $35,143.30. Additionally, the plaintiff claims pharmaceutical costs at $45.00 per week and equipment needs of $7,190.50.

363 The defendant submits that Professor Robinson allowed $3,456.00 for domiciliary nursing which overlaps with the care/services claim. The defendant further says that Professor Robinson has allowed more than $10,000.00 for medication, yet the plaintiff has made claim for another $9,165.15 for pharmaceutical costs. Thirdly, the defendant says that Professor Robinson also allowed for hospital admissions but this was based upon some speculation due to complications and should be separately discounted. The defendant says that the claim should be reduced to an amount in the order of $20,000.00.

364 I accept that there is some overlap between the amounts allowed by Professor Robinson on the one hand and the claim for care/services and pharmaceutical costs on the other hand. I also accept that there should be some discount for the allowances made by Professor Robinson for hospital admissions. I do not think that these matters are capable of precise arithmetic calculation. I allow an amount for $35,000.00 for future out of pocket expenses.

Interest on past out of pocket expenses (on non-Medicare and non-Medibank items only)

366 The plaintiff is entitled to judgment in the sum of $537,032.99.