R v KARGER No. SCCRM-98-224 [2001] SASC 64

Supreme Court of SA|2007-04-05|Before: Kearns J

CITATION : (re Rowley) The University of Adelaide v BI (Contracting) Pty Limited [2007] NSWDDT 1

PARTIES : The University of Adelaide BI (Contracting) Pty Limited

Dust Diseases Tribunal :- cross claim duty of care of sprayer to bystander state of knowledge in 1961 as to the health risks associated with asbestos CATCHWORDS: breach of duty of care causation of exposure to mesothelioma where exposure was for five to ten minutes' duration analysis of McNeill's case extent of contribution between tortfeasors

Dust Diseases Tribunal Act 1989 LEGISLATION CITED: Health Act 1956 Wrongs Act 1936 (SA) Civil Procedure Act 2005

James Hardie & Co Pty Ltd v Seltsam Pty Ltd (1998) 196 CLR 53; R v Karger [2001] SASC 64[67]; Jones v Scully [2002] FCA 1080[82-5]; Bux v Slough Metals Limited [1973] 1 WLR 1358; Seltsam Pty Limited v McNeill [2006] NSWCA 158; CASES CITED: BI (Contracting) Pty Limited v Myer Emporium Limited (2005) 3 DDCR 142; BI (Contracting) Pty Limited v Public Trustee of South Australia (2005) 3 DDCR 161; A.W. Baulderstone Holdings Pty Limited v Bradford Insulation (SA) Pty Limited [2006] NSWDDT17; Seltsam v Minehan (1996) 13 NSWCCR 410; Julia Farr Services Inc v Hayes [2003] NSWCA 37; Adelaide Chemical and Fertilizer Company Limited v Carlyle (1940) 64 CLR 513, 534

DATES OF HEARING: 30.10.06, 31.10.06, 01.11.06, 02.11.06, 11.12.06, 12.12.06, 05.04.07

Messrs M J Neil RFD QC and J C Sheller, instructed by Thompson Cooper, appeared for the cross claimant LEGAL REPRESENTATIVES: Mr T G R Parker SC, instructed by Makinson D'Apice, appeared for the cross defendant

JUDGMENT: 65 Dust Diseases Tribunal of New South Wales Matter No. DDT00073/2003/CC1 (re Derrick Rowley, Plaintiff)

BI (Contracting) Pty Limited (BIC), when it undertook insulation spraying in 1961, could have undertaken some simple steps that would have prevented Professor Rowley from being exposed to asbestos dust and fibre and contracting mesothelioma, from which he died. The statement of that proposition, whilst it might appear to provide the key to the resolution of this case, does not. It does not because that statement hides a number of issues that were contested in this case and that need resolution. Further, it is a statement going to the issue of breach of duty of care and it cannot be made good without an antecedent issue being determined in the affirmative. That antecedent issue is whether BIC owed Professor Rowley a duty of care at all. That was the main issue in this case.

Professor Rowley died as a result of contracting mesothelioma. For the contraction of that disease, he sued the parties to these proceedings. Those parties are the cross claimant, The University of Adelaide (the University) and the cross defendant, BIC. The University employed Professor Rowley. BIC sprayed asbestos insulation at the medical school at the University in 1961.

His case against the University and BIC was that he contracted his illness as a result of exposure to asbestos dust and fibre over a period of about five to ten minutes on one day in 1961 when some asbestos spraying was being conducted at the medical building at the University.

His case against the University and BIC commenced in Adelaide on 12 November 2003 when oral evidence was given and documents were tendered. During the currency of the case on the following day, Professor Rowley settled his case against BIC. The effect of the settlement was that he would receive nothing from BIC and, in due course, a verdict would be entered in favour of BIC in his claim against it. The University had an interest in that settlement and, for that reason, the verdict to be entered in favour of BIC was not entered at the time Professor Rowley settled his case with BIC. The reason for this was to overcome the effect of the High Court decision in James Hardie & Co Pty Ltd v Selstam Pty Ltd (1998) 196 CLR 53. As the matter was done in this way, the University's right to any claim for contribution it might have against BIC was preserved.

To return to the short historical narrative of the matter, after Professor Rowley's case against BIC was settled, he proceeded with his case against the University. The case continued on 18 December 2003, 16 February 2004 and 17 February 2004 when further oral evidence was given and documents were tendered. On 17 February 2004, Professor Rowley's case against the University was settled. It was settled by the entry of a judgment in his favour in the sum of $250,000, plus costs.

In these proceedings, the University seeks a contribution from BIC towards the amount of the judgment and costs it has paid to Professor Rowley.

The parties informed me that there was a question as to whether the applicable law to apply for the purpose of determining the contribution claim was the law of New South Wales or the law of South Australia. It was agreed, however, that it was a question that did not arise, because there was no material difference in the interpretation and application of the two pieces of legislation.

At the commencement of the hearing, the University applied to amend its cross-claim by adding additional particulars of negligence, in particular, that the so-called Dreessen standard had been breached. A ruling on that application was deferred. I do not consider any prejudice has flowed to BIC from the proposed amendment and I allow it.

After Mr M Neil of Queen's Counsel, who appeared with Mr Sheller of Counsel, for the University, opened the case, Mr Parker of Senior Counsel, who appeared for BIC, stated the issues.

It is apparent that these proceedings give rise to numerous issues. The issues concern the state of knowledge as to the health risks associated with asbestos in 1961 and also numerous evidentiary issues.

In a crude sense, the issue may be described as being whether approximately five to ten minutes of exposure to asbestos dust and fibre during the course of a spraying operation in 1961 was enough:

· to give rise to a duty of care, the content of which required the University and BIC to take reasonable steps to prevent Professor Rowley being harmfully exposed to asbestos dust and fibre; · if the answer to the above point is affirmative, to give rise to a breach of that duty; · to have caused Professor Rowley's mesothelioma.

In the course of the conduct of these proceedings numerous evidentiary questions arose. Senior counsel for both parties took the position that, rather than dealing definitively with each tender as it arose, I could receive all the evidence and make my final ruling on it during the course of these reasons.

In the end, the contentious evidence really finished up in two categories. There was evidence that was allowed in, but without prejudice to the right of either party to make appropriate objections and deal with it in the course of submissions and then there was evidence on the voir dire which, strictly speaking, would need to be dealt with differently. The only reason this needs to be expressed in these reasons is so that it is made clear that whichever category the evidence fell into, it was not intended to be treated in any different way to the other. All the contentious evidence, whether received subject to the right of the parties to deal with its admissibility in the course of submissions or whether received on the voir dire, was intended to be dealt with on the basis that the final disposition of that evidence would rest on my rulings which would be made during the course of these reasons.

Professor Rowley was exposed to asbestos dust and fibre from the spraying process of BIC at the medical school at the University in 1961

The statement contained in this heading includes two issues that were contested. They were whether BIC did the spraying at the medical school and whether it was asbestos that was sprayed.

In the course of the University's submissions in reply on the last day of hearing, Mr Parker SC announced that he did not contest that BIC was the party responsible for the spraying. That saves me setting out reasons why I would have made such a finding in any event. That simply leaves the issue as to whether it was asbestos that was sprayed.

Evidence supporting the fact that it was asbestos that was sprayed comes from a number of sources as follows:

(a) Mr Caon's evidence - Exhibit CX 9 paragraphs 6 and 9, Exhibit CX 83, 22.02 and Exhibit CX 85 paragraph 36. Objection was taken to his use of the term "asbestos" as evidence of the fact, but because of his lengthy experience as a lagger from 1953 including the spraying of asbestos, I accept his evidence on this point; (b) the University had a contract for work at the medical school in 1961 (Exhibit CD 4, Tab 7), the specifications of which included fire proof asbestos spraying (Exhibit CD 4, Tab 4 clauses 35 and 95);

(c) Mr Cushway (Exhibit CX 7) started at the University in 1979 as an engineer and in 1984 became Building and Estates Officer and Director of Property Services. Soon after he started in 1979 he became aware that asbestos had been used throughout the construction at parts of the University and this was considered to create a danger to those who may be exposed to asbestos. An asbestos register was maintained. Over time, the University sought to identify places where asbestos had been used and contracted for its removal. Asbestos was identified in the old medical school on Frome Road. The contracting for the removal of asbestos included asbestos located on the steel beams within the old medical school. I allowed much of this evidence over objection. I consider Mr Cushway's position equipped him to give the evidence he did; (d) documentary material evidences the presence of asbestos in the medical school in Frome Road - Exhibit CD 4, Tabs 14, 15, 19, 20, 29, 31, 43 and 47. It comprised 70%-90% amosite. By 8 December 1981, it had been removed - Tab 50.

I find that in 1961 for about five to ten minutes, Professor Rowley was exposed to asbestos dust and fibre at the medical school at the University when BIC was spraying asbestos insulation.

Professor Rowley was not otherwise exposed to asbestos dust and fibre

There is the possibility of some later exposure arising from Professor Rowley's continued work at the University. The evidence on this is flimsy. In the end, the further exposure was not pressed and I say no more about it other than that I am not satisfied on the evidence that there was any later exposure.

The nature and extent of Professor Rowley's exposure

I set out part of paragraphs 14 and 15 of Professor Rowley's affidavit.

While I was present at the building site, some of the workers sprayed a material on to the steel beams. There were workers on the ground spraying the beams and there were also workers on platforms spraying higher up…
The area where the spraying was being carried out was very dusty. The material that was sprayed was a dirty whitish-grey colour. I was in the vicinity of the spraying for about five but probably closer to ten minutes. I was keen to get out of there because it was not a particularly pleasant environment to be in. I commented to Geoff Harrison about how dusty the place was and that it did not seem very healthy for workers to be working in such a dusty environment…

Professor Rowley also gave evidence in his case and the transcript became evidence in these proceedings (Exhibit CX 83). He described being on the floor when the spraying was done and said it was very dusty. I mean there were clouds of dust everywhere (T.3.43). Professor Rowley walked all around the floor on which the spraying was being done including standing at the bottom of a ladder from which the sprayer was working. At this point, he must have been under some spray and dust cloud (see next paragraph). Over the whole of that floor It was dusty more or less everywhere to a greater or lesser extent. (Exhibit CX 83, p9.11)

Mr Caon swore an affidavit dated 29 October 2003 (Exhibit CX 9). He referred to there being a lot of dust around. Clouds of dust went into the air when bags of asbestos were tipped into the back of the asbestos spray machine. When the asbestos was sprayed, dust also went into the air. Some of the asbestos did not stick and went in to the air and on to the ground. He could see asbestos dust in the air. It looked like snow flakes. There was not a lot of ventilation at the medical school. In cross examination, this was qualified, in part, when he said that bags of asbestos were opened and, from the bag, handfuls of asbestos were put into the machine (Exhibit CX 83, 25.04). This evidence has a significance because it reveals that, apart from the asbestos spray, which was probably mixed with cement, there was also pure asbestos liberated into the atmosphere.

Mr Caon also gave evidence in Professor Rowley's case (Exhibit CX 83). His evidence was consistent with his affidavit. He stated that the asbestos spray on the girders was about one inch thick. This was in accordance with the specification (Exhibit CD 4, Tab 4, clause 95). The further removed from the source of spray, the finer the dust in the air became. He said there was a roof on the building as he had never been on a building that did not have a roof on it before he started.

Mr Caon also swore another affidavit. This was on 5 October 2005 and was in his own case. It became Exhibit CX 85. It is more extensive than his other affidavit and his evidence, but so far as concerns the spraying at the medical school, it is consistent with his other evidence.

On this material alone, which I accept, I am satisfied that Professor Rowley was exposed to asbestos dust and fibre for a period of five to ten minutes on a day in about mid to late 1961. The time in 1961, I take from Exhibit CD 4, Tab 7, from which it would seem work started probably at the beginning of March 1961. The timing of the spraying would then probably be mid to late 1961. Throughout that period of five to ten minutes, a process of spraying asbestos on the steel girders was being undertaken. It was an extremely dusty process. The asbestos dust and fibre in the atmosphere was very thick near the source of the spraying and thinned out over a distance removed from the source. Though the asbestos dust and fibre was thinned out over a distance removed from the source, it was still visible in the atmosphere at all places where Professor Rowley was on the floor over that five to ten minute period. Professor Rowley's exposure over the five to ten minute period encompassed exposure in the thickest of the dust and fibre and also where it had thinned out.

Even on a layman's view of it, this description of Professor Rowley's exposure exposed him to a level considerably in excess of ordinary background exposure that any member of the community is subject to. This, of itself, has a relevance on causation which I deal with from paragraphs 140-145.

I would add that this Tribunal, as a specialist tribunal, is well aware that spraying is one of the dustiest processes undertaken with asbestos if adequate steps are not taken to suppress the dust. I would add also that the content of the dust sprayed at the medical school had a high concentration of asbestos. The specification required a one inch thickness of asbestos (Exhibit CD 4, Tab 4, clause 95). That was applied (see paragraph 22). The asbestos mix also required some cement and a bonding agent.

(b) Other materials relevant to the extent of Professor Rowley's exposure

It is not uncommon for evidence to be given in this Tribunal that if dust is visible in the atmosphere in ambient light its concentration in the atmosphere is at least 5 million particles per cubic foot (5 mppcf). There was evidence to that effect in this case and, though there were qualifications, I accept that evidence. This evidence was given by Mr Stewart (T.106.42) although, with qualifications, he put it as high as 10 mppcf (Exhibit CX 113.47) and Professor Henderson (Exhibit CX 83, 15.40). Professor Henderson's qualifications to give that evidence were challenged, but for reasons given in paragraph 152, I accept he is able to give that evidence.

This evidence was also given in material tendered under section 25(3) of the Dust Diseases Tribunal Act, for example, Mr Kilpatrick (Exhibit CX 50; CX 51, 427T, 449H), Professor Ferguson (Exhibit CX 55, 99U; CX 74, 591), Dr Joseph (Exhibit CX 60, 78I, 149I) and Mr Stewart (Exhibit CX 71, 248F; CX 79, 43N). I note, especially, Mr Kilpatrick's practical experience in observing dusts in the atmosphere and undertaking laboratory assessments, relative to those observations.

There was evidence about the significance of visible dust. It is true that visible dust is not a scientific test of the concentration of asbestos dust and fibre in the atmosphere, nor of the concentration of respirable dust and fibre, nor of fibre type. However, it is a useful test to get some idea of the extent to which Professor Rowley was exposed where a spraying process, with a high concentration of asbestos, was being undertaken.

In the light of all this material, I find that Professor Rowley over the whole period of exposure during the spraying process was exposed to concentrations of asbestos dust and fibre in the atmosphere well in excess of 5 mppcf. I am unable to make a finding as to the precise level.

There was also some literature about the concentration of asbestos in the atmosphere in a spraying process as follows:

(1) article in 1971 by PG Harries (Exhibit CX 4). This was a study of the use of asbestos in naval dockyards. Records of dust sampling during spraying in 1951 showed asbestos fibre counts of 173-322 fibres per cubic centimetre and 3121-5957 particles per cubic centimetre of other dusts. These figures are not very helpful because it was agreed they could not be converted to an assessment of particles per cubic foot. It is, however, more evidence that spraying is a very dusty process;

(2) article in 1976 by Robert Barnes (Exhibit CX 24). This was a study of the process of spraying. The process was described. The process included spraying with a fine water mist, with a mix of chrysotile and small amounts of mineral oil and cement powder. The water mist was to give the mixture an adhesive quality when it hit the surface to be covered. It was sprayed to a depth of a quarter of an inch to two fifths of an inch. That may be contrasted with a spray depth of one inch at the medical school. Despite the use of water, fibres of asbestos contaminated the workers' environment and floated in the air for a considerable time. Concentrations as high as 150 mppcf had been registered in the vicinity of sprayers. Tests in Sydney in 1972 were said to give results varying from 15 to 80 fibres per cubic centimetre, although I note a reading of 5 fibres per cubic centimetre;

(3) chapter from Tweedale's book in 2000 (Exhibit CX 15). This chapter covers a number of matters, but, for present purposes, it is sufficient to note reports on measurements from spraying operations ranging from 4 f/cc (p204) to 1827 f/cc (p203). It demonstrates that spraying can give rise to very dusty conditions and not so dusty conditions where there is damping; (4) part of an article by Tweedale (Exhibit CX 14). This describes the spraying process. It notes that asbestos and cement were usually in a mix of 60/40 and that mineral oil and water were used. It went on to describe the process as obviously a very dusty technique and spoke of dangerous levels of fibre to many including bystander workers doing other jobs (p87). Measurements from 50 fibres per cubic centimetre to 1827 fibres per cubic centimetre were noted (p95). 32. In my view, these articles are not defining evidence as to what the concentration of asbestos was in the atmosphere at the medical school in 1961. Without knowing that conditions were comparable they could not be. The articles do give weight to spraying being a very dusty process and they do provide some indications of concentrations of asbestos that can prevail in certain conditions. They also offer support for the opinion expressed by Professor Henderson as to the probable concentration of asbestos in Professor Rowley's atmosphere (see paragraph 154 below).

Objection was taken to the tender of these articles. A useful statement of the law and the admissibility of scientific articles is to be found in the judgment of Mullighan J in R v Karger [2001] SASC 64[67]. I think they are admissible, not to prove the precise concentration of asbestos dust and fibre to which Professor Rowley was exposed, but to prove that spraying can be a very dusty process. Whether it is in any particular case then depends on the circumstances of the occasion and I have dealt with that especially in paragraphs 19 to 22. Professor Henderson has adopted the Harries article and the Tweedale measurements (T.42.17) and, accordingly, they are admissible. In my view, the Barnes article, being to the same effect, is admissible. There was an objection as to whether this comes within Professor Henderson's expertise in any event and, as already indicated, I deal with that in paragraph 152.

Mr Parker SC tendered an article by Bell (Exhibit CD 2). BIC relied on this to seek to demonstrate that spraying was not hazardous. The paper covered a number of matters including the investigation of asbestos concentrations in shipyards. Spraying of limpet asbestos carried the opinion no hazard. Wetting process at application of nozzle effective. Like Harries, Tweedale and Barnes, this is not defining evidence of the conditions at the medical school in 1961. It is, however, admissible. I do not find it of use in assessing the concentration of asbestos when Professor Rowley was exposed. The wetting process may have been effective in the Bell study, but it was not effective at the medical school.

Other evidence consistent with the fact that spraying can be a dusty process is to be found in Exhibit CX 45. This was a note of discussion on a number of papers that had been presented to the pneumoconiosis conference in 1968 and, in the course of discussion, Dr McNulty at p511 made an observation about asbestos spraying as follows.

The only reference I can find to asbestosis occurring in asbestos sprayers was a casual reference by Gilson in his Wyeth Memorial Lectures in which he mentioned that asbestosis was becoming less common in the textile industry and more common in laggers, asbestos sprayers, etc. There is no doubt that asbestos sprayers work in a very heavily contaminated and dusty atmosphere but there is a sort of pious hope that because the asbestos spray comes out surrounded by a collar of water that this causes aggregation of the smaller particles and that the eventual dust is not respirable.

This literature simply reinforces my view that Professor Rowley was exposed to high concentrations of asbestos dust and fibre when he visited the floor of the medical school on which spraying was being done in 1961.

There was a confounding factor in relation to the concentration of asbestos in the atmosphere where Professor Rowley was. That factor concerned the extent to which cement was added to the asbestos. I am satisfied there was some cement. The contract provided for it. There was no direct or circumstantial evidence as to the extent of cement being added to the asbestos. Two articles are not very helpful. Exhibit CX 24 describes the process of spraying as involving a mix of asbestos with small amounts of mineral oil and cement powder. The Tweedale article (Exhibit CX 14) refers to a proportion of asbestos to cement as being 60/40. This material does not enable me to make any specific finding about the content of the cement. I am satisfied, however, that asbestos was by far the predominant component of the spray mix. This confounding factor does not affect my view that Professor Rowley was exposed to a level of asbestos considerably in excess of ordinary background exposure, nor my view that his exposure was well in excess of 5 mppcf. In saying this, I am especially mindful of the fact that at all times Professor Rowley was standing or moving in dust visible in the atmosphere and also the fact that one of the sources of that dust was pure asbestos liberated into the atmosphere when it was removed from the bag to the machine.

What was the state of knowledge available in 1961 as to the risks to health associated with asbestos?

One of the circumstances to be taken into account in determining whether BIC owed Professor Rowley a duty of care will be the knowledge available to it in 1961 of risks to health associated with asbestos. In this regard, I note that all the knowledge and learning that was available in 1961 was in fact known to BIC. Mr Parker SC accepted BIC was as knowledgeable as any other informed industry participant in Australia in 1961 - submissions 74.48. I proceed to examine the state of knowledge.

A note in The Lancet (Exhibit CX 13) on 20 February 1932 referred to "the existence of chronic industrial pulmonary asbestosis" and noted that the first fatality from asbestosis was recorded in 1900. Later in the note, concern was expressed about the expectation in years to come of a large increase in pulmonary asbestosis.
Later, in response on 5 March 1932, the inventors of the process for insulating the London tube railways, explained the method they were to use. They noted that an incoming supply of fresh air would remove any possible traces of dust from the vicinity of the worker. Also, sufficient liquid was to be used to prevent the possibility of dry particles of fibre escaping into the surrounding atmosphere. Even at that stage in 1932, a fairly meticulous approach to ensuring the safety of the workers and others resulting from the process of spraying asbestos in 1932 was being expressed.

Report in 1930 by ERA Merewether, MD & CV Price (Exhibit CX 25). This report noted that the effects of dust, and this includes asbestos, on the lungs could vary from slight to severe and even fatal. The study, the subject of the report, examined manufacturing processes where there was exposure to pure, or near pure, asbestos. It did not study cases where there was exposure to asbestos mixed with other dusts. It thus has a qualification of not having studied cases of lower exposure than those that were studied to see what, if any, pulmonary consequences resulted. Nevertheless, the report draws a conclusion that pulmonary disability was likely as a consequence of the concentration of dust to which a person was exposed and the length of exposure. Amongst the cases studied, there was no fibrosis amongst 89 subjects who were employed in an asbestos process for a period of 0-4 years. There were three cases with less than five years' exposure, although it was considered that there was some earlier exposure to other dusts in these cases. The report noted that further research was necessary. A large section of the report dealt with preventative measures. It its summary, it stated The appropriate methods for the suppression of dust may only fully be determined when the harmful effects of comparatively low concentrations of asbestos dust are duly appreciated.

(a) Paper in 1933 by ERA Merewether, MD (Exhibit CX 26) - This paper noted that exposure to asbestos from less than five years can result in the development of a degree of asbestosis sufficient to cause death. The author stated it would be wrong to assume that so long as the period of exposure did not exceed five years, the risk of contracting asbestosis was almost negligible. He went on to say that this would occur if a worker was exposed to a dense concentration of dust. Development of asbestosis would not occur below a certain concentration of dust.

(b) If a certain, but unknown, amount of asbestos dust is trapped in the lungs, death due to the development of asbestosis is inevitable. The paper considered it important to consider what amount of dust would produce that result, or conversely, what amount of dust, from the practical standpoint, could be inhaled with impunity. (c) The paper went on to consider various processes and spinning was considered to be the process giving off the least concentration of dust. The level that emanated from that process was considered to be a safe level. The safe level was unknown. Further, the acceptance of the level given off by spinning as a safe level was with the reservation that it was subject to alteration and conformity with further medical evidence. It was a safe measure for practical purposes. (d) The paper noted that a practical maxim of the greatest value was that every translation of fiberised asbestos in the factory produces dust which, if not controlled is dangerous, although it was thought the outlook was bright if levels were kept to the safe level earlier mentioned. It noted that one could not be dogmatic that it was a safe level but nothing had arisen to cast doubt on its validity. 43. (a) Study in 1938 by W.C. Dreessen and others (Exhibit CX 12). The paper came to be commonly called, "the Dreessen standard". This study found that the incidence of asbestosis increased with increasing dust concentrations and also length of exposure. It was a study in industrial settings. The study found no cases of asbestosis where dust concentrations were below 2.5 mppcf. There were three doubtful cases of asbestosis that fell in the range of 2.5 to 4.9 mppcf. One of the difficulties pointed out was that there were very few workmen exposed for long periods of time to low concentrations of asbestos dust.

(b) In comments made in setting the value, the paper noted:

From a practical standpoint, one of the most important results of a medical and engineering study such as this is the definition of safe working conditions in the industry under study. (emphasis added)

(c) It was seen as desirable to use such data as are at hand to define tentative safe working conditions that may serve as standards for the guidance of factory managers and engineers until more complete data are available. (p91). (emphasis added)

(d) The value was then set at 5 mppcf tentatively … until better data are available (p91).

(e) The standard had recognised deficiencies: (1) technical difficulties in obtaining accurate measurements; (2) difficulties in evaluating the potency of particular particles perhaps highlighted by the fact that all particles under 50 microns can carry asbestos to the lungs, yet in the particle count in applying the standard, there was no distinguishing between a particle of 50 microns and one of one micron where the former would carry fifty times as much asbestos to the lungs as the latter (p60).

This demonstrates one of the problems of relying too heavily on scientific learning.

(f) The paper did note that it was thought that if asbestos dust concentrations in the air breathed were kept below the limit, new cases of asbestosis would not appear.

7th February, 1945 - Gazettal of the Victorian "Harmful Gases, Vapours, Fumes, Mists, Smokes and Dusts Regulations 1945" (Exhibit CX 22). The preamble noted that health was endangered by excessive quantities of certain products in the atmosphere and that, in order to safeguard health, it was necessary to limit the quantities of such products in the atmosphere to quantities that would not endanger or impair health. It then provided that an occupier of premises or part of any premises should not allow concentrations in excess of specified amounts in the air likely to be inhaled by certain persons including those in the vicinity of the place where the process was carried on. In the case of asbestos, the limit was set at 5 mppcf of air.

1948 Report of the Director of General Public Health of New South Wales (Exhibit CX 27). Of note was an examination of the use of asbestos as heat insulation in a steel foundry. Asbestos was used to reduce the escape of heat from molten metal held in a crucible. The exposure was intermittent and of short duration, about five minutes at each pouring, and was only being done two to three times per week. The dust hazard was considered to be small. However, in view of the dangers associated with asbestos dust, it was advised that a substitute… be used.

1952 Journal of the Commonwealth Department of Health (Exhibit CX 28). Doubt was expressed as to whether any dust could be regarded as harmless if the exposure was sufficient. Steps to eliminate health risks associated with dusty processes were suggested.

1953 (estimated) - Survey by C G Roberts & H M Whaite (Exhibit CX 29). This confirmed a quantitative relationship between dust exposure and onset and development of asbestosis. Methods of dust suppression were suggested.

11 July 1956 Declaration of Certain Trades to be Dangerous Trades (Exhibit CX 30). The Governor of Victoria declared, amongst other things the trade of asbestos lagging or spraying to be a trade which, unless preventative measures were adopted, may be dangerous to the health of persons employed therein, to be a dangerous trade within the meaning of the Health Act 1928. There was tendered with this an extract from the Victorian Health Act 1956. It was the Health Act 1928 in place at the time, but it contained a like relevant provision authorising the Declaration.

19 January 1957 article by D L G Thomas in The Medical Journal of Australia (Exhibit CX 32). This is a report on a 1952 survey to determine the sources and incidences of pneumoconiosis. Different occupations were surveyed including 300 asbestos workers of whom 47 were found to have pneumoconiosis. That 47 did not present the full picture because pulmonary fibrosis from asbestos is insidious in onset and the 47 were established cases. Others may have developed later. Asbestos workers surveyed covered a range of occupations including spraying. The paper commented that it was imperative that conditions improve in dusty trades. It noted that industry in Victoria was becoming very dust conscious. It added,

The use of respiratory devices is recommended only when the hazard is of short duration and when other methods cannot be used effectively. (Emphasis added.) It added that asbestos regulations were awaiting gazettal and that they were very stringent. 50. (a) 1960 paper by J C Wagner and others (Exhibit CX 33). This paper disclosed 33 cases of mesothelioma, all but one of which had probable exposure to asbestos. It implicated asbestos as the cause. The paper was described as a preliminary publication and the problem is being intensively investigated. Some case histories revealed industrial exposure and others revealed relatively short exposure. The findings suggested that mesothelioma occurred 20-40 years after exposure.

(b) Historically, the Wagner paper recorded that the first case of carcinoma of the lung associated with asbestos was described in 1935. By 1955, according to Doll, a total of 61 cases had been reported including one mesothelioma. Carter (1952) mentioned two cases of mesothelioma. A further three cases were described by van der Schobt in 1958.

March 1961 National Health and Medical Research Centre - Schedule of Recommended Maximum Concentrations of Atmospheric Contaminants for Occupational Exposures (Exhibit CX 34). This set 5 mppcf of air as the recommended value for asbestos dust. The introductory notes state that the values are intended as guides in the control of health hazards, not as fine lines between safe and dangerous concentrations. They represent conditions to which, it is believed, workers except hypersensitive persons, may be exposed without adverse effects for eight hours a day for five days a week.

Thereafter, there was a number of papers (Exhibits CX 35-47) post 1961. As they all post-date 1961 when Professor Rowley was exposed, they do not assist in terms of the state of knowledge that was available in 1961. It would seem that the parties had the same view about this as I was not referred to the content of any these exhibits, with the exception of Exhibit CX 35 where I was referred to the recommended concentration of asbestos in the atmosphere being limited to 5 mppcf.

Mr Parker SC objected to evidence of witnesses on this issue unless they were witnesses practising in the field at the time Professor Rowley was exposed and could, by reason of that fact, give evidence of the state of knowledge in 1961 or of what an appropriate expert might advise as to safety at that time. I do not think this submission is right. It would mean that in the case of an event at a time when no practising expert was alive, a person who later became an expert could not give evidence of an earlier state of knowledge based on his learning. I think this is historical material about which these persons may give evidence - see, for example, Jones v Scully [2002] FCA 1080[82-5].

Mr Stewart gave evidence in Professor Rowley's case (Exhibit CX 84) and was also called to give evidence on this cross-claim. Evidence he had given in other cases was also before me pursuant to section 25(3) of the Dust Diseases Tribunal Act. I detail the effect of his evidence hereunder.

Mr Stewart's qualifications were attacked. Even though he is not a medical practitioner, I consider he was suitably qualified to give evidence as to safety standards applicable in 1961 and his knowledge of such standards then. I consider he was also qualified to give evidence of the extent to which asbestos was a risk to health and I do not think that it is a pure medical question. I think it is a question covered by different disciplines, including Mr Stewart's.

From 1952, he was employed by the Department of Health in Victoria as a Scientific Officer - Industrial Hygiene. He retired from there in 1965 and took up a position as Industrial Hygiene Engineer with Mt Isa mines. When he worked in the Victorian Department of Health, he was aware of the Victorian 1945 Harmful Gases, Vapours, Fumes and Mists, Smokes and Dusts Regulations. Although he had not read it, he was aware of what was called the Dreessen standard. He was aware of the "standard" of 5 mppcf.

In the 1950s, he was made aware of principles associated with industrial hygiene. This was through the medical department and through reading books and industrial health papers and through discussions with scientific staff and formal discussions within the department.

· the 1945 Victorian Harmful Gases, Vapours, Fumes and Mists, Smokes and Dusts Regulations;

· the 1956 Declaration under the Victorian Health Act of 1928;

· article by Dr Thomas in The Age newspaper in 1956 and a report by Dr Thomas in 1957;

· generally reading books and industrial health papers though the literature he had read by 1961 on matters related to the Dreessen standard was limited; · regular discussions with scientific staff, inspectors and medical officers and formal discussions within the department where he worked;

· visits to factories where dusts were present even though such may not have been directed to asbestos dust;

· on his observations on his visits to factories where dusts were present, reporting on those observations, taking laboratory measurements for dust counts of dust in factories he had visited;

· communications with people working in other departments in other states.

In the mid-1950s if Mr Stewart visited a factory and saw dust in the atmosphere of a workplace, that was an indicator that there could be a risk to persons exposed to that dust. He thought asbestos was capable of producing a very serious pneumoconiosis if inhaled, that it was an extremely dangerous dust and that it could produce asbestosis, a progressive condition which could be lethal. He did not comment at that stage in giving his evidence as to the extent of exposure capable of producing such results.

· if dusts could be seen in the atmosphere of a workplace, that was an indication it could be a risk to persons exposed (Exhibit CX 84, 89.30, 93.29);

· the absence of visible dust did not necessarily indicate there was no risk (Exhibit CX 84, 93.30);

· asbestos was an extremely dangerous dust; its effects could be progressive and lethal (Exhibit CX 84, 91.23). He did acknowledge that his view may not have been correct (Exhibit CX 84, 107.39);

· if dust exceeded the standards, then ameliorating responses were required. If the dust could be life threatening, the exposure had to be minimised and this applied particularly to dusts such as asbestos that could be cumulative in their effect (Exhibit CX 84, 93.47);

· if a workplace did not meet the criteria for exposure level it was unsatisfactory whatever the length of time that failure to meet the criteria lasted (Exhibit CX 84, 102.32);

· in circumstances similar to those prevailing when Professor Rowley was exposed, Mr Stewart, if he had the authority, would have instructed that the site be cleared of persons not directly involved in the operation (Exhibit CX 84, 104.39). He gave evidence to similar effect at Exhibit CX 84 T.117.10-31;

· it was never the view that there was a body of thought that asbestos was not dangerous to a worker so long as he was not exposed to high levels of dust over a long period of time (Exhibit CX 84, 107.03);

· the standard used in the 1945 Regulations was not a standard that would guarantee that one would not get sick (T.130.06).

Before 1961, Mr Stewart did not have a view as to what level of exposure would have eliminated health risks from asbestos. He agreed he did not have the scientific expertise to form an opinion as to what was a safe level of exposure. The conclusion put to him does not necessarily follow and that is that as he did not have the expertise to form an opinion as to a safe level of exposure, therefore, he could not form an opinion that a particular level, for example, the Dreessen level, was not safe. It is consistent that Mr Stewart or anybody could have an opinion that exposure above a particular level was not safe, but have no idea at what level exposure was safe. This is because exposure above a particular level may have been determined to be not safe, yet the learning may have been ignorant or undecided as to exposure below that level.

Dr McNulty's report (Exhibit CX 10) opines that it was not reasonably foreseeable in 1961 that a person might contract an asbestos related disease if he was exposed to conditions that Professor Rowley was exposed to.

Dr McNulty gave evidence in Professor Rowley's case (Exhibit CX 11). He is a medical practitioner. In 1958, he knew nothing about asbestos, but he then became interested in the relationship between asbestos and asbestos related lung disease. He visited the Wittenoom mine about four times from 1959 to 1965. The atmosphere there was extremely dusty. He did not take any precautions on those visits. He did not think he was exposing himself to a risk of lung disease.

The standard for the level of asbestos in the atmosphere was reduced over time.

In cross-examination, Dr McNulty agreed that dust in the workplace generally throughout the 20th century was regarded as bad occupational hygiene.

Dr McNulty learned of asbestos in the late 1950s. He learnt that asbestos fibre was a dangerous fibre. He agreed that exposure to that fibre that could be avoided should be avoided. It was known that individuals varied greatly in their capacity to deal with dust. There were idiosyncratic differences between different persons. The reasons for that were not known and are still not known. In the late 1950s, as a principle, one avoided any unwarranted or unnecessary exposure to that sort of dust.

He agreed with the content of a letter from 1945 from the Chief Inspector of Factories. The letter was in the context of shipbuilding and ship repairs and included the following statement.

It is important that even if work will only be temporary, all reasonable practical steps should be taken to reduce the risk to a minimum. The letter also set out recommended steps for avoiding unnecessary or unwarranted exposure and Dr McNulty agreed those steps were in accordance with our recommendation.

By 1950, pulmonary cancer was recognised as a disease of persons working with asbestos.

He stated that the general principle was to eliminate the hazard insofar as humanly possible. If that could not be done, then stick to a limit of international acceptance. If that could not be done, then wear protection.

In 1961, he would have been concerned about persons working in clouds of asbestos dust and concerned if there were no precautions and would have recommended the principles mentioned in the previous paragraph. He wondered whether ten minutes' exposure would be harmful, but he would not have recommended such exposure.

He stated that the practice described in paragraph 45 was most undesirable. That was intermittent minor exposure described in 1948.

Dr McNulty had received the Wagner article probably in 1960 (T.138). It set out a number of case histories of mesothelioma, including housewives, domestic servants, cattle herders, farmers and accountants. They were removed from heavy concentrations of exposure, but they were exposed to environmental pollution. Reading especially the Wagner paper, one was left with the suspicion that a combination of individual idiosyncrasy and minimal exposure may be dangerous.

Dr McNulty was referred to an article in the British Medical Journal on 30 April 1960 where asbestos dust was said to be most toxic and the amount needed to cause asbestosis was not known, so constant vigilance and new preventative methods were needed if the disease was to be abolished. Dr McNulty agreed this was all good sense in 1960.

In re-examination, Dr McNulty agreed that in 1961, he did not consider that a person with a brief exposure to asbestos would have incurred an asbestos related disease. I do not consider that undoes the evidence he gave in cross-examination as to risks to persons who had brief exposure. His view that such a person would not have suffered an asbestos related disease is not inconsistent with his evidence that they were at risk and at risk because a safe level of exposure was not known and there could be variations between persons exposed and it was not known and is still not known why there are such variations.

Professor Henderson, in giving evidence in Professor Rowley's case, apparently agreed with Mr Rundle, then counsel for the University, that 5 mppcf was a safe level of exposure (Exhibit CX 83, T.19).

(a) However, there was an ambiguity in the evidence and it was not clarified (Exhibit CX 83, T.19). The following exchange occurred.

Q. But as you say it was regarded though for some years as the, for want of a better word, a safe level.

A. It was regarded as an exposure standard at the time.

Q. Viewed that it was safe but unfortunately it has not worked out that way.

A. It hasn't worked out that way, no, it hasn't. I agree with you.

(b) The premise in the first question was not justified. Professor Henderson had not said that the level was regarded as a safe one. That appears to be reflected in his answer to the question. The next question asserts the viewing of the standard as safe and then adds another subject matter to the question. The answer no is probably meant to be yes. That is, Professor Henderson was agreeing with what had been put to him and that seems evident from his next answer. It is a problem often raised with an answer in the negative when the question contained a negative. However, the cross-examiner in suggesting to Professor Henderson that he was agreeing with him has not made it clear whether the agreement is with the first part of the question, the second part or both parts. The fact that he was trying to clarify a negative upon a negative suggests that the last question was directed to the second part of the previous question. The answer to the last question seems to be founded on that too. I take it that Professor Henderson's agreement with the cross-examiner was that the standard had not worked out to be safe, not that it was viewed as safe. Mr Kilpatrick's evidence

Exhibit CX 52 at 465V to 466I, he thought that though a reasonably prudent employer who wished to protect his workers against asbestosis might have felt comfortable if he had adopted a standard below 5 mppcf, the Wagner article might have made some people think.

In 1962-65, there were almost no academically qualified occupational physicians practising in private industry in Australia (Exhibit CX 61).

In short, Professor Ferguson's view was that as at 1960 for asbestos to cause asbestos related illness, it required intense exposure over a long period of time, for example, day-in-day-out, eight hours per day in some sort of asbestos process to cause asbestosis (Exhibit CX 56, 765). The same was true of lung cancer (Exhibit CX 56, 778C). See also Exhibit CX 61, CX 66,820H. He thought the cases of mesothelioma in the Wagner paper were of considerable exposure (Exhibit CX 53).

Illustrative of the lack of appreciation of the hazard to other than prolonged and intense exposure were two episodes Professor Ferguson gave evidence about. A senior industrial hygienist colleague of Professor Ferguson in 1966 spent six months measuring dust levels at Wittenoom without taking protective measures and the industrial hygienist responsible for testing respiratory protective devices in Australia did not, in about 1967, know of the relationship between crocidolite and mesothelioma. I do not consider this evidence to be of much weight and nor do I consider it to be evidence that all industrial hygienists or others working in that field had that level of lack of appreciation for the following reasons:

(1) if truly the industrial hygienist in 1967 did not know of the relationship between mesothelioma and crocidolite, he should have. Not only had the 1960 Wagner paper been published, but there were developments following that paper - see, for example, the Newhouse & Thompson paper in 1965 (Exhibit CX 36);

(2) this does not tell us what the full extent of the industrial hygienists' state of knowledge was as to the relationship between asbestos and mesothelioma or other lung diseases;

(3) that a senior industrial hygienist in 1966 did not take precautions might tell us: (a) that he was not up-to-speed with the learning in the area when he should have been; or (b) that he was foolhardy or turning a blind eye to his own safety; or (c) both;

(4) at most, this tells us that in particular situations, two industrial hygienists did not consider they were at risk. Other industrial hygienists or persons working in that field might have taken a different view. In the 1950s, Mr Stewart was using a mask or respirator.

Cross-examination of Professor Ferguson elicited qualifications to his position that prolonged exposure to asbestos was required to cause lung disease and also elicited other relevant evidence and I proceed to look at some of that evidence.

It was known by 1930 that asbestos was a dangerous fibre (Exhibit CX 56, 805L) and that asbestosis was a debilitating, progressive disease that could kill (Exhibit CX 56, 803N). It was insidious and persistent (Exhibit CX 65, 197R). Different people exposed to asbestos could have different susceptibilities (Exhibit CX 65, 214H).

By the end of the 1930s, there were numerous reports in literature available in Australia of an association of asbestos with lung cancer (Exhibit CX 56, T.806Q).

It was well recognised through the 1940s that all asbestos was toxic (Exhibit CX 56, 809O) in sufficient quantity (Exhibit CX 56, 809U).

The 1947 Inspector of Factories report in Australia presented strong evidence of the link between asbestosis and lung cancer (Exhibit CX 56, T807T-808E). In 1955, the association was confirmed beyond reasonable doubt (Exhibit CX 61). As at 1961, the view was that one needed to have asbestosis to have lung cancer from exposure to asbestos (Exhibit CX 66, 827G).

He agreed that in 1961 asbestos dust was most toxic and the amount needed to cause asbestosis was not known, so constant vigilance and new preventative methods were needed if it was to be abolished (Exhibit CX 57, T.870T-W).

He agreed that mesothelioma and lung cancer kill and asbestosis is capable of killing. All may come on many years after inhaling asbestos. Unnecessary exposure to that fibre in 1950 should have been avoided. By 1959/60, because of the growth of knowledge, that was even more desirable (Exhibit CX 57, 880-881). He qualified some of this evidence in re-examination, but not in a way that, in my view, lessens the burden of his earlier evidence.

Alarm bells rang around the world with the Wagner article (Exhibit CX 65, 200P). The authors of the 1960 Wagner article called their observations preliminary and recommended further research. The Wagner finding immediately became the subject of further research. The article was enough to alert everyone working in the field that further investigation was needed (Exhibit CX 65, 193W).

Any dust should be avoided (Exhibit CX 56, 801O). It is one of the principles of occupational health to reduce exposure to the minimum practically achievable (this was speaking as at the 1950s) (Exhibit CX 56, 801S).

Then at Exhibit CX 56, T810T-V, he stated that as at 1950 there was a general principle in occupational medicine that it was desirable to reduce unnecessary exposures, not only having regard to reducing the exposure just below a putative safe limit, but to as low a level as was reasonably attainable. This was even if exposure was to a level that was not thought to cause disease (Exhibit CX 65, 198D-H).

The Dreessen standard of 5 mppcf did not set a safe limit (Exhibit CX 57, 861N). It was a standard to which people could be exposed with reasonable safety until a better standard was evolved. It tended to be adopted because there was nothing else people had to go on (Exhibit CX 57, 868U). It was a temporary standard until better data became available (Exhibit CX 61). It was clear at the time that Dreessen was underestimating the hazard (Exhibit CX 66, 840S). It was acknowledged to be marginal in terms of safety (Exhibit CX 81, 271V). In that context, Professor Ferguson would recommend that dust be reduced as much as reasonably feasible (Exhibit CX 66, 841E; CX 74, 593).

Any occupational physician reading the Dreessen paper would have got the message that 5 mppcf was not a safe lower limit (Exhibit CX 81, 300R).

In Exhibit CX 56 at 805V to 806D were the following question and answer:

Q. …if I can just put you to what the Chief Inspector wrote in 1938. "There can be no doubt that dust if inhaled, physiologically is undesirable. Moreover dust that is thought today to be harmless may, following research, be viewed in another light tomorrow. It's not many years ago when the dust of asbestos was regarded as innocuous while today it is recognised as highly dangerous." (emphasis added)

Professor Ferguson was clearly of the view that scientific knowledge in the field of asbestos and its known risks was something that had evolved over the years (Exhibit CX 56, 805V-806D). Also as at 1961, there was not, in the scientific learning a known and established safe level of exposure (Exhibit CX 65, 193W). And there are limitations in science in predicting unknown risks (Exhibit CX 74, 566, 583).

There is always a delay before initial findings of studies are accepted by the occupational health profession and years more before regulatory action follows (Exhibit CX 68, p21).

It would seem Professor Ferguson approached the matter from the point of view of the risk occurring without regard to the consequences of the risk. The questions and answers at Exhibit CX 74, 582 and 583 appear to support that.

He thought it was unlikely that a person would develop asbestosis if he was exposed to less than 5 mppcf for less than five years. It was a matter of the product of the concentration and time of exposure so that if exposure was less than 25 particle years, the chances of getting asbestosis were quite small (Exhibit CX 60, 117-8). He interpreted the Dreessen standard to mean there was no risk to health if a person worked at a level below the standard (Exhibit CX 60, 127). This is not a correct interpretation of the document. Nor, does it accord with other evidence. It is also undermined by evidence in another case where he said in 1958 nine months' exposure was sufficient to cause asbestosis (Exhibit CX 60, 144). The Dreessen paper itself speaks of two cases of asbestosis with less than 25 particle years of exposure (Exhibit CX 60,150). I do not accept the interpretation Dr Joseph put on the Dreessen paper.

He referred to the Dreessen paper as having some cases of asbestosis with an exposure of less than 5 mppcf (Exhibit CX 69, 152Q). He referred also to a paper in 1934 by Wood & Gloyne with three reported cases of asbestosis with less than a year of exposure (Exhibit CX 69, 162Q). He noted that the 1949 Merewether paper reported a lung cancer risk with asbestosis (Exhibit CX 69, 165G). He commented that the 1955 Doll paper reported three cases of lung cancer without asbestosis (Exhibit CX 69, 165L).

At Exhibit CX 69, 189P, Dr Leigh was asked a lengthy question about the Dreessen paper and whether, on the information available in it, an end-user might be seen to be at risk in 1938 of contracting asbestosis. He gave a lengthy answer, not entirely responsive, but it does seem to imply that there was a risk.

Asbestos has been recognised as a toxic substance since the 19th century (Exhibit CX69,177P). As at 1947, it was a dictum in the field of occupational hygiene to have the lowest possible exposure to a toxic substance (Exhibit CX 69, 179W).

The risk of mesothelioma should have been known in 1960 (Exhibit CX 69, 197P). The requirement for dust control to reduce it should have been known then (Exhibit CX 69, 197T). I am not really implying there how much reduction for mesothelioma would be required because the quantitative aspects of that were only worked out subsequently. (Exhibit CX 69,197Q). The requirement for dust control and respiratory protection to reduce the risk of mesothelioma should have been known in 1960 (Exhibit CX 69, 197T). This should have been known to executives of companies, such as James Hardie, but I'm not suggesting they should have known that it should be reduced to nothing. (Exhibit CX 69, 197X).

The following questions and answers appeared at Exhibit CX 69,199D-G.

Q. Does it come to this that you are of opinion that the executives of my client company ought reasonably to have given the Wagner paper some consideration and ought reasonably to have awaited developments in the profession. A. Yes, that's reasonable.

Q. You do not suggest therefore, that they ought to upon their receipt of the paper, accepted what was is in it as gospel and implemented alterations within their enterprise in response to it. A. Not immediately on receipt of the paper.

At T.203C-E, the following question and answer appeared.

Q. Would you agree with this proposition, "The existence of mesothelioma as a specific entity was not accepted by the world's leading cancer authority Professor Rupert Willis nor was its relationship to asbestos appreciated prior to the mid 1960s with the exception of a few deeply involved experts. A. By mid 1960 - by 1960, if you put 1960 there rather than mid 1960s.

As to the Dreessen standard, it was known in the 1940s and 1950s that measurement devices at the time were unreliable and accordingly dust levels should be kept as low as possible. That was the general premise of occupational hygiene at the time (Exhibit CX 73, 421U).

Mr Rogers's approach to worker safety is one that does not necessarily conform with the obligations of a person under a duty of care. He did not agree that obedience to legislation and protecting the health of persons exposed to asbestos might be two entirely different matters (Exhibit CX 73, 445R). I would add here that compliance with legislation or standards is not inconsistent with negligence. Statutory regulations or standards do not supersede a common law obligation - Bux v Slough Metals Limited [1973] 1 WLR 1358.

In speaking of the standard of 5 mppcf, he reported that effective fibre counting methods were not available until the 1970s. Hence, the conventional standard would have provided no safeguard against mesothelioma. On an empirical basis, it was assumed to reduce the risk of asbestosis (Exhibit CX 67, para 3.1.8).

He reported that prior to the Doll survey of 1955, lung cancer was associated with asbestosis with about two exceptions (Exhibit CX 67, 3.4.2).

He reported that the existence of mesothelioma as a specific entity was not accepted by the world's leading cancer authority, Professor Rupert Willis, nor was its relationship to asbestos appreciated prior to the mid-1960s, with the exception of a few deeply involved experts (Exhibit CX 67, para 2.7). He must have been talking of established scientific proof here, because at paragraph 2.24, he reported that the association of mesothelioma with asbestos was suspected in South Africa in 1958 and confirmed in 1960.

He was not particularly impressed by the Wagner paper (Exhibit CX 75, 606E). It was an exceedingly interesting paper, but one he put to one side for a year or so (Exhibit CX 75, 606H).

He agreed that if a substance was known to be dangerous or toxic in 1950, it was a basic tenet of industrial or occupational hygiene to minimise or eliminate the exposure to such a substance (Exhibit CX 82, 194H).

Findings of the State Coroner of Victoria, 18 June 2004, Case No. 2598/03. This concerned the death from mesothelioma of a Donald Rawson. It does contain a record of the history of asbestos exposure and knowledge of the risks associated therewith over time. However, this is really a second hand and truncated account of the Coroner of reports of other persons. I take no note of it, especially in the presence of more direct evidence put before me in the form of articles, reports and evidence in this and other cases. It lists many articles and reports that were not tendered in this case. I do not propose to take note of them.

Report by G Major and A J Rogers, Commonwealth Institute of Health, The University of Sydney, 11 August 1981. This was a report of an examination of asbestos in the University buildings in 1981 and an assessment of the safety aspects thereof. They dealt with safety aspects generally. One thing they commented on was the NH&MRC document and Threshold Limit Values for different types of asbestos. In this context, they wrote,

It is useful to point out that just as experienced occupational hygienists do not interpret the TLVs as fine lines between safe and dangerous concentrations, they do not support the wilful exposure of workmen to air contaminants. It is their practice to ensure that all exposures are kept at a level as low as is reasonably achievable and this is governed by their knowledge of the toxicology of the material and environmental, industrial and other practices. They would therefore recommend on occasions the adoption of prudent practices to limit exposure irrespective of the actual concentration of any contaminant to which persons are exposed.

Messrs Major and Rogers did not use respirators when inspecting the areas where asbestos was as they did not perceive themselves to be at any greater risk than that to which they were exposed during their normal working day. That might be their perception. Others might take a different view. This has been dealt with in paragraph 80. They added,

We do not think that tradesmen, either, are at any excess risk to their health when doing minor work but there are occasions when we would think it prudent for them to take certain limited precautions such as wearing a respirator and taking greater care with the house-keeping.

In large measure, this case was argued around McNeill. On the face of it, that case does have a special application to this case because Father McNeill's exposure was in 1961, the same year as Professor Rowley's exposure.

In 1961, Father McNeill assisted in placing a roof over a rumpus room at his sister's house. In doing that, he cut, drilled, rasped and fixed some corrugated asbestos cement sheeting. He did it on two to three Mondays for two to four hours on each occasion, totalling not more than about 10 to 12 hours' exposure at the most. The sheeting contained between 10 and 15% content of asbestos fibre. He contracted mesothelioma as a result. He sued the manufacturer of the sheeting for this injury.

Judge Duck found that what was foreseeable in the circumstances was the development of lung disease from exposure to the asbestos dust. The Court of Appeal disagreed with that and held that there was no duty of care owed to Father McNeill.

On the question of duty, it was held that in the context of those exposed to asbestos, it is not right to adopt one broad class of end-users to whom risk of exposure to asbestos was foreseeable. This was because there is a vast array in the degree to which end-users may be exposed, with some exposed to undiluted asbestos for hours per day over several years down to exposure of the kind suffered by Father McNeill. Father McNeill was in a class of persons to whom the body of knowledge of risk associated with asbestos use did not extend. The body of knowledge dealt with industrial disease risk where the intensity of exposure was different to that of Father McNeill. The person whose reasonable foreseeability of risk must be considered is and must remain a home handyman who does not encounter the product in an industrial or commercial continuing situation [38]. It would be a legal error to treat all end-users of a manufactured product uniformly.

I consider that there are several points of distinction between McNeill and this case and they are:

· McNeill was an end-user case. Professor Rowley was not a user at all. This is not an end-user case;

· in McNeill, the manufacturer had, for some time before Father McNeill used the product, ceased to have control of it. Here, BIC was in control of the spraying operation;

· in McNeill, there was no physical proximity between the manufacturer and Father McNeill. Here, BIC and Professor Rowley were physically proximate;

· an aspect of the control distinction is that the manufacturer in McNeill could do nothing practical at the time Father McNeill was using its product. Here, BIC had the opportunity to undertake simple, practical measures to avoid Professor Rowley being exposed. I shall come to those later;

· Father McNeill had a very light exposure over two to three broken periods. Professor Rowley had a short period of exposure, but it was intense;

· Father McNeill was exposed to the dust of a product which comprised about 10 to 15% asbestos. Professor Rowley was exposed to a product with a far higher concentration of asbestos;

· Father McNeill was exposed in a small, backyard home handyman situation. Professor Rowley was exposed in the course of a commercial, industrial enterprise.

These are, in my view, differences of significance, such that I do think McNeill is truly distinguishable and does not apply to this case. The learning up to 1961 must be looked at in the circumstances of Professor Rowley's exposure.

I proceed to make findings on that learning which I have summarised above and to consider whether that learning, together with other circumstances, gives rise to a duty of care in this case.

BIC owed Professor Rowley a duty of care when it conducted its spraying operation in 1961

I make the following findings as to the learning of the dangers of asbestos that was available in 1961:

(b) toxic effects included, but were not limited to, asbestosis, cancer and mesothelioma;

(d) the effects of exposure to asbestos were not immediate and took many years to develop;

(e) it was known that exposure to a level of 5 mppcf over a sufficiently prolonged period would produce asbestosis and could produce lung cancer. There had been cases of asbestosis at levels below 5 mppcf and where the exposure was less than prolonged;

(f) there were cases of mesothelioma attributed to relatively light exposure to asbestos;

(h) light exposure to asbestos in certain processes, for example, that described in paragraph 45 was recognised to be hazardous even if the hazard was small;

(i) individuals were known to have different capacities to deal with dust; there were idiosyncratic differences;

(j) further investigation and study were required and were being undertaken;

(k) Dreessen understated the hazard and was marginal in terms of safety. The Dreessen value was a temporary one until better data became available;

(l) dust in the workplace was regarded as bad occupational hygiene. Any dust should be avoided. Exposure should be limited to the minimum practically achievable;

(m) because asbestos was a dangerous dust and fibre, if exposure to it could be avoided, it should be;

(n) the general principle was to eliminate the hazard insofar as humanly possible;

(o) responsible industrial hygienists in 1961 would have recommended against the exposure to asbestos dust in circumstances in which Professor Rowley was exposed;

(p) a combination of individual idiosyncrasy and minimal exposure might be dangerous. 122. The learning as to the dangers of asbestos up to 1961 had progressed in a way such that, at each new development, it was learned that asbestos was more dangerous than it had been understood to be up until then. Some, but not all, developments illustrating this were:

(a) in 1900, the first fatality from asbestosis was recorded;

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