Lo Presti v Ford Motor Company of Australia Ltd [No 2]
[2008] WASC 12
•19 FEBRUARY 2008
JURISDICTION : SUPREME COURT OF WESTERN AUSTRALIA
IN CIVIL
CITATION: LO PRESTI -v- FORD MOTOR COMPANY OF AUSTRALIA LTD [No 2] [2008] WASC 12
CORAM: BEECH J
HEARD: 24, 26-28 SEPTEMBER, 2-5, 8-11, 15, 17 & 18 OCTOBER 2007 (FINAL WRITTEN SUBMISSIONS FILED 4 DECEMBER 2007)
DELIVERED : 19 FEBRUARY 2008
FILE NO/S: CIV 1583 of 2003
BETWEEN: ANTONINO LO PRESTI
Plaintiff
AND
FORD MOTOR COMPANY OF AUSTRALIA LTD
Defendant
Catchwords:
Torts - Negligence - Personal injury arising from exposure to asbestos - Whether duty of care exists - Defendant manufacturer or supplier of cars with brake linings containing asbestos and supplier of such brake parts - Whether risk of injury to professional mechanics foreseeable
Torts - Negligence - Personal injury arising from exposure to asbestos - Whether breach of duty of care - Whether reasonable care called for defendant to give warnings - If so, to whom, in what form and by what means
Torts - Negligence - Personal injury arising from exposure to asbestos - Causation - Whether plaintiff's pulmonary fibrosis arose from exposure to asbestos or is idiopathic
Legislation:
Nil
Result:
Judgment for the plaintiff
Category: A
Representation:
Counsel:
Plaintiff: Mr J R C Gordon & Mr M J Magazanik
Defendant: Mr R J Burbidge QC & Dr M J Maxwell
Solicitors:
Plaintiff: Slater & Gordon
Defendant: Clayton Utz
Case(s) referred to in judgment(s):
Aerospace Engineers Services Pty Ltd v Ibrahim [2007] WASCA 33
Amaca Pty Ltd v Hannell [2007] WASCA 158; (2007) 34 WAR 109
Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307
Bennett v Minister of Community Welfare (1992) 176 CLR 408
City of Stirling v Tremeer [2006] WASCA 73; (2006) 32 WAR 155
CSR Ltd v Wren (1997) 15 NSWCCR 650
CSR Ltd v Young (1998) 16 NSWCCR 56
Donoghue v Stevenson [1932] AC 562
Dovuro Pty Ltd v Wilkins (2003) 215 CLR 317
Ellis v South Australia [2006] WASC 270
EM Baldwin & Son Pty Ltd v Plane (1998) 17 NSWCCR 434
Freidin v St Laurent [2007] VSCA 16; (2007) A Tort Rep 81‑875
Graham Barclay Oysters Pty Ltd v Ryan (2002) 211 CLR 540
Homestyle Pty Ltd v Perrozzi [2007] WASCA 16; (2007) 33 WAR 209
Julia Farr Services Inc v Hayes [2003] NSWCA 37; (2003) 24 NSWCCR 138
Makita (Australia) Pty Ltd v Sprowles [2001] NSWCA 305; (2001) 52 NSWLR 705
March v E & M H Stramare Pty Ltd (1991) 171 CLR 506
Medlin v State Government Insurance Commission (1995) 182 CLR 1
Mount Isa Mines Ltd v Pusey (1970) 125 CLR 383
Mulligan v Coffs Harbour City Council [2005] HCA 63; (2005) 223 CLR 486
Neindorf v Junkovic [2005] HCA 75; (2005) 80 ALJR 341
Pollock v Wellington (1996) 15 WAR 1
Pownall v Conlan Management Pty Ltd (1995) 12 WAR 370
Roman Catholic Church Trustees for the Diocese of Canberra v Hadba [2005] HCA 31; (2005) 221 CLR 161
Scanlon v American Cigarette Co (Overseas) Pty Ltd (No 2) [1987] VR 281
Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262
Tame v New South Wales [2002] HCA 35; (2002) 211 CLR 317
Thomson v Johnson & Johnson Pty Ltd [1991] 2 VR 449
Vairy v Wyong Shire Council [2005] HCA 62; (2005) 223 CLR 422
Van Der Sluice v Display Craft Pty Ltd [2002] NSWCA 204
Western Australia v Watson [1990] WAR 248
Wyong Shire Council v Shirt (1980) 146 CLR 40
Table of Contents
Introduction
Background facts
The pleadings and the issues
The plaintiff's work exposure to dust during the relevant period
Duty issues
Duty of care: legal principles
Duty of care; foreseeability; the evidence
Dr Leigh
Professor Musk
Dr Francis
Mr Stewart
Dr Egilman
Some of the relevant literature
The defendant's evidence
Dr Paustenbach
Other evidence relied upon by the defendant
Conclusions on foreseeability as at 1970
What the defendant knew or ought to have known during the period 1970 to 1987
Duty of care: the defendant's submissions
Duty of care: conclusions
Breach issues
Legal principles
Did the defendant breach its duty of care?
Causation issues
Causation - would a warning label or insert have been heeded?
Causation - does the plaintiff have asbestosis?
Dose estimates
Outline of the evidence
Dr Francis
Dr Egilman
Mr Rogers
Dose estimates: conclusion
Epidemiological evidence
Medical witnesses
Overview of medical evidence
The matters relevant to the diagnosis question: the common ground and the issues
Is there a threshold level of exposure for contracting asbestosis?
Other matters said to be relevant to diagnosis
Observations on Associate Professor McKenzie's evidence
Observations as to the evidence of Professor Robinson and Professor Musk
Conclusion as to plaintiff's fibrosis
Was the plaintiff's asbestosis caused by the defendant's negligence?
Conclusion
BEECH J:
Introduction
The plaintiff suffers from serious fibrosis of his lungs. The plaintiff's case is that his condition is asbestosis and that it was caused by his exposure to asbestos in the course of his work as a motor mechanic. Asbestosis is, by definition, pulmonary fibrosis caused by asbestos. The defendant's case is that the plaintiff's condition is not asbestosis but is a pulmonary fibrosis of unknown cause (termed idiopathic pulmonary fibrosis).
The defendant manufactures Ford motor vehicles. It is common ground that during the period 1970 to 1987 (the relevant period) Ford motor vehicles had brake linings which contained asbestos.
The plaintiff worked as a motor mechanic for two Ford dealerships in Western Australia from 1970 to 1987.
The plaintiff claims damages for the tort of negligence. He claims that his asbestosis was caused by the failure of the defendant to warn of the dangers of working with brake linings containing asbestos and of the need to take measures to prevent or minimise the release and inhalation of asbestos dust and fibres.
The defendant raises issues in relation to all three of the elements of the tort of negligence: duty, breach and causation. The major groups of issues arise in relation to the questions of duty and of causation.
The parties have agreed the quantum of damages at $840,000.
It is convenient to begin by outlining some background facts, which are largely uncontroversial, before turning to the pleadings to identify the issues raised.
Background facts
The plaintiff was born on 9 July 1949 in Sicily. He left school at the age of 11 and commenced an apprenticeship as a motor mechanic. His apprenticeship was with a motorcycle dealership. He continued working there until 1970. He was not aware of any exposure to asbestos in that employment and none was suggested in evidence at the trial.
There is no evidence of any specific exposure to asbestos outside the plaintiff's work as a mechanic from 1970 onwards.
In 1970, when he was 20, he migrated to Australia.
After he arrived in Australia he obtained employment with Anderson Ford, then located at 151 Adelaide Terrace in Perth. He worked as a mechanic for Anderson Ford from 1970 to 1975.
For the first two or three years of his employment with Anderson Ford he worked in the main workshop. This was a large workshop where dozens of mechanics worked performing a range of repairs and services to vehicles.
There was no mechanical ventilation in the workshop.
A number of issues arose in the course of the trial as to the extent and frequency of the activities by which asbestos dust was said by the plaintiff to have been generated in the workshop. The evidence in this regard will be analysed in more detail later in these reasons. At this stage I propose only a general outline.
In the course of servicing cars, the brakes were checked. This did not occur on all services, but did occur for 'major' or 'big' services. In the course of checking the brakes, the wheels and brake drums were removed and both the brakes and the drums were blown with compressed air. (Dust from within the brake drums would be blown out in the course of this.)
In the 1970s and 1980s, Ford motor vehicles were fitted with brakes lined with a friction material that included asbestos, of the type known as chrysotile. There are two main groups of asbestos: serpentines, which include chrysotile, and amphiboles, which include crocidolite and amosite. The risk of contracting cancer from exposure to asbestos varies according to the type of asbestos fibre. Chrysotile gives rise to the least risk; then amosite, then crocidolite.
The friction material was embedded in resin and bonded to metal brake shoes for use in drum brakes. In the case of vehicles fitted with disc brakes, the friction material was bonded to a metal backing plate for brake pads used in the disc brakes.
The defendant led expert evidence that the heat generated in the course of the braking process caused the breakdown of the vast majority of the asbestos in the friction material into non‑fibrous material including forsterite. This evidence will be referred to further when I give consideration to the question of the level of exposure of the plaintiff to asbestos.
In the course of servicing vehicles, brakes were also, on occasion, rubbed with emery paper, a rough sandpaper‑like cloth. There is also mention in the evidence of the need, from time to time, to chamfer or file the edge of a new brake lining to ensure it fitted correctly.
The floor of the work area was regularly swept.
For about two years, from 1973 to 1975, the plaintiff worked in a designated area known as the 'Quick Service area'. This was a smaller separate area with enough room for four vehicles.
As the name suggests, the purpose of the Quick Service area was for as many cars as possible to be serviced each day. A team of five men worked in the Quick Service area. One man was in the pit underneath the two cars, one man worked on the wheels, one man did the 'lubes', with another two doing the motors. There was also a supervisor.
Substantially the same tasks relevant to this case were undertaken in the Quick Service area. They were done in a more confined area and at a greater speed. The Quick Service area was very dusty.
The plaintiff did not know that the brake linings contained asbestos and did not know or believe that inhalation of the dust could be hazardous and that steps should be taken to reduce any exposure and inhalation. Nor did his workmates at Anderson Ford.
In 1975 the plaintiff left Anderson Ford. He moved to a small country town in Western Australia called Narembeen. For about six months he worked on a wheat farm, assisting his father‑in‑law.
He then returned to work as a motor mechanic. From late in 1975 until 1988 he worked as a mechanic for Col Commons & Son in Narembeen. Col Commons was a Ford dealership.
At Col Commons the plaintiff did a wide range of mechanical work. He worked primarily on cars and occasionally on trucks.
Compressed air was used to blow out the brakes of cars in the course of servicing them. If the brakes were glazed, emery paper was used to rub them down.
The workshop would be swept at the end of the day.
In 1988 the plaintiff left Col Commons and returned to Perth. He worked in a service station as a mechanic from 1988 to 1994. This service station did not service Ford vehicles exclusively.
In 1994 the plaintiff commenced worked at Tom's Auto Repair in Osborne Park as a mechanic. At Tom's Auto, different procedures were used in the course of servicing brakes. Brakes were washed out with water. Compressed air was not used.
When the plaintiff used compressed air on the first day of his job at Tom's Auto, his employer told him that compressed air was not to be used and that water was used instead. The employer said that compressed air was dusty and dangerous.
Before that, the plaintiff did not know (or believe) that exposure to brake dust and fibres was or might be dangerous and that measures should be taken to reduce the generation and inhalation of dust.
Until the late 1990s the plaintiff was an active man in good health. He enjoyed boating, fishing and gardening (among other things).
The plaintiff described that in the late 1990s he noticed that he would become tired and breathless.
His medical records (exhibit L) reveal that he saw his general practitioner Dr Angelo Carbone in March 1997 on account of coughing and having a wheezy chest. An antibiotic was prescribed and a description of the problem as 'bronchitis and bronchiolitis, acute' was recorded.
The plaintiff saw Dr Carbone again twice in July 1999. He described having been short of breath on exertion for two months. Bibasal crepitations (crackling sounds) were recorded as having been heard on examination.
In March 2000 he spent some days as an in‑patient at St John of God Hospital in Subiaco. The records suggest that the reason for admission was that the plaintiff had been struck in the face by an object at work. Chest x‑rays taken at this time were recorded as suggesting some changes in the left lower lobe consistent with bronchopneumonia.
The plaintiff referred in his evidence to having spent a week or so in St John of God Hospital. He thought that that was in 1998 but when questioned in cross‑examination he was, understandably, unsure of the dates. He is likely to have been referring to his admission in March 2000.
In September and October 2000 the plaintiff saw Dr Bernard Hockings, a cardiologist. Medication was prescribed to attempt to lower the plaintiff's high blood pressure.
In the course of the year 2000, the plaintiff saw Dr Carbone on occasions. There were continued references to feeling tired and having a cough. Bibasal crepitations were recorded. Further chest x‑rays were done.
There were considerable further investigations during the first half of 2001, including further radiological examination.
In June 2001 Dr Carbone referred the plaintiff to Professor Bruce Robinson, a consultant chest physician.
In July 2001 Professor Robinson diagnosed the plaintiff as suffering from asbestosis.
The plaintiff stopped work, because of his poor health, in September 2001.
The plaintiff has become substantially disabled from leading a normal life by his condition. He requires oxygen 24 hours a day. His breathlessness is continuing to get worse, as is his condition generally.
The defendant is, indirectly, a wholly owned subsidiary of Ford Motor Company (Ford US). There is and at all relevant times was also a Ford company operating in Britain called Ford Motor Company Limited (referred to at trial as Ford UK).
I turn to the pleadings and to the identification of the major issues in the trial of this action.
The pleadings and the issues
The plaintiff pleads that in the course of working as a motor mechanic at Anderson Ford between 1970 and 1975, and Col Commins between 1975 and 1987, he handled and cleaned asbestos brake linings and components and was exposed to and inhaled asbestos dust, particles and fibres.
In the particulars it is said that, in the course of servicing vehicles, the plaintiff would use compressed air to blow the dust from each brake drum, would inspect, remove and replace asbestos brake linings, and would handle asbestos brake linings by filing or grinding back the edges to enable them to be fitted into the brake drum. Further, it is said that his work duties included regularly dry sweeping the floor of the work areas after vehicles had been serviced. Fellow employees also cleaned, handled and worked with asbestos brake linings and components, and the plaintiff worked in the vicinity of these employees.
The defendant denies that filing and grinding occurred but otherwise admits that the alleged activities occurred, but without any admission as to the regularity or frequency of the sweeping.
The plaintiff puts his negligence case in two alternative ways. First, he sues the defendant as the manufacturer of the brake linings or of the vehicles fitted with the brake linings. Secondly, he sues the defendant as the supplier of the vehicles containing the brake linings and components and as the supplier of brake spare parts.
The defendant denies any role in the manufacture of any brake linings or brake components. It admits that various motor vehicles manufactured by it were fitted with brake linings containing asbestos but denies that any other brake component in vehicles manufactured by it contained asbestos.
The defendant admits that from time to time during the relevant period it supplied brake linings containing asbestos to its licensed dealers and distributors, but denies that it supplied any other brake component containing asbestos.
The alleged duties of care as manufacturer and supplier are pleaded in corresponding terms in par 6 and in par 10 of the statement of claim respectively. Each is built upon a foundation of what it is said that the defendant knew or ought to have known. In summary, it is pleaded that the defendant knew or ought to have known that:
(a)inhalation of asbestos fibres and dust was extremely injurious to human health and caused diseases including asbestosis, lung cancer and mesothelioma;
(b)the asbestos brake linings and components manufactured or supplied by it, or contained in vehicles manufactured by it, would, in the course of cleaning, handling and working, be likely to release asbestos fibres and dust;
(c)persons working as motor mechanics would be exposed to asbestos fibre and dust as a result of cleaning, handling or working of the brake linings and may suffer injury unless measures were taken to prevent or minimise the release and/or inhalation of asbestos fibres and dust;
(d)if the defendant did not provide warnings, it was unlikely that any sufficient measures would be taken to prevent the release of asbestos fibres and dust and inhalation by mechanics.
Three sets of detailed particulars have been provided of the facts relied upon in alleging that the defendant knew or ought to have known the matters pleaded in par 6 and par 10 of the statement of claim. I do not propose to detail them here.
The defendant admits that, by 1970, it knew that exposure to certain types of asbestos fibre, in sufficiently large quantities and duration, could cause asbestos related disease. However, it denies that it knew (or that it was the case) that exposure of the kind claimed by the plaintiff would, or could, increase his risk of contracting any asbestos related disease.
The duty of care said to arise as manufacturer or supplier of the asbestos brake linings and components or vehicles which included asbestos brake lining is pleaded in corresponding terms. In substance, the duty is said to be to take all reasonable care to give two categories of warnings: first, a warning to motor mechanics and/or their employers that handling, working and cleaning asbestos brake linings and components was extremely injurious to health and caused diseases including asbestosis and mesothelioma; secondly, to issue warnings to motor mechanics and/or their employers that it was essential that measures be taken when handling, cleaning or working with asbestos brake linings to prevent or minimise the release of asbestos dust and fibres into the atmosphere and their inhalation.
It can be seen, therefore, that the pleaded duty of care is in terms of a duty to warn, rather than a more general duty to avoid foreseeable risk of injury to mechanics.
It is then pleaded that the defendant negligently exposed the plaintiff to the risk of inhalation of, and to the actual inhalation of, asbestos dust and fibres. The particulars of negligence complain of five failures:
(a)the failure to warn the plaintiff and his fellow employees who cleaned, handled and worked with asbestos brake linings against using compressed air to clean brake drums, against filing and grinding asbestos brake linings and components, and against dry sweeping work areas in which asbestos brake linings and components were cleaned, handled and worked;
(b)failing to warn the plaintiff's employers, as receivers or purchasers of asbestos brake linings and components, against those matters;
(c)failing to advise the plaintiff and fellow employees of appropriate safety measures; namely using wetting or damping down cleaning methods; using an industrial vacuum cleaner with an adequate filter system; and using a respirator when handling, filing, grinding or cleaning asbestos brake linings and components;
(d)failing to advise the plaintiff's employers of those matters; and
(e)failing to warn the plaintiff, his employers and his fellow employees of the risks and dangers of asbestos inhalation, including the risks of asbestosis, lung cancer and mesothelioma.
It is pleaded that as a result of the alleged breaches of duty the plaintiff suffered injury, namely asbestosis and other problems.
The defendant denies that the plaintiff's injuries are caused by his inhalation of asbestos from brake linings manufactured or supplied by the defendant or by the defendant's negligence. Further, the defendant says that the plaintiff is not suffering from asbestosis but suffers from lung fibrosis of an idiopathic nature.
The major issues may be summarised as follows.
First, there are issues whether the defendant owed any duty of care to the plaintiff and, if so, issues as to the content of that duty. There are both factual and legal issues in that regard. The factual issues relate to what the defendant knew or ought to have known or foreseen as to the risks to motor mechanics arising from the presence of asbestos in brake linings.
Secondly, there are issues respecting the question of breach of any duty of care. Did reasonable care on the part of the defendant require it to give any warnings and, if so, by what means, in what terms, and to whom?
Thirdly, there are a number of issues concerning the question of causation. Most fundamentally, there is a diagnosis related causation issue: is the pulmonary condition from which the plaintiff suffers asbestosis, or is it of an idiopathic nature? The parties invite attention to evidence relating to a number of topics as being relevant to this question, including the following:
(a)evidence of lay witnesses, including the plaintiff, as to the activities which occurred in the course of the plaintiff's work as a motor mechanic, and the extent to which and circumstances in which he was, in that context, exposed to asbestos fibres;
(b)evidence from occupational hygienists who provided estimates of the level of exposure to asbestos fibres experienced by the plaintiff;
(c)expert evidence as to whether there was any threshold exposure level below which it is accepted that asbestosis will not occur;
(d)epidemiological evidence as to whether there is any association between work as a motor mechanic and the level of incidence of asbestos related diseases including mesothelioma, lung cancer and asbestosis; and
(e)expert medical opinion relating to whether the plaintiff's condition is asbestosis or is idiopathic in nature.
It is convenient to begin by making factual findings, based upon the evidence of the lay witnesses, in relation to the plaintiff's work as a motor mechanic and the frequency of those activities undertaken which gave rise to exposure to asbestos and associated topics. Thereafter, I propose to deal in turn with the issues of duty, breach and causation.
The plaintiff's work exposure to dust during the relevant period
The plaintiff gave evidence regarding his work environment at Anderson Ford and at Col Commons during the relevant period. He called four other witnesses who had worked at Anderson Ford: Mr Ian Hinkley, Mr Kenneth Hood, Mr Giuseppe (Joe) Lenzo and Mr Colin Bushby.
Mr Hinkley worked at Anderson Ford from 1969 to 1999. (At some stage during this period, subsequent to the plaintiff's departure from Anderson Ford, the business name changed to Centre Ford). Mr Hinkley was the supervisor of the Quick Service section for the whole of the time that the plaintiff worked at Anderson Ford.
Mr Hood worked for Anderson Ford from 1969 to 1979. Until 1974 he spent most of his time in the general workshop, with short periods in the Quick Service section. From 1974 to 1979 he worked in the Quick Service section. When Mr Hinkley was away, Mr Hood deputised as the Quick Service supervisor. Mr Hood was cross‑examined on very few aspects of his evidence.
Mr Lenzo worked at Anderson Ford from 1968, where he started as an apprentice, until 1987. He spent some of his time in the Quick Service area and worked there with the plaintiff. He was not cross‑examined.
Mr Bushby worked for Anderson Ford/ Centre Ford, for some 18 years. His recollection was that he started work at Anderson Ford in about September 1975. From his commencement at Anderson Ford he worked in the Quick Service area. He was unable to put a face to the name of the plaintiff and was, in the end, unsure of whether they had both worked at Anderson Ford at the same time (ts 343, 361 ‑ 362).
The defendant submits that it should be concluded that Mr Bushby commenced work at Anderson Ford after the plaintiff left and that, consequently, his evidence is of no assistance. I accept the first part of that submission but do not accept the second part of it. The tenor of the evidence of the other witnesses who worked at Anderson Ford through the 1970s and 1980s seems to me strongly to support a conclusion that there were few, if any, changes of substance in the relevant work practices and environment between 1974 and 1975 and in the years shortly thereafter. Of course, if and to the extent that Mr Bushby's evidence is materially different in a given respect from the evidence of those working at the time the plaintiff worked, I would rely upon the evidence of those working with the plaintiff. However, insofar as Mr Bushby gave evidence which is generally consistent with the others, while fleshing out or explaining matters in more detail than other witnesses, it seems to me that Mr Bushby's evidence is of assistance.
Leaving aside the plaintiff, there was no suggestion, in cross‑examination or submissions on behalf of the defendant, that any of the lay witnesses called on behalf of the plaintiff were doing other than giving their best recollection of the working conditions which they experienced and observed and of the other matters the subject of their evidence.
There was no challenge, in the course of cross‑examination, to the credibility of the plaintiff. In closing submissions the defendant submitted that the plaintiff's estimates of the mix of work done and the number of cars worked on and matters of that kind were estimates 'made in hindsight with the obvious incentive of financial reward'. I do not consider that the plaintiff was influenced, in his evidence as to his work practices, by any tendency, conscious or unconscious, to maximise his exposure to dust in order to assist his case. In that regard his evidence was supported by and consistent with the other witnesses who worked at Anderson Ford. For example, other witnesses gave descriptions of the level and intensity of the dust which were as vivid and graphic as those given by the plaintiff.
Unsurprisingly, the witnesses' evidence was not to identical effect in all respects. On matters of detail, there were some differences.
On the basis of the evidence of the five witnesses, I make the following findings of fact in respect of the plaintiff's work at Anderson Ford.
From 1970 until 1973 (or perhaps late 1972) the plaintiff worked in the main workshop at Anderson Ford. In the main workshop there were 15 car bays and up to that number of cars would be worked on at one time. About 40 to 50 cars per day were done in the workshop.
Approximately 50% of cars serviced received what was called a 'big' service, with the other 50% having a 'small' service. Brake work was done on big services but not in the course of small services.
In the course of a big service, the brakes would always be removed, 'de‑dusted' and checked. The de‑dusting process involved removing brake drums, tapping them on the floor to remove some of the dust, blowing them out with compressed air and then blowing out the wheels with compressed air. The plaintiff described the generation of dust in this way in par 27 of his witness statement (exhibit 3A):
When I used compressed air to blow out the brakes it would generate large amounts of dust containing asbestos which would blow up into my face and stick to my clothes and hair. It would cause a cloud or haze in the air and fall down in the area where I was working. The dust would get stirred up as I worked in it. The same would happen when the men beside me blew out brakes too, or anywhere else in the building. Sanding and filing the shoes would also cause asbestos dust.
See also ts 287; the evidence of Mr Lenzo at exhibit 10 par 12; and the evidence of Mr Hinkley at ts 309 ‑ 310.
If, on inspection, the brakes were glazed, they would be rubbed back with emery paper, so as to roughen them up and prevent squeaking (exhibit 3A par 25, see also ts 248 ‑ 249).
Further details and descriptions of the process of rubbing brakes with emery paper were given by Mr Hinkley and Mr Bushby. The evidence was given in the context of work in the Quick Service section but seems to me to be of general application. Mr Hinkley said that emery paper was used in about 50% of brake services to give the pads and the drum 'a hell of a rub' which created 'tons of dust' (exhibit 5 par 30). See also Mr Bushby's evidence at ts 351, 368.
Sometimes, when a new set of brake shoes was being installed, the edge of the shoe and lining would be chamfered or filed off (see exhibit 3A par 27, exhibit 5 par 31 - Mr Hinkley; and the evidence of Mr Bushby at ts 349 ‑ 350).
The workshop would be swept, generally at the end of the day, at least if time permitted.
The bulk of the detailed evidence regarding the plaintiff's exposure to dust related to the Quick Service section, to which I turn.
The Quick Service workshop was small and unventilated. A large number of cars were serviced each day. Several witnesses said that they would often service up to 40 cars per day. Mr Hood said that in Quick Service they got through about 40 cars per day (exhibit 9 par 8). He was not cross‑examined in that respect. Mr Lenzo said that it was pretty common for them to get through 40 cars a day in Quick Service (exhibit 10 par 7). He was not cross‑examined. See also Mr Bushby's evidence at ts 345.
The defendant's submissions fixed on evidence of the plaintiff, in cross‑examination, to the effect that he estimated that it took them one hour to do a small service and three hours to do a big service. The defendant submits that 40 is an unrealistically high number of cars to service in one day.
The plaintiff's evidence as to these estimates was, it seemed to me, directed to the question of the expected or permitted estimate of time for these tasks upon which the charge to the customer was calculated. I refer to the plaintiff's evidence in re‑examination (ts 290) and to the evidence of Mr Hinkley explaining the way in which those working in Quick Service were remunerated based upon the estimated or permitted time for the service (see exhibit 5 pars 11 ‑ 14).
While no doubt the number of cars serviced in a given day varied, I accept that it was not uncommonly in the region of 40 and, at other times, somewhat less.
As in the main workshop, the processes of using compressed air to remove dust, sanding brake shoes and, from time to time, filing brake shoes all created dust in the Quick Service workshop.
Something more than half of the cars that came through the Quick Service section had their brakes checked, and thus de‑dusted, using the compressed air as already described.
Mr Lenzo described the creation of dust in the Quick Service area. He said as follows (exhibit 10 par 12):
The way it actually happened is that you would pull the drums off and tap them on the floor and get all the dust out on the floor and then blow out the wheels and then you would even blow the dust away from around you. There was so much of that dumping of dust and blowing out during the day that as the day wore on there would be more and more asbestos dust around and you would be blowing out not just the dust out of the drum that you were taking out but all the other dust that had accumulated around you.
The brakes on about half of the cars having their brakes serviced would be rubbed with emery paper, as already described.
The evidence of all the witnesses who worked in the Quick Service area was to the effect that it was an extremely dusty environment. Mr Hinkley said that 'lots of dust was being blown up into the air and into the pit. There was heaps of dust and you could see it in the air. You would often get it in your mouth and your teeth and up your nose and in your hair and everywhere' (exhibit 5 par 34). See also the evidence of Mr Hinkley (exhibit 5 pars 29, 37), Mr Hood (exhibit 9 par 9), the plaintiff (exhibit 3A pars 37, 41) and Mr Bushby (ts 346, 354).
The room did not have any mechanical ventilation and had poor natural ventilation. There were walls on three sides of the room. One wall partitioned the Quick Service area from the main workshop. This wall was solid except for an area of mesh at the top. There were high windows on one of the other walls. Those windows opened only partially and did not allow much natural ventilation. See, in this regard, the evidence of Mr Lenzo (exhibit 10 par 8) and Mr Bushby (ts 343, 378).
The dust was not removed in the course of the day. Accordingly, and given the lack of ventilation, the dust accumulated in the course of the day.
There were regular complaints about the dust. In response, the only thing that was done was that some fans were provided. These provided some relief from the heat but merely kept the dust airborne without removing it.
Five men worked in the Quick Service section. One was on wheels. He was responsible for the work on the brakes. Another was in the pit. The person on wheels was most exposed to the dust. The pit was also very dusty. But the Quick Service workshop as a whole was a very dusty environment. Dust would cover Mr Hinkley's desk in the corner of the room.
The evidence in the witness statements was to the effect that the plaintiff rotated between the five tasks but spent a higher proportion of his time on the brakes because he was short and worked fast on the wheels. However, the evidence of both the plaintiff and Mr Hinkley, in the course of cross‑examination, was to the effect that the plaintiff did one week in five on the wheels. See the plaintiff's evidence at ts 267 and Mr Hinkley's evidence at ts 306 and, especially, at ts 308, where Mr Hinkley was asked, in plain terms, whether the plaintiff took his part in the rotation and did one week in five like each other person, to which he answered yes. I have not overlooked the evidence of Mr Hinkley in re‑examination at ts 317 ‑ 321, upon which reliance is placed by the plaintiff. However, I am not satisfied that the plaintiff spent the majority of his time on wheels, although he may well have spent a little more time in that role than in other roles.
The accumulated dust was, generally, swept once a day, mostly at the end of the day. If time did not permit sweeping to occur at the end of the day this may be done in the morning. There was also evidence that, at least on some occasions, a hose was used in the sweeping process.
Disc brakes were also de‑dusted with compressed air. However, they did not accumulate dust to the same extent, and so released less dust in the process of cleaning.
Some attention was given, in the evidence and in cross‑examination, to the question of the relative proportion of cars serviced which had disc brakes as distinct from drum brakes.
By the mid‑1970s virtually all new Ford vehicles had disc brakes installed on the front wheels. However, according to Mr David Ford, a witness called by the defendant, there would, in that period, still have been 'lots and lots' of vehicles with drum brakes at front and back (ts 734).
The evidence of those who worked at Anderson Ford as to the distribution of drum brakes and disc brakes in the first half of the 1970s was not consistent. Mr Hinkley and Mr Hood said that most cars had disc brakes at the front (ts 314, 317, 332). The plaintiff thought that the majority of cars, around 60% to 70%, had drum brakes at the front (as well as at the back) (ts 243). Mr Bushby's evidence was that when he started work there were predominantly drum brakes on the front wheels (ts 347). Mr Hinkley and Mr Hood both worked for Anderson Ford for extended periods which spanned the early and late 1970s. By contrast, Mr Bushby did not commence until 1975. On balance, I consider that Mr Bushby's evidence as to the position when he commenced is likely to be reliable. Mr Hood and Mr Hinkley may well be identifying the position as at a later time, rather than during the first half of the 1970s.
Accordingly, I find that the majority of cars serviced at Anderson Ford while the plaintiff worked there had drum brakes both at the front and back of the vehicle.
The only evidence respecting the 11 years during which the plaintiff worked at Col Commons was the evidence of the plaintiff himself.
The plaintiff said it was common practice to use compressed air to blow out the brake drums while he was working at Col Commons. He estimated that he blew the drums on every second car that he worked on (exhibit 3A par 68). If the brakes were glazed, he would use emery paper to rub them down (exhibit 3A par 69). He estimated that he would change a set of brakes twice a week on average, and would service three or four cars a day, using compressed air on two of them on average (exhibit 3A par 72).
In cross‑examination he acknowledged that by the 1980s more cars had disc brakes at the front (ts 275).
He also described in some detail the work which would be done on the brakes of trucks. I accept his evidence in that regard. However, given his evidence that the brake linings on a truck were replaced only two or three times a year (ts 276), this is not of great significance.
The workshop floor would be swept at the end of the day, either by the plaintiff or by an apprentice if there was one.
I turn to the question of whether the defendant owed a duty of care to the plaintiff.
Duty issues
It is convenient to begin with some relevant general principles.
Duty of care: legal principles
The well known dictum of Lord Atkin in Donoghue v Stevenson [1932] AC 562, 580 remains relevant to the question of identification of persons to whom a duty of care is owed. In Tame v New South Wales [2002] HCA 35; (2002) 211 CLR 317 [9], Gleeson CJ observed that it is the reasonableness of a requirement that a defendant should have certain persons and certain interests in contemplation that determines the existence of a duty of care.
In general terms, a necessary, but not sufficient, condition of the existence of a duty of care is reasonable foreseeability by the defendant of the kind of injury that has been suffered by the person to whom the duty is owed: Tame [12]; Amaca Pty Ltd v Hannell [2007] WASCA 158; (2007) 34 WAR 109 [299]. Reasonable foreseeability is to be understood and applied with due regard to whether it is reasonable to require a person to have in contemplation a risk of the kind of injury that eventuated: Tame [12].
The 'kind of injury' which must be foreseeable is a reference to the different categories of injuries such as personal injury, property damage or pure economic loss. The particular injuries suffered need not be foreseeable: Mount Isa Mines Ltd v Pusey (1970) 125 CLR 383, 402; Amaca Pty Ltd v Hannell [299].
In Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307, 332 the New South Wales Court of Appeal held that it was not necessary for the plaintiff to prove that it was foreseeable that he might contract the particular injury of mesothelioma from the asbestos exposure of which he complained. It was sufficient that he could contract an injury of the kind which he suffered, namely personal injury from the inhalation of asbestos.
In deciding whether the defendant owed the plaintiff a duty of care, the tribunal of fact must first ask itself whether a reasonable man in the defendant's position would have foreseen that his or her conduct involved a risk of injury to the plaintiff or to a class of persons including the plaintiff: Wyong Shire Council v Shirt (1980) 146 CLR 40, 47.
A risk of injury which is remote, in the sense that it is extremely unlikely to occur, may nevertheless constitute a foreseeable risk. A risk which is not far‑fetched or fanciful is real and therefore foreseeable: Wyong Shire Council v Shirt (48); Dovuro Pty Ltd v Wilkins (2003) 215 CLR 317 [60]; Amaca Pty Ltd v Hannell [300].
The test of reasonable foreseeability is to be applied at the time of the alleged breach and thus without hindsight: Amaca Pty Ltd v Hannell [301]; Homestyle Pty Ltd v Perrozzi [2007] WASCA 16; (2007) 33 WAR 209 [143].
In Bendix Mintex the New South Wales Court of Appeal held that a plaintiff does not have to show that the particular asbestos fibre type (there, as here, chrysotile) was known to be dangerous (332). If that approach is adopted the task of the plaintiff in establishing a duty is thereby made less onerous, given that the type of fibre here is the least dangerous. However, in the light of the factual findings I make, it is not necessary to decide whether that approach ought be taken on the foreseeability question.
The plaintiff invited my attention to findings of foreseeability, in respect of the hazards of asbestos, in numerous decided cases. For example, in EM Baldwin & Son Pty Ltd v Plane (1998) 17 NSWCCR 434, Fitzgerald AJA referred to other decisions of the New South Wales Court of Appeal, including CSR Ltd v Young (1998) 16 NSWCCR 56, in which it was accepted that 'the known toxicity' of asbestos dust, and 'the known uncertainty' as to the effects of exposure to asbestos dust, together with knowledge that injury or illness might not emerge for many years, give rise to a risk which could not be dismissed as remote, slight, far‑fetched or fanciful [110].
Similarly, it has been observed that foreseeability can turn on knowledge of the dangers of any exposure to asbestos, including in the calculus for breach of duty, and is not confined to knowledge of the dangers of exposure to high levels of asbestos or levels of asbestos above any particular standard: Julia Farr Services Inc v Hayes [2003] NSWCA 37; (2003) 24 NSWCCR 138 [125] (Giles JA). In that case Spigelman CJ agreed with Giles JA and observed [2] that decisions of the New South Wales Court of Appeal established the proposition that breach of duty can be made out on the basis that there was no known safe dose of asbestos, taking into account the test of foreseeability enunciated in Wyong Shire Council v Shirt.
However, the conclusion that, in a particular case, a particular hazard was found to be foreseeable is a fact‑based conclusion derived from the evidence in the particular case; it is not a conclusion of law. See, for example, Julia Farr Services [106] ‑ [110]. The same point was made in relation to decisions on the question of breach of duty by Gleeson CJ and Kirby J in Vairy v Wyong Shire Council (2005) 223 CLR 422 [2] ‑ [4].
Of course, that is not to say that decided cases are not of assistance in relation to questions of the existence and scope of duty of care. To the contrary, where the existence and scope of a duty of care is settled by authority it is unnecessary to identify and apply the legal principles that govern the determination of those questions (see, for example, Amaca Pty Ltd v Hannell [348]). Whether a duty of care arises from given facts is a question of law: Vairy [62].
The plaintiff invokes general principles respecting the duty of care of a manufacturer and a supplier. It is well established that a manufacturer owes a duty to a consumer to take reasonable care to prevent the product causing injury to a consumer: Dovuro Pty Ltd v Wilkins (2003) 215 CLR 317 [29]. In Amaca Pty Ltd v Hannell [354] there was reference to the manufacturer's duty to take reasonable care to avoid injury being suffered by persons using the product in an intended or normal way. See also CSR Ltd v Wren (1997) 15 NSWCCR 650, 655.
The question is, however, as to the scope of the class of persons to whom the duty is owed. The duty is owed only to those in respect of whom it is reasonably foreseeable that injury or harm might result. In Amaca Pty Ltd v Hannell, for example, the factual conclusion (at [347]) on foreseeability of harm to the home handyman, favourable to the plaintiff, in the joint reasons of Steytler P and McLure JA was the foundation for the duty of care found by their Honours in that case.
In the same way, reasonable foreseeability of the risk of harm to motor mechanics is a critical factual foundation of the plaintiff's case on duty of care. If that factual foundation is made out it seems, contrary to some of the submissions on behalf of the defendant, a small step to find that a duty of care arose. If (and only if) reasonable foreseeability of harm to mechanics is established, mechanics thereby become one of the classes to whom the manufacturer or supplier of vehicles fitted with asbestos brake linings or of brake lining spare parts owed a duty to take reasonable care to avoid the product causing injury.
Both parties accepted that the question of reasonable foreseeability was significant to whether the defendant owed a duty of care to a class of persons of which the plaintiff was a member. However, the parties appeared to differ as to what it was that was required to be foreseeable, in order that a duty of care arose.
The duty of care pleaded by the plaintiff is said to be owed to motor mechanics. In the course of opening, counsel for the plaintiff specified that that was intended to refer to professional motor mechanics.
The plaintiff submitted that the foreseeability question is whether the defendant ought reasonably to have foreseen a possibility of asbestos inhalation injury from asbestos exposure to mechanics as a result of working with Ford vehicles with asbestos in the brake linings, and that such possibility was not far‑fetched or fanciful (no matter how unlikely).
The defendant submitted that the question of foreseeability was whether it was reasonably foreseeable by the defendant that a motor mechanic might contract an asbestos related disease as a consequence of exposure to the level or quantities of asbestos associated with his working on brakes fitted to the defendant's vehicles.
The plaintiff took particular issue with the reference, in the defendant's formulation, to 'the level of asbestos'. The plaintiff contended that there was no necessity to foresee any particular level in order that a duty of care arises. Insofar as the reference to a level is intended to refer to a specific numerical level, I accept the plaintiff's submission that such is not required.
On the other hand, I accept that, in determining whether the defendant owed a duty of care to professional mechanics, regard is to be had to the extent of exposure of mechanics which might foreseeably arise from asbestos dust and fibres released from asbestos in brake linings. If, having regard to that, and taking into account what was known or believed at the time, harm to mechanics was not reasonably foreseeable, no duty of care would be owed to mechanics.
Of course, in taking account of the extent to which mechanics might foreseeably be exposed to asbestos from brake linings, account must be taken of the wide range of possible work practices and environments, and of the prospect that a mechanic may work on servicing and changing brakes on Ford vehicles for many decades.
In short, what must have been reasonably foreseeable by the defendant is that a professional motor mechanic might contract an asbestos inhalation disease arising from the release of asbestos from the brake linings of Ford vehicles.
The duty of care pleaded by the plaintiff is expressed as a duty to give warnings. That invites attention to the question of the particularity of the formulation of a duty of care. A duty of care should not be formulated with such particularity as has the effect of obscuring the proper inquiry into the reasonable response to a foreseeable risk at the breach stage of the analysis: Graham Barclay Oysters Pty Ltd v Ryan (2002) 211 CLR 540 [191] ‑ [192].
In some cases the duty question involves a determination of whether a defendant owes the plaintiff a duty to warn. That may be the position in novel situations where a more general formulation of the duty would be at such a high level of abstraction as to be of no practical assistance. See the discussion in Amaca Pty Ltd v Hannell [350] ‑ [352]. If that occurs, the duty analysis must take account of the same considerations as are relevant in determining whether the specific breaches relied on would constitute a breach of any duty however formulated.
Ordinarily, the question whether the provision of a warning is within the scope of a duty of care in a particular case is determined at the breach stage of the analysis, by assessing whether a failure to warn constitutes a breach of duty: see Amaca Pty Ltd v Hannell [353] and cases there cited. However, as is there remarked, the result should be the same regardless of the approach.
I will return to those issues in the course of stating my conclusions in respect of the duty issue.
That brings me to the evidence as to whether it was reasonably foreseeable by the defendant that, if no protective measures were taken, professional mechanics might be at risk of contracting an asbestos inhalation injury or disease arising from the release of asbestos from the brake linings of Ford vehicles.
Duty of care; foreseeability; the evidence
An enormous volume of evidence was tendered by the parties in relation to the issue of what the defendant knew, or should have known, or reasonably foreseen as at 1970, and during the period from 1970 to 1987.
By way of overview, the plaintiff relied upon the following main categories of evidence:
(a)the defendant's admissions;
(b)various items of evidence bearing upon what the defendant knew;
(c)knowledge of Ford US and Ford UK, which was said to bear upon the defendant's position in two ways:
(i)knowledge of the foreign companies was said to be attributable to the defendant because of common directorships or senior executives within those organisations;
(ii)alternatively, knowledge held by Ford US and Ford UK was part of what the defendant ought to have known, because such information was readily available to it in the circumstances calling for inquiry by the defendant; and
(d)expert evidence as to readily available information regarding the hazards of asbestos, said to be supported by voluminous scientific literature and other publications tendered by the plainitff.
The plaintiff's claim is that the defendant owed him a duty from 1970 through to 1987. That being so, the question of the actual or constructive knowledge of the defendant falls to be determined, first, as at 1970, and, then, throughout the period from 1970 to 1987. Much of the evidence relied upon by the plaintiff as to what the defendant knew, and as to what Ford US and Ford UK knew, pertains to the period from 1970 to 1987. Very little of it bears on the position as at 1970.
The defendant led very little evidence as to what it knew regarding asbestos and the brake linings used in its vehicles and supplied by it. Substantially the only evidence led by the defendant in this regard was the evidence of Mr Ford, a former senior executive of the defendant. Although he worked for the company from about 1969, his evidence as to the defendant's relevant knowledge related primarily to the period from 1980 onwards.
Given that there appears to be little evidence bearing directly upon what Ford knew, as at 1970, the question of what Ford knew, at that time, will, it seems to me, overlap to a significant degree with what the defendant ought to have known at that time. The subject matter, source and circumstances of publication of some matters may (or may not) give rise to an inference that the defendant knew of them, as well as to (or not) a conclusion that the defendant ought to have known of them. In any case, it is sufficient for the plaintiff to establish that the defendant either knew or ought to have known of relevant matters.
The defendant's case in respect of foreseeability relied on the following main categories of evidence:
(a)expert evidence, primarily from Dr Dennis Paustenbach and also from Mr Alan Rogers;
(b)scientific and other literature relied upon by those experts as supporting their views; and
(c)a bundle of material (exhibit W) containing documents regarding threshold limit values for asbestos between 1970 and 1987 and setting out legislative and regulatory duties of occupiers of premises between 1970 and 1987.
The plaintiff points to admissions made by the defendant. In the course of the trial, senior counsel for the defendant made the following admission on its behalf (ts 456):
The defendant accepts that it understood or knew, if you wish, that there was asbestos in brake linings and it knew also that in a general sense if there was sufficient exposure of asbestos to people occupationally exposed, asbestos related disease could result. Those admissions are plain and we don't resile from that.
It was, plainly, foreseeable by the defendant that motor mechanics who serviced and repaired Ford vehicles would, in the course of so doing, service, clean, install and replace brakes. It did not appear to be in dispute that Ford was aware of the various steps involved in servicing and repairing Ford vehicles and I so find. It was foreseeable that work by mechanics might involve blowing brake dust from brake drums and filing or grinding the edge of a brake shoe to ensure that it fitted, for example.
The question is whether it was reasonably foreseeable by the defendant that a mechanic might suffer an asbestos inhalation injury caused by the asbestos in the brake linings of vehicles manufactured or supplied by the defendant, or from brake parts supplied by the defendant.
The level of risk required in order that a risk be reasonably foreseeable is not high. It is enough that it is not far‑fetched or fanciful and thus is real, even though it may be extremely unlikely to occur.
I propose to begin the review of the evidence relating to foreseeability issues with the expert evidence. In undertaking that review it should, it seems to me, be borne in mind that the question of foreseeability is not limited to the question of risk of asbestosis. It is broader than that and extends at least to reasonable foreseeability of any life threatening disease, including mesothelioma (see Bendix Mintex). At times, the defendant's submissions on foreseeability approached the question by reference only to the foreseeability of asbestosis.
I will deal first with the experts called by the plaintiff.
Dr Leigh
Dr James Leigh is a consultant occupational physician. He has extensive qualifications in medicine and mathematics. He is a fellow of the Australasian Faculty of Occupational Medicine and the Australasian Faculty of Public Health Medicine. In 1999 he was a consultant to the World Trade Organisation on asbestos issues. He was the head of the Epidemiology and Surveillance Unit of the National Occupational Health and Safety Commission from 1988 to 1996 and head of the Research Unit of that Commission from 1996 to 2001. He was co‑ordinator of the Australian Mesothelioma Register from 1988 until 2001.
His first report (exhibit 24A) dealt at length with the development of knowledge about the risks of health arising from exposure to asbestos. Some of the points made in the report may be summarised as follows:
(a)by 1955 the issue of asbestos exposure as a cause of lung cancer was put beyond doubt in a published study by Doll;
(b)an article in Industrial Medicine by Cooke in 1942 pointed out the need for physically measuring dust concentration of asbestos, and not relying on sight only, because the then applicable 5 million particles per cubic foot risk level would not necessarily be visible to the naked eye; and
(c)in 1952, Hueper wrote that:
'Since we did not know the minimum effective dose of any of the many occupational carcinogens it seems obvious that they should be completely eliminated wherever that is practicable. This can be done by using or producing suitable non‑carcinogenic substitutes.
Hueper went on to describe other control measures including enclosure, wetting and ventilation.
Dr Leigh also referred to a conference in England in 1969 at the Essex offices of Ford UK. The chairman of the conference was the chief medical officer of Ford UK. The conference was on the subject matter of exposure to asbestos during brake and clutch maintenance. The hazards and appropriate control measures were discussed. Control measures such as dilution and exhaust ventilation, vacuum funnels and brushes and respirators were described and their effectiveness demonstrated. The conference papers were published in 1970 in the journal the Annals of Occupational Hygiene, 1 ‑ 41. That publication was document 30 within the bundle of documents comprising exhibit 37, which I will denote as exhibit 37/30. Further reference to these conference papers will be made later in these reasons.
At pp 7 ‑ 12 of his report Dr Leigh referred to substantial scientific literature relating to short or low asbestos exposures and mesothelioma. The following summarises some of the points made:
(a)In the course of the 1960s various reports were made of occurrences of mesothelioma from asbestos exposure, in many of which no fibre type distinctions were made.
(b)In 1964 an editorial in the British Medical Journal drew attention to the occurrence of mesothelioma at low exposures and did not distinguish between the hazards of different fibre types.
(c)In 1965, in the British Journal of Industrial Medicine, Newhouse & Thompson (exhibit 37/216) described 83 mesothelioma cases, 40 of which gave a history of occupational or domestic exposure.
(d)In 1965 and 1971 two authoritative reviews of the epidemiology of asbestos cancers were published. Both recognised the possible differential effects of different fibre types but neither claimed that chrysotile did not cause mesothelioma.
(e)By 1970 the dangers of asbestos in causing mesothelioma were well known in Australia. All types were thought to cause mesothelioma with, from 1965, a common theory held by the majority that crocidolite was the most potent, followed by amosite and then chrysotile. However, there was a fairly strong minority that felt that all types should be regarded as equally potent in causing mesothelioma, based on animal inhalation and implantation studies showing roughly equal effects per unit dose. This is reflected in the International Agency for Research on Cancer (IARC) Evaluation (1976 p 80). (The IARC Evaluation is exhibit 37/141).
(f)A 1982 report by the Australian National Health and Medical Research Council (NHMRC) on the health hazards of asbestos commented on the impossibility of determining a safe threshold below which no adverse effect of asbestos exposure existed, and recommended as a result that exposure to all forms of asbestos be kept as low as reasonably practical. (The 1982 NHMRC report is exhibit 41/15 and will be referred to later in these reasons.)
Dr Leigh was not cross‑examined.
Professor Musk
Professor A W (William) Musk is an eminent respiratory physician and research scientist who has specialised in the area of asbestos related diseases for many decades. He gave evidence in relation to the diagnosis of the plaintiff, to which reference will be made later in these reasons. At that stage more will be said about his expertise.
At pp 8 ‑ 36 of his substance of evidence (exhibit 18A) Professor Musk gave evidence relating to the development of knowledge in relation to asbestos related diseases and as to standards and regulations applying to asbestos exposure. By the mid‑1960s Professor Musk said that it was widely accepted that asbestos could cause asbestosis, lung cancer and mesothelioma. It was accepted that small doses, particularly of crocidolite, could cause mesothelioma. The need for the protection of workers exposed to all forms of asbestos was known. Following a 1964 conference (held in New York) on the biological effects of asbestos, the overview of proceedings was said to be that 'it is abundantly clear from the evidence presented at the conference that in future much greater care must be taken to eliminate unnecessary exposure to asbestos dust wherever it occurs'.
Professor Musk referred to the British Occupational Hygiene Society Hygiene Standards for Chrysotile Asbestos Dust published in about 1968 (1968 BOHS Standards) (exhibit 37/50). He pointed out that the committee considered the standards were the best that could be obtained from scanty data and hoped to supplement them in due course. It was unable to specify any air concentration of asbestos which was known to be free of risk from cancer. New United Kingdom asbestos regulations came into effect in May 1970. These regulated all activities where asbestos or asbestos‑containing compounds were used, and required that where asbestos might be liberated into the atmosphere capable of causing harm, exhaust ventilation or personal protection was to be used.
Professor Musk concluded as follows. The material he had referred to would have led a reasonable employer, occupier or product supplier to have been aware of the necessity to minimise the risk of inhalation of asbestos well before 1970 onwards and to warn of the potential dangers. By 1961 the serious dangers to health occasioned by even small exposures should have been known by persons responsible for exposing other persons to asbestos and appropriate warnings and safeguards should have been implemented. By the mid‑1960s, no person should have been exposed to asbestos, especially (but, by implication, not exclusively) blue asbestos (ie crocidolite), without exposure being reduced to a minimum and appropriate warnings of the risks being given to those exposed. The amounts of asbestos to which persons were being exposed could and should have been quantified during the 1960s as a consequence of these serious dangers and risks to health. By the 1970s medical researchers in the field were considering not whether there was a safe level of exposure, which had never been asserted, but whether asbestos should be banned completely.
Professor Musk was not cross‑examined in relation to these matters.
The defendant submitted that Professor Musk's evidence did not take account of three critical factors and their impact on an assessment of what hazard may have existed for mechanics. The factors were: asbestos type; exposure levels and duration; and characteristics of specific asbestos‑related diseases.
I do not accept that submission. The summary set out above reflects Professor Musk's opinion that, at the relevant time, no safe level of exposure for any variety of asbestos had been demonstrated or was believed to exist, and that all exposure to any asbestos (of whatever type) should, consequently, have been reduced to a minimum, with appropriate warnings. As to the third factor referred to by the defendant, the foreseeability issue is, as I have already found, not to be tested only by reference to asbestosis.
Dr Francis
Dr Eva Francis is an occupational hygienist with almost 30 years of practical experience in the area. She has had a particular interest in the area of asbestos since the early 1970s. She gave evidence estimating the asbestos dose experienced by the plaintiff. That evidence will be referred to later in these reasons. Some of the points arising from her evidence as to foreseeability may be summarised as follows:
(a)By 1970, and through to 1987, asbestos was recognised among occupational health specialists as causing asbestosis and as a carcinogen.
(b)Mesothelioma occurrence in garage workers was reported in the UK and in Canada by Newhouse & Thompson (1965) (exhibit 37/216), McDonald et al (1970) (exhibit 37/182) and by Greenberg & Lloyd Davies (1974) (exhibit 37/177).
(c)As a result, the United States National Institute for Occupational Safety and Health (NIOSH) recommended a procedure for asbestos brake and clutch servicing requiring respiratory protection, vacuuming of brake drum dust and localising of grinders and machinery in a workshop with dust extraction in its Current Intelligence Bulletins of 8 August 1975 (1975 NIOSH bulletin) (exhibit 37/75).
(d)In a United States publication by Lorimer et al in 1976 (exhibit 37/295), asbestosis and pulmonary function loss was said to have been demonstrated in 25% of automotive workers examined.
(e)In 1970, and up to and including 1987, it was recognised by health scientists and occupational health specialists that all exposures to carcinogens, and hence to asbestos, should be minimised as far as practical. It was accepted that there was a need to reduce all exposure to carcinogenic agents to the lowest achievable level of exposure (Dr Francis referred in this respect to a publication by Conklin in 1949). There was the view that carcinogens were extremely dangerous and should be treated with comprehensive care.
(f)A comprehensive compilation of the international medical literature has always been available in Index Medicus, and the Industrial Hygiene Digest has provided abstracts of findings in occupational health. Major industrial companies in the 1970s would have been abreast to these two sources of references, with the latter being sent monthly to members of the Industrial Hygiene Foundation;
(g)Thus a prudent and responsible producer, user or manufacturer and distributor of asbestos and products containing asbestosis would have known in 1970 and through to 1987 that the inhalation of asbestos dust could be injurious to persons using, repairing and maintaining asbestos products.
Dr Francis was not cross‑examined in relation to this aspect of her evidence.
Mr Stewart
The plaintiff also relied upon evidence from Mr Gordon Stewart. From 1953 to 1966 Mr Stewart worked in the industrial hygiene section of the Department of Health and then from 1966 ‑ 1985 for a private company. Since then he has worked in the industry as a private consultant.
Mr Stewart referred to publications in the United Kingdom and in New South Wales in the 1940s which emphasised the need to minimise exposure to asbestos, even if the exposure arose only from temporary work or the exposure was only intermittent. He referred to the 1970 Queensland Rules under the Factories and Shops Act which prescribed measures to be taken whenever a process involved asbestos or an article partly comprising asbestos, or any work involved the use or handling of asbestos or any article containing asbestos. He referred to the 1975 NIOSH bulletin to which reference has already been made. He concluded that there was significant knowledge available throughout the period 1970 to 1987 as to the significant risks from asbestos inhalation, and that exposure and inhalation of dust derived from the manipulation, drilling, grinding and shaping of asbestos containing products such as brake and clutch parts and from cleaning by sweeping or blowing out such parts could give rise to such risks.
The brief cross‑examination of Mr Stewart did not touch upon these matters.
Dr Egilman
Finally, in this respect, the plaintiff relied upon evidence from Dr David Egilman. He canvassed a very large volume of academic literature, some of which was referred to by various others of the plaintiff's experts. I have not found it necessary to rely upon his evidence and, accordingly, do not propose to review his evidence.
I propose, next, to review some of the literature and other documents to which reference was made by the plaintiff's experts, before turning to the defendant's evidence.
Some of the relevant literature
It is not practical to summarise, in these reasons, the contents of voluminous material relied upon by the parties' experts. I propose to set out excerpts from, or summarise, only a small selection of the material. Wherever, in the summary of the plaintiff's expert evidence set out above, I have referred by number to a particular exhibit, I have considered it and am satisfied that it supports the proposition for which it is relied upon in the summary I have given.
I start with the 1968 BOHS standards (exhibit 37/50). The defendant emphasised pars 1 ‑ 3 of the summary and recommendations at the commencement of the document. These were in the following terms:
1. As long as there is any airborne chrysotile dust in the work environment there may be some small risk to health. Nevertheless, it should be realised that exposure up to certain limits can be tolerated for a lifetime without incurring undue risks.
2. The committee believes that a proper and reasonable objective would be to reduce the risk of contracting asbestosis to 1 per cent of those who have a lifetime's exposure to the dust. By 'asbestosis' this committee means the earliest demonstrable effects on the lung due to asbestos.
It is probable that the risk of being affected to the extent of having such early clinical signs will be less than 1 per cent for an accumulated exposure of 100 fibre years per cm3. That is, for example, a concentration of 2 fibres per cm3 for 50 years, 4 fibres per cm3 for 25 years or 10 fibres per cm3 for 10 years.
3. It is recommended that exposures which lie in certain ranges of dustiness be designated by categories according to the following scheme:
DUST CATEGORY CONCENTRATION AVERAGED OVER
3 MONTHS (FIBRES/CM3)
Negligible 0‑0.4
Low 0.5‑1.9
Medium 2.0‑10.0High over 10.0
However, as was common ground between the experts, and as anyway would appear to be common sense, regard must be had to the whole of the contents of the document, which included the following passages:
CRITERIA OF RISK
As long as there is an appreciable amount of dust in the air, the committee recognises that there may be some risk to health.
If there is a threshold concentration, below which nobody is adversely affected, one could not argue from a limited number of dust measurements that a worker will never be exposed to this concentration, but only that the possibility is remote. Thus, in practice, one can show only that the risk of a worker's exposure exceeding such a threshold is small. Consequently, whether or not there is a threshold exposure, one can show only that the risk of a worker being affected by asbestos is minimal.
Knowledge of the relationship between airborne dust exposure and the risk of asbestosis is not in itself sufficient to establish a hygiene standard. Another important problem, and one which is very difficult to resolve, is that of balancing the risks to health against the consequences of demanding excessive dust reduction.
However, the committee believes that it is reasonable to reduce to 1 per cent the risk of getting asbestosis through having worked for a lifetime with asbestos. By 'asbestosis' the committee has in mind the existence of the earliest demonstrable effects on the lung due to asbestos.
ESTIMATION OF THE STANDARD AIR CONCENTRATION
The way in which risk and dust concentration are related is not fully understood. However, it seems reasonable to assume that at zero concentration of asbestos there will be zero risk and that there will be an increase in risk corresponding to an increase in concentration. (p 4)
...
Good industrial hygiene practice tends towards controlling exposures below the hygienic maximum rather than maintenance at the maximum. (p 6)
...
PERIODIC MEDICAL EXAMINATIONS
In all types of pneumoconiosis too little is known about the variability of the response of different individuals to a given dose of dust to allow complete reliance on dust monitoring as a means of reducing the risk to a specified level ...
CANCER
...
There can be little doubt that these risks will be least in the lowest concentration (Knox, Doll and Hill 1965), but the quantitative relationship between asbestos and cancer risk is not known, nor is it known exactly why these two are related, nor even whether all kinds of asbestos present a risk. Consequently it is not possible, at this time to specify an air concentration which is known will be free of risk in this respect. (pp 7 ‑ 8)
Consideration of the whole of the document seems to me to provide support for the conclusions about it drawn by the plaintiff's experts. The acknowledgement, in the concluding paragraph of the document, that it is not possible to specify an air concentration which is known to be free of cancer risk is of some significance.
The papers which were presented at the conference held at the central office of Ford UK in March 1969 were published at pp 1 ‑ 41 in the 1970 Annals of Occupational Hygiene, a journal published for the British Occupational Hygiene Society (exhibit 37/30). It was, I think, common ground between the parties that these papers are part of what the defendant knew or ought to have known, as from around the time of its publication. In any event, I would so find.
In a preface, the context in which the conference arose is set out. Pages 17 ‑ 21 are an article on exposure to asbestos during brake maintenance by Hickish & Knight. Further reference to this article will be made later in these reasons in the context of analysis of exposure levels. The conclusion of the authors was as follows:
Our investigations show that exposure to asbestos during brake maintenance is not as severe as was anticipated, and in the situations we examined, the personal exposure of the operators was below the limit corresponding to 50‑year exposure [a reference to the 1968 BOHS standards already referred to in these reasons].
It is however recommended that care should be exercised during brake cleaning to avoid inhalation of the dust produced, and the development of cleaning procedures which would reduce air contamination is desirable. The present trend towards the introduction of 'flow line' servicing at dealers works, in which one individual may be engaged in almost entirely on brake servicing, emphasises this point.
Our environmental studies have not included maintenance procedures which involve the filing or grinding of brake lining material, and we would envisage that these would give rise to considerably increased air contamination by chrysotile asbestos, with the attendant need for strict precautions to prevent the inhalation of fibres.
The Hickish & Knight study also referred to the observed fact that the percentage of asbestos fibres in the drum dust and airborne dust was much lower than in the dust formed from the original lining material (about 1% as against 40% ‑ 60%). There is reference to enquiries about how that occurs.
A reasonable person reading the Hickish & Knight paper would conclude that the asbestos in brake linings would or might lead to respirable asbestos fibres in brake dust and would lead to respirable asbestos fibres in any dust formed from the original brake lining material, such as by grinding or filing.
Pages 23 and 24 are a paper by Luxon of the Factory Inspectorate of the Department of Employment and Productivity. The paper sets out a number of cautionary notes respecting questions of measurement and dose. The paper describes the figures produced by Hickish & Knight as, to a large extent, reassuring in that they indicate that the exposure levels of those servicing braking systems are likely to be below the level of 2 fibres per cm3 considered, in the light of past knowledge, to be a safe one for chrysotile. The author went on to note the increasing tendency to carry out brake overhauls on a production line basis making the development of adequate precautionary measures even more important. He states, 'Certainly we should not be blowing out brake dust, even if it contains only a few per cent of asbestos'.
The 1975 NIOSH bulletin was issued on 8 August 1975 (exhibit 37/75). It referred to a meeting on 21 July 1975 convened by NIOSH to discuss the present state of knowledge with respect to the potential health hazards for persons exposed to asbestos during the servicing of motor vehicle brake and clutch assemblies. It stated that data from the Mount Sinai School of Medicine in New York indicated that workers engaged in the maintenance and repair of automobile and truck brake linings are exposed to potentially hazardous levels of airborne asbestos dust. It continued in the following terms:
Previous studies of the extent of asbestos emissions from automobile brake lining wear showed that only a very small fraction of the original asbestos content of the brake lining is found in brake drum dust. It was presumed that this is due to thermal degradation of the fibres during braking. The present findings indicate that enough asbestos is preserved to produce significant exposures during certain brake servicing procedures.
The full extent of asbestos‑related disease in brake servicing personnel is not known at present because this particular occupational group has not been studied systematically up to now. However, a review of the scientific literature on the association between asbestos exposure and mesothelial tumors of the pleura and peritoneum has revealed at least four cases of these rare tumors in persons who were employed in jobs involving automobile brake servicing.
For your information and guidance, we are enclosing pertinent references, estimates of the population at risk, a NIOSH interim recommendation for brake and clutch servicing procedures, and a copy of the Department of Labor standard covering exposure to asbestos in the work place.
The environmental studies of brake lining servicing operations outlined above together with observations of mesothelial tumors in persons so employed affirms the necessity for instituting and maintaining recommended control measures in this industry so that the health hazards of asbestos are minimized. (references omitted)
Attached to the bulletin were recommended procedures for asbestos brake and clutch servicing. Attention should be given to all of the measures there referred to which included the use of a rag soaked in water to clean brake drums. It was said that 'under no circumstances shall compressed air or dry brushing be used for cleaning'.
The 1982 NHMRC report (exhibit 41/15) on the health hazards of asbestos was relied upon by the plaintiff's experts and also as part of the defendant's case. It included the following three passages:
Given the inability to precisely identify a threshold level and the nature of biological variations in persons exposed, it is possible that a small proportion of workers may be affected at or below a hygiene standard. Good occupational hygiene practice requires that exposures be reduced to the best practical minimum below the hygiene standard. The Sub‑committee [for the report] agreed that this was particularly important where asbestos and other carcinogens were concerned ... (p 8)
The Sub‑committee, having accepted the existence of a threshold of risk and taken account of the uncertainties regarding it, concluded that it is at present impossible to establish an exact line of demarcation between safety and hazard with respect to exposure to asbestos and the subsequent development of mesothelioma. The Sub‑committee therefore supports the view that there should be a continuing requirement to reduce the exposure to all forms of asbestos to the minimum that is reasonably practical. (p 9)
Recommendation 1
Expert evidence suggests that it is not possible to establish a threshold value below which a carcinogenic effect of asbestos cannot be identified, although some recent evidence suggests that such a threshold may exist. The Subcommittee recommends that exposure to asbestos should, in all phases of the asbestos industry, be reduced to the lowest practicable level by the most efficient technology currently available and enforced through:
•extension of the provisions of State asbestos regulations to cover all work processes where exposure to asbestos dust may occur;
•statutory prohibition of all asbestos spraying;
•the licensing of contractors engaged in the repair, removal and replacement of asbestos‑containing insulation materials;
•compliance with the NH & MRC recommended codes of practice;
•delegation of responsibility for safety precautions to principal contractors in the building industry. (emphasis in the original text) (p 10)
Observations as to the evidence of Professor Robinson and Professor Musk
Professor Musk was cross‑examined at some length. He was asked a number of questions relevant to the differential diagnosis as between asbestosis and IPF. However, the diagnosis of NSIP was not put to him and he was asked no questions about it. Professor Robinson was asked numerous questions as to the diagnostic choice between asbestosis and IPF. He was asked only two questions about NSIP, being the last two questions of his cross‑examination (ts 629).
Those matters are, I think, relevant to whether the opinion of Associate Professor McKenzie, that the plaintiff has an idiopathic form of pulmonary fibrosis which is either NSIP or IPF, and more probably NSIP, should be accepted in preference to the opinions of Professor Musk and Professor Robinson.
The defendant pointed in submissions to Professor Musk's evidence in cross‑examination (ts 557) that only two lines of investigation into the correct diagnosis were left open. The first, Professor Musk said, was to consult an industrial hygienist to look at the actual exposure of the plaintiff; the second, to look at the epidemiological evidence to see whether anything is to be learned from that area. The substance of that evidence, as I understood it, was that these were the two areas, beyond the information already available to Professor Musk, which were or may be capable of assisting in determining the diagnosis question.
However, I have made findings that the evidence of the industrial hygienists does not provide a reliable dose estimate for the plaintiff. I have also found that, for the reasons given, the epidemiological evidence does not assist in any significant way.
In that light, the two lines of inquiry contemplated by Professor Musk have, in the event, proved not to assist in the diagnosis question. That returns attention to the opinions of the experts based upon the information available to them. In any event, as already observed, Professor Robinson differed from Professor Musk on the question of the utility of dose estimates and the epidemiology.
Each of Professor Robinson and Professor Musk has expressed the opinion that, taking into account what he knows of the plaintiff's history and the presence of the pleural plaques, the probabilities favour the conclusion that the plaintiff's condition is asbestosis.
As already explained, Professor Robinson gave significant but not controlling weight to the presence of pleural plaques. Professor Musk has, I think, taken a similar approach. Such an approach seems to me to have been appropriate and open to be taken. I refer to the earlier discussion of the significance of the presence of pleural plaques.
Professor Robinson explained in his evidence that individual sensitivity and reaction to the presence of asbestos fibres varies substantially. He referred to it as 'host reactivity' and found it to be a relevant consideration in his diagnosis of the plaintiff (see, for example, ts 619, 627 and 631). I accept that it is appropriate to take into account variations in host sensitivity and reaction to asbestos in determining the diagnosis.
Each of Professor Musk and Professor Robinson approached the diagnosis question in a way which was, each considered, and, I find, consistent with the 2004 ATS guidelines.
In support of a submission to the contrary, the defendant argued that in order to satisfy the third criterion of the 2004 ATS guidelines: exclusion of alternative diagnoses, alternative diagnoses must be excluded as reasonable possibilities. I do not accept that submission. Rather, the criterion, as I would understand it, requires the doctor to exclude, on balance, alternative diagnoses. That is what Professor Robinson did, as he explained.
The defendant submitted that the reasoning of Professor Musk and Professor Robinson was at variance one with the other. However, the defendant did not, when asked, identify particular respects, of any real significance, in which their reasoning was at variance. They differed on the utility of epidemiology and of a dose estimate from an industrial hygienist to the diagnosis. However, the defendant accepted that that was not significant for present purposes. That is because neither in fact relied upon any epidemiology or dose estimate in making their diagnosis or expressing their opinion in court. Of course, given that quite different questions, at times respecting different topics, were asked of each of them, some aspects of their reasoning have been articulated in greater detail by one rather than the other. An example of this is, I think, to be found in Professor Robinson's 'mathematical approach', to be discussed shortly.
Next, the defendant pointed to the evidence of Professor Robinson to the effect that, because of the low level of the plaintiff's exposure, it was likely that there had been some amphibole contamination of the asbestos dust (ts 634 ‑ 637). The defendant submits that there is no basis to postulate amphibole contamination other than working backwards from the (assumed) diagnosis of asbestosis and then having regard to the low level of exposure to asbestos. Rather, the defendant submits, the low level of asbestos exposure should lead to a conclusion that the disease is IPF rather than asbestosis. Accordingly, a fatal flaw in Professor Robinson's reasoning is said to have been revealed.
I do not accept that submission.
There is no specific evidence before me as to the composition of Ford brake linings during the relevant period, although clearly it was generally understood and accepted that they contained chrysotile (being serpentine, not amphibole, in nature). Thus the possibility of amphibole contamination, perhaps for a part of the relevant period, cannot be definitely excluded. However, there is nothing in the evidence which positively supports it having occurred.
Professor Robinson was, from the time he first saw the plaintiff, aware of the source and nature of the plaintiff's exposure to asbestos. The possibility of amphibole contamination of what was understood to be chrysotile asbestos was not a matter mentioned in his reports. It emerged only at the conclusion of his oral evidence. Professor Robinson said (and I accept) that his diagnosis does not hinge upon a view that there was amphibole contamination. I find that that possibility was not a central part of Professor Robinson's reasoning in reaching (and maintaining) his opinion that the plaintiff has asbestosis.
I accept that, to the extent that the level of exposure was thought to be so low as to suggest that there was or may have been amphibole contamination, that should lead to further consideration of the question of whether the fibrosis was caused by asbestos at all. However, I do not accept that Professor Robinson failed to do that in forming (and maintaining) his opinion that, on the probabilities, the plaintiff's fibrosis was caused by asbestos.
In the end, Professor Robinson says, the diagnosis question is a question of likelihood. An apparently important part of his reasoning in preferring a diagnosis of asbestosis as being more likely than IPF was articulated in the course of re‑examination. At ts 631 ‑ 632 Professor Robinson said as follows:
one makes a judgement call based really on likelihoods. For example, he has asbestos in his lung. It is causing disease. Cryptogenic fibrosing alveolitis, the alternative diagnosis, is a very rare disease. It is about 3 in 100,000. So, for example, if you have a high level of asbestos exposure, let's say you worked in the mill at Wittenoom or some intense exposure, you might have a lifetime risk of 30%. With moderate exposure it might be 3%. That means 97% of people with that exposure won't get it, so 3% is still pretty high. If you have low‑level exposure it might only be .3% so that means 99.7% of people in that occupation won't get it so epidemiological studies often won't show that up but .3% is still 100 times .003%, which is the background incidence of IPF, so anyone who has got asbestos exposure who has an IPF or asbestosis‑like pattern, 99 of them, on sheer mathematical grounds, who have had low exposure have probably got asbestosis and one IPF. When a patient comes to see me and I weigh this up and I make the statement, 'On balance one has to ascribe the interstitial lung disease to asbestos,' it's as much a mathematical thing; that is, that there are 99 chances out of 100 that it's due to asbestos, or something like that. I mean, IPF is a rare disease.
See also ts 634 ‑ 635 where the same point was made, and where he said that even if asbestos being the cause was 10, 20 or 30 times more likely than it being a case of IPF, that would still influence the diagnosis.
Professor Robinson did not identify (and was not asked to identify) the sources of the probability figures which he used in his explanation of his view of the competing probabilities. There is other evidence, to which I will come, as to the incidence (more correctly, prevalence) of IPF, suggesting it is higher than the level referred to by Professor Robinson. The incidence or prevalence of the disease is a matter where there is evidently available data. However, given that the plaintiff's exposure level was, from Professor Robinson's perspective, unquantified, it would seem unlikely that there is published data from which figure for the probability of the plaintiff contracting asbestosis can be directly derived.
I do not take Professor Robinson's figures as to the probability of contracting asbestosis to be intended as mathematically precise. Rather, they seem to be illustrative numbers used to explain his thinking. The thrust of his thinking is that, given the presence of the plaques and the plaintiff's history of exposure, the probabilities of asbestosis exceed the probabilities of IPF by more than an order of magnitude, ie at least a factor of 10.
Professor Robinson's vast experience and research, over more than 20 years, in relation to asbestos related diseases might be thought to provide a reasonable foundation for making a ball park assessment of the kind which he explained.
A similar line of reasoning was, I think, taken by Professor Musk, although it was developed in less detail. In the course of agreeing that the lower the exposure of the plaintiff the less likely the disease is to be asbestosis, he observed, 'but IPF is not a common disease so I think virtually any measurable exposure is likely to be important' (ts 568).
The defendant criticised this reasoning, which it termed Professor Robinson's 'mathematical approach', in two respects. First, it pointed to evidence to the effect that the prevalence of IPF is higher than the 3 in 100,000 referred to by Professor Robinson. Associate Professor McKenzie said (ts 1006 and 1057) that the literature suggests the prevalence of IPF is somewhere between 5 per 100,000 and 20 per 100,000. He suggested that the higher figures were more recent, and that the literature suggested an increase in incidence of the disease. The ATS/ERS joint statement (exhibit V/13) had some reference to prevalence estimates varying from 3 to 6 per 100,000, with more recent figures for one county in New Mexico revealing a prevalence of 20 per 100,000.
There was also evidence from Dr Goodman which suggested a prevalence figure for IPF which was higher again. He referred to Table 5 of an article by Demedts et al (exhibit V/17). That was based primarily upon the study in the county of New Mexico (also referred to in the ATS/ERS joint statement) which had identified (using round figures) a prevalence for males of 20 per 100,000 and an incidence for males of 10 per 100,000. Elsewhere in the Demedts et al paper, there is reference to a study showing a prevalence of 3 ‑ 6 per 100,000 for males; and another indicating a prevalence of 20 per 100,000 for males (see p 9).
I accept Associate Professor McKenzie's evidence to the effect that the prevalence of IPF is now thought to be somewhere between 5 and 20 per 100,000.
In this context, the defendant appeared also to place reliance on evidence to the effect that the prevalence of asbestosis generally is falling. I do not find such evidence to be of any assistance in assessing the likelihood of whether the plaintiff, with the history which he has, and with pleural plaques, has asbestosis.
Thus I have found that the prevalence of IPF is now thought to be higher than the 3 per 100,000 figure used by Professor Robinson. However, given the scale of the differences in the ball park figures used by Professor Robinson, that, in itself, does not seem to me to invalidate his reasoning (although, plainly, it makes the position less clear cut). Moreover, it is unclear whether Professor Robinson was referring to the prevalence of IPF in Australia specifically, as against its prevalence throughout the world.
Secondly, and perhaps more fundamentally, the defendant also criticised the logic and methodology inherent in Professor Robinson's response. The defendant contended that the logic of Professor Robinson's response would lead to the conclusion that, whenever there was an exposure to asbestos at whatever level (albeit non‑trivial, in that it had caused pleural plaques), pulmonary fibrosis would always be attributed to the asbestos. As it was put in oral submissions, it is said not to be appropriate to disregard the prevalence of IPF, whatever the level of prevalence is, by attributing all cases where some exposure to whatever levels of asbestos existed, as being asbestosis. The 3 (or 6 or whatever the figure) are actual cases and should not be mathematically consigned to be asbestosis on the basis that 'they are nearly all asbestosis therefore we will treat them all as asbestosis' (ts 1374).
At a statistical or general level, I see some force in the submission made by the defendant. However, the question for Professor Robinson (and the question for the court in this case) involves identifying, on the probabilities, the more likely conclusion as to whether the plaintiff's fibrosis is or is not caused by asbestos. In the context of determining that question, I see no flaw in Professor Robinson's logic or methodology in taking account of his views as to the relative probability of IPF and asbestosis in the known circumstances. To the contrary, it seems to me appropriate to take account of those matters.
Conclusion as to plaintiff's fibrosis
In the preceding discussion I have found that:
(a)Professor Robinson and Professor Musk took into account all relevant significant matters in assessing whether the plaintiff had asbestosis or IPF (or, to the extent it was raised, NSIP);
(b)(unlike Associate Professor McKenzie) Professor Robinson and Professor Musk took only relevant matters into account in their opinion as to diagnosis;
(c)Professor Robinson and Professor Musk had regard to their understanding of the work practices and environment leading to the plaintiff's exposure, which was substantially consistent with my findings;
(d)Professor Robinson and Professor Musk gave appropriate consideration to alternative diagnoses, in particular IPF (in Professor Robinson's case that was spelled out in his first report);
(e)Professor Robinson and Professor Musk gave appropriate but not determinative weight to the presence of pleural plaques;
(f)Professor Robinson and Professor Musk gave appropriate consideration to the features of the plaintiff's condition which were atypical for, but not inconsistent with, asbestosis, but concluded that these features did not assist in choosing between asbestosis and IPF;
(g)Professor Robinson and Professor Musk approached the diagnosis in a way which was consistent with the 2004 ATS guidelines;
(h)Associate Professor McKenzie took into account his view that asbestosis would not occur at an exposure level below 25 fibre/ml years, a view which I have not accepted;
(i)Associate Professor McKenzie also took into significant account the radiography, as favouring a diagnosis of IPF/NSIP, whereas I have found that (beyond the common ground) the radiography does not assist in the diagnosis question; and
(j)there were various aspects of Associate Professor McKenzie's evidence which bore adversely upon the weight to be given to it.
For the reasons given, in the light of the findings and observations already made, I conclude as follows:
(a)I accept the opinion evidence of Professor Robinson and Professor Musk that the plaintiff suffers from asbestosis;
(b)I do not accept the evidence of Associate Professor McKenzie to the effect that the plaintiff has IPF or NSIP;
(c)on the balance of probabilities, I find that the plaintiff suffers from asbestosis.
Was the plaintiff's asbestosis caused by the defendant's negligence?
In the realm of negligence, causation is essentially a question of fact to be resolved as a matter of common sense. In resolving that question, the but‑for test has an important role to play but it is not a comprehensive and exclusive test of causation; value judgments and policy considerations intrude: Bennett v Minister of Community Welfare (1992) 176 CLR 408, 412 ‑ 413; March v E & M H Stramare Pty Ltd (1991) 171 CLR 506, 515 ‑ 519, 522 ‑ 524; Medlin v State Government Insurance Commission (1995) 182 CLR 1, 6.
Situations where it has been recognised that the 'but‑for' test is inadequate as an exclusive test for causation include where there is said to be an intervening cause or an alternative sufficient cause, or where the connection between the defendant's wrong and the plaintiff's damage is insufficient to warrant the attribution of legal responsibility. An example of the last category of case is where the defendant's wrong merely secures the presence of the plaintiff at the time and place of the damage (without thereby having increased the risk of injury). Thus it is not enough that something contributes an essential condition (in the but‑for sense) to characterise it as a cause for the purpose of attribution of legal responsibility. However, this case does not raise considerations of any of these characters.
I have made the following findings:
(a)the plaintiff has asbestosis;
(b)the only asbestos exposure of any significance experienced by the plaintiff occurred during his work as a mechanic;
(c)had the defendant provided the required warning, the protective measures referred to in that warning would have been implemented;
(d)if those protective measures had been implemented, the plaintiff's exposure to asbestos during his work from 1970 to 1987 would have been considerably diminished;
(e)the higher the dose of asbestos, the greater the risk of contracting asbestosis.
I find that had the required warning been given, on the balance of probabilities, the plaintiff would not have contracted asbestosis.
In so finding, I have taken account of the fact that the plaintiff also worked as a mechanic in a service station not associated with Ford from 1988 to 1994. However, taking into account the evidence as to the extent of exposure during the 1970s at Anderson Ford, and the medical evidence as to the latency of asbestosis, I find that, had the required warnings been given, the plaintiff would not have contracted asbestosis.
Thus the question of causation in fact is answered in favour of the plaintiff. That leaves only the question of whether the defendant is in law causally responsible for the damage: Bennett (412 ‑ 413); City of Stirling v Tremeer [2006] WASCA 73; (2006) 32 WAR 155 [73]; Amaca Pty Ltd v Hannell [389].
I am satisfied, on the findings just summarised, that the defendant's negligence is properly to be seen as a cause of the plaintiff's asbestosis so as to attribute legal responsibility to the defendant. The defendant had a duty to take steps to reduce the risk of asbestos inhalation injury to a class of persons including the plaintiff. The defendant breached its duty. Had the defendant performed its duty, the plaintiff would not have contracted asbestosis.
I find that the defendant's negligence caused the plaintiff's asbestosis. Accordingly, the defendant is liable to the plaintiff for damages for his asbestosis arising from the defendant's negligence.
Conclusion
The plaintiff is entitled to judgment for damages in the sum of $840,000.
JURISDICTION : SUPREME COURT OF WESTERN AUSTRALIA
IN CIVIL
CITATION: LO PRESTI -v- FORD MOTOR COMPANY OF AUSTRALIA LTD [No 2] [2008] WASC 12 (S)
CORAM: BEECH J
HEARD: ON THE PAPERS (WRITTEN SUBMISSIONS FILED 4 MARCH 2008)
DELIVERED : 19 FEBRUARY 2008
SUPPLEMENTARY
DECISION :12 MARCH 2008
FILE NO/S: CIV 1583 of 2003
BETWEEN: ANTONINO LO PRESTI
Plaintiff
AND
FORD MOTOR COMPANY OF AUSTRALIA LTD
Defendant
Catchwords:
Costs - Indemnity costs - Calderbank offer - Whether gives rise to prima facie entitlement to indemnity costs - Whether rejection of Calderbank offer ground for ordering indemnity costs
Legislation:
Rules of the Supreme Court 1971 (WA) O 24A
Result:
Defendant to pay the plaintiff's costs on a party-party basis
Category: B
Representation:
Counsel:
Plaintiff: No appearance
Defendant: No appearance
Solicitors:
Plaintiff: Slater & Gordon
Defendant: Clayton Utz
Case(s) referred to in judgment(s):
Alpine Holdings Pty Ltd v Warwick Entertainment Centre Pty Ltd [2003] WASC 53 (S)
Calderbank v Calderbank [1976] Fam 93
Colgate‑Palmolive Company v Cussons Pty Ltd (1993) 46 FCR 225
Flotilla Nominees Pty Ltd v Western Australian Land Authority [2003] WASC 122 (S); (2003) 28 WAR 95
Fyna Foods Australia Pty Ltd v Cobannah Holdings Pty Ltd (No 2) [2004] FCA 1212
Globaltech Pty Ltd v Pareek [2006] WASC 30 (S)
Gove v Black [2006] WASC 298 (S)
Gretton v Commonwealth of Australia [2007] NSWSC 149
Jones v Bradley (No 2) [2003] NSWCA 258
MGICA (1992) Pty Ltd v Kenny & Good Pty Ltd (No 2) (1996) 70 FCR 236
Multicon Engineering Pty Ltd v Federal Airports Corporation (1996) 138 ALR 425
NMFM Property Pty Ltd v Citibank Ltd (No 11) [2001] FCA 480; (2001) 109 FCR 77
SMEC Testing Services Pty Limited v Campbelltown City Council [2000] NSWCA 323
Townsend v Collova [2005] WASC 4 (S)
Unioil International Pty Ltd v Deloitte Touche Tohmatsu (No 2) (1997) 18 WAR 190
BEECH J: On 19 February 2008 I delivered reasons for decision after the trial of this action. I concluded that the plaintiff was entitled to judgment for damages in the agreed sum of $840,000. Judgment in that amount was entered on that day.
The plaintiff seeks an order that the defendant pay his costs on an indemnity basis, or alternatively on a solicitor and own client basis. No other special costs orders were sought by the plaintiff.
The plaintiff relies primarily upon the rejection, by the defendant, of an offer of settlement. On 12 September 2007 the plaintiff offered to settle his claim for $450,000 plus indemnities for certain repayments to Medibank Private and the Health Insurance Commission, plus costs to be taxed if not agreed.
The offer was expressed to be without prejudice except as to costs. The letter stated that if the offer was not accepted and the judgment entered after trial was more favourable to the plaintiff than the offer, the plaintiff would apply for costs on a solicitor-own client basis from the date of the letter, in accordance with the principles applied in Calderbank v Calderbank [1976] Fam 93.
The offer was rejected on 13 September 2007.
The trial commenced on 24 September 2007.
It is convenient to begin by outlining some general principles relevant to the exercise of the discretion to award costs.
The usual costs order is that the successful party in an action is awarded its costs on a party and party basis. An order for indemnity costs will be made only if there is some special or unusual feature in the case to justify departure from the ordinary practice. The court has power to make an indemnity costs order whenever justice requires it: Unioil International Pty Ltd v Deloitte Touche Tohmatsu (No 2) (1997) 18 WAR 190, 191; Flotilla Nominees Pty Ltd v Western Australian Land Authority [2003] WASC 122 (S); (2003) 28 WAR 95 [8].
The categories of cases in which the discretion to award indemnity costs may be exercised are not closed: Colgate‑Palmolive Company v Cussons Pty Ltd (1993) 46 FCR 225, 233 ‑ 234; Unioil (191).
Most of the situations in which indemnity costs have been awarded have involved an element of improper or unreasonable conduct on the part of the parties or their advisors in the conduct of the case: Flotilla [9]; Colgate‑Palmolive (233 ‑ 234).
An offer of compromise is capable of being a ground relevant to the award of indemnity costs. However in my opinion, the rejection by a defendant of an offer of compromise which subsequently proves to be more favourable to the defendant than the result of the trial does not necessarily or presumptively lead to an award of indemnity costs for the plaintiff. All the circumstances must be considered in determining whether justice requires the exceptional exercise of the power to award indemnity costs.
The plaintiff relies upon the decision of Roberts‑Smith J in Alpine Holdings Pty Ltd v Warwick Entertainment Centre Pty Ltd [2003] WASC 53 (S). In that case, his Honour followed the decision of Rolfe J in Multicon Engineering Pty Ltd v Federal Airports Corporation (1996) 138 ALR 425 in holding that an offer of compromise, whether made under the Rules of Court or pursuant to a 'Calderbank letter', gives rise to a prima facie presumption of indemnity costs in the event that the result of the trial was less favourable to the recipient of the offer than was the terms of the original offer [72].
The decision in Multicon Engineering was not followed by Lindgren J in MGICA (1992) Pty Ltd v Kenny & Good Pty Ltd (No 2) (1996) 70 FCR 236, 240. Lindgren J pointed to decisions of judges of the Federal Court who had taken an approach different from that stated by Rolfe J. There seems to me to be considerable force in the matters referred to by Lindgren J as supporting the view that non‑acceptance of a Calderbank offer does not give rise to a prima facie entitlement to indemnity costs. See also SMEC Testing Services Pty Limited v Campbelltown City Council [2000] NSWCA 323 [37]; Jones v Bradley (No 2) [2003] NSWCA 258 [9]; Gretton v Commonwealth of Australia [2007] NSWSC 149 [10].
In any event, in the light of the amendments to O 24A of the Rules of the Supreme Court 1971 (WA) which took effect on 1 March 2007, it does not seem to me to be necessary to decide whether the approach of Roberts‑Smith J in Alpine should be followed. That is because his Honour's approach was founded upon the then prima facie entitlement of a plaintiff who had made an offer under O 24A to indemnity costs in the circumstance that the result of the trial was less favourable to the defendant than the terms of the offer. His Honour adopted the view that the same prima facie entitlement to indemnity costs should arise from a Calderbank offer. The amendments to O 24A which took effect on 1 March 2007 mean that there is now no such prima facie entitlement under O 24A. See O 24A r 10(4). Thus the foundation for his Honour's view that rejection of a Calderbank offer can give rise to a presumption in favour of indemnity costs no longer exists.
In this regard, I note that in Townsend v Collova [2005] WASC 4 (S), Le Miere J held that rejection by a plaintiff of a Calderbank offer did not give rise to a prima facie entitlement to indemnity costs. In so holding, Le Miere J distinguished Alpine Holdings and Multicon Engineering on the basis that those were cases in which the plaintiff had made a Calderbank offer. In Townsend, the Calderbank offer had been made by the defendant. Under the provisions of O 24A, a defendant had (and has) no prima facie entitlement to indemnity costs in circumstances where a plaintiff has rejected an offer from a defendant that is more favourable to the plaintiff than the outcome of the action.
The amendments to O 24A in 2007 have equated the position of a plaintiff offeror under O 24A with the position of a defendant offeror.
For these reasons, in my opinion the making of an offer of settlement which is more favourable to the offeree than the outcome of a trial does not give rise to any prima facie entitlement to indemnity costs.
The relevance of the rejection of what proves to be a favourable offer of settlement to the award of indemnity costs has been stated in different ways in various decisions. For example, it has been said that rejection of a settlement offer may lead to indemnity costs where the rejection is 'imprudent' (Colgate‑Palmolive (233); NMFM Property Pty Ltd v Citibank Ltd (No 11) [2001] FCA 480; (2001) 109 FCR 77 [82]); 'plainly unreasonable' (NMFM [82]); or simply 'unreasonable' (Globaltech Pty Ltd v Pareek [2006] WASC 30 (S) [17]; Fyna Foods Australia Pty Ltd v Cobannah Holdings Pty Ltd (No 2) [2004] FCA 1212 [5]).
In Gove v Black [2006] WASC 298 (S) [45] ‑ [46], Templeman J adopted the approach that a failure to accept an offer may give rise to costs on an indemnity basis if the failure to accept the offer was so unreasonable in all the circumstances that an order for costs on a party and party basis would not be just. That is the formulation which I would adopt.
In assessing any question of the reasonableness of the rejection of an offer, it is of the first importance that the assessment be made without the benefit of hindsight. See, for example, Gretton [24], [38].
In my opinion, in the circumstances of this case the defendant's rejection of the plaintiff's offer of settlement falls well short of being so unreasonable as to mean that it is just to order indemnity costs.
The defendant had a case of substance, supported by a substantial body of expert evidence. In some instances (Mr Rogers, Associate Professor McKenzie), the evidence of the defendant's experts conflicted directly with the plaintiff's experts. In other cases, the questions were as to the weight to be given to expert evidence on a subject (for instance, epidemiology), in determining the cause of the plaintiff's fibrosis.
The defendant cannot be expected to have been able to predict what my findings would be in determining the various issues regarding the expert evidence. Many of the plaintiff's submissions in support of an award of indemnity costs seem to me to involve, implicitly, expecting the defendant to have been able to do so.
The defendant's conduct in deciding to have the court decide the substantial issues arising from the expert evidence was, in my opinion, not unreasonable and certainly not so unreasonable as to make it just to order indemnity costs.
The plaintiff submitted that the defendant ought to have recognised that it faced a real risk in the litigation. I accept that that is so, but that fact alone does not provide an adequate basis for the award of indemnity costs.
Nor, in my opinion, is the question to be determined (as some of the plaintiff's submissions suggest), by whether the defendant reasonably held the view that it was 'likely' to succeed in its defence. That is a judgment which the court is not well placed to make, in that the views expressed by those who advised the defendant are not available. (The defendant's submissions contain various statements as to what the defendant 'believed' prior to trial, in various respects. As these assertions are not supported by evidence I have not had regard to them.) In any event, a decision to litigate a case of substance which had a reasonable prospect of success (albeit that such prospects were thought to be less than 'even money') in the face of an offer to settle, would not, in the absence of further facts, give rise to a sufficient ground to order indemnity costs.
It follows that I do not accept the plaintiff's submission that 'the defendant having chosen to take the risk of litigating, there ought to be a price to pay beyond party/party costs'. The 'price to be paid' by the defendant includes the excess of its liability under the judgment compared to the settlement offer, its own costs after the offer was rejected, as well as its liability for the plaintiff's costs on a party-party basis. In any case, for the reasons I have sought to explain, I do not consider that the plaintiff's submission in this regard reflects a proper basis for the award of indemnity costs.
This was not an instance where a party's case was doomed to fail, or suffered from a fatal flaw which was pointed out by the other party in the Calderbank offer; see NMFM [87].
The plaintiff emphasised that the defendant rejected his offer within one day of receiving it. In the circumstances of this case I do not consider that that fact affords any support for a conclusion that the rejection was hasty or pre‑emptory and so unreasonable in the sense that I have explained.
The plaintiff also submitted that the relative ability of the parties to bear the additional costs of the trial is relevant. I do not accept that the differing means of the parties provides any ground for ordering indemnity costs.
In my opinion, neither the defendant's rejection of the offer of settlement, nor any other aspect of the defendant's conduct referred to in the plaintiff's submissions provides any sufficient basis to order indemnity costs.
The plaintiff seeks, in the alternative, costs on a solicitor-own client basis. No separate submissions were made in support of that application.
For the reasons already stated I am not satisfied that it is appropriate in this case to depart from the usual order for costs on a party-party basis.
For these reasons I order that the defendant pay the plaintiff's costs of the action, including any reserved costs, such costs to be taxed if not agreed.
10
33
1