Father Robert McNeill v Seltsam Pty Limited - [2005] NSWDDT 43

No judgment structure available for this case.

Dust Diseases Tribunal

of New South Wales

CITATION:
Father Robert McNeill v Seltsam Pty Limited [2005] NSWDDT 43

PARTIES:
Father Robert McNeill (Plaintiff)
Seltsam Pty Limited (Defendant)

MATTER NUMBER(S):
84 of 2005

JUDGMENT OF:
Duck J at 1

CATCHWORDS:
Damages :- Light exposure
Foreseeability of risk of injury
Duty of manufacturer to end users of the product
Duty to warn
Damages

LEGISLATION CITED:
Dust Diseases Tribunal Act s 25(3)

CASES CITED:
- McCusker v James Hardie and Coy Pty Limited DDT 176 of 1996;
- CSR Limited v Wren (1997) 15 NSW CCR 650 at 655;
- Peter Bradley v James Hardie and Coy & Ors DDT58 of 1995;
- David Scutt v James Hardie and Coy Pty Limited DDT 199 of 1996;
- Wyong Shire Council v Shirt (1979-1980) 146 CLR 40;
- Tame v New South Wales (2002) 76 ALJR 138;
- Julia Farr Services Corporated v Hayes (2003) 79 ALJR 565 at 108;
- Swain v Waverley Municipal Council (2005) 79 ALJR 565 at 108;
- Berrigan Shire Council -v Ballenini and Ors (2005) VSCA 159;
- Bolton v Stone (1951) AC 850;
- The "Wagon Mound" [No2] 1967 AC 617 at 643-644;
- Seltsam Ltd v Minahan (1996) 13 NSW CCR 410;
- Rolls Royce Industrial Power (Pacific) Ltd v James Hardie and Coy Pty Limited (No 4) (1999) 18 NSW CCR 653 at 685;
- Mt Isa Mines v Pusey (1970) 125 CLR 383;
- Bendix Mintex Pty Ltd v Barnes (1997) 42 NSW LR 307;
- Malec v JC Hutton Pty Limited (1990) 169 CLR 638;
- Nielsen v Seltsam Pty Limited DDT 280 of 2003;
- Wright v Dunlop Australia Co Ltd (1972) 13 KIR 255;
- Thompson v Johnson and Johnson Pty Limited (1991) 2 VLR 449 at 490

DATES OF HEARING: 2, 3, 4, 5,16 and 18 August 2005

DATE OF JUDGMENT:

09/05/2005

LEGAL REPRESENTATIVES:
FOR PLAINTIFF:
Mr J Rush, QC instructed by Turner Freeman
FOR DEFENDANT
Mr J Fernon, SC instructed by Makinson and D'Apice

JUDGMENT:

59

Dust Diseases Tribunal of New South Wales

Matter No DDT 84 of 2005

Father Robert McNeill

v

Seltsam Pty Limited

5 September 2005

JUDGMENT

DUCK J

1. The plaintiff suffers from mesothelioma. He sues the defendant as the supplier of asbestos cement sheeting which the plaintiff fixed as a roof to a rumpus room in his sister’s backyard in Miranda in 1961. The work was done over several hours on each of two or three Mondays. The plaintiff alleges the defendant was negligent in exposing him to the inhalation of asbestos dust and fibre associated with the work. The basic allegation of negligence is failure to warn about the risks of breathing in asbestos dust. The fundamental issue between parties is what should the defendant have reasonably known about the risks in 1961. This knowledge or lack of it may go to whether or not the defendant owed the plaintiff any duty of care. It may also go to whether or not if such a duty existed the defendant was in breach of the duty ie acted in a way other than the way in which a reasonable person in the defendant’s position would have acted.

2. The plaintiff was born on 7 June 1927. He grew up in Sydney. The last year of his schooling was completed at St Columba’s College Seminary at Springwood. In 1952 the plaintiff was ordained a priest in the Catholic Church. He then worked as a priest at various places in Sydney and in Victoria. He worked as a priest until retiring in 1990. The evidence suggests that throughout his working life as a priest the plaintiff was not exposed to asbestos other than at his sister’s place and perhaps also at his mother’s house at Maroubra. (See generally PX1 para 6; T13.32-33, see T22.32-33)

3. The possible exposure to asbestos at his mother’s place occurred, apparently in 1960 or perhaps a couple of years before that. (PX1 para 7-8; T17.30-31) His mother’s house was at 10 Wilson Street, Maroubra. His father had built a veranda and room at the back of the house. They did not have a ceiling. After the plaintiff’s father had died his mother asked him to install a ceiling in the room so she could sell the house. (PX1 para 7) The plaintiff installed a ceiling as requested using fibro sheets that he believed contained asbestos. The room was about 9 ft wide and 14 – 16 ft long. The plaintiff cut the fibro sheets to size and nailed them into position to form a ceiling. He believed that he rasped the edges of the sheets. He did not need to drill them. He thought that in all there were five or six sheets of fibro used. (T17.22-23)

4. While the plaintiff believes that the materials used at his mothers house in Maroubra contained asbestos, because of objection by the defendant the evidence was received about the nature of the sheeting as proving the plaintiff’s state of mind not as proving in fact that the sheets contained asbestos. There is no evidence to prove that the fibro in fact contained asbestos.

5. The plaintiff carried out the necessary work at Miranda over two or three Mondays for up to four hours each time. (PX1 para 10; T9.27-30) He was assisted by a friend Father Williams who handed him the fibro up onto the roof and helped lay it down (T21.27-33 and T23.43-45)

6. The corrugated sheets were dusty to handle. (PX1 para 11; T10.1-2). There was dust visible when he sawed the sheet. Dust got onto the sheets when they were cut. (T10.10-12; T21.44-45) The plaintiff breathed in the dust. (PX1 para 11)

7. The plaintiff did all of the cutting (T10.8-9; T20.33-35)

8. The plaintiff also drilled holes in the sheets using a hand drill (PX1 para 11; T23.25-45) The plaintiff said (at 21.39): “In all the work there was plenty of dust”. The plaintiff estimated that he drilled three or four holes per piece of timber (T10.22-23)

9. At the end of each days work the plaintiff cleaned up by picking up with his hands the broken pieces of fibro sheeting and put them in the rubbish tin. (See T11.1-2)

10. The plaintiff said that he breathed in the dust while working on the rumpus room roof. (See T10.46-48)

11. The fibro sheets used were stamped with “Wunderlich Durasbestos”. (Annexure to PX1; DX9 the report of Mr G Pickford pg 2 and pg 8) Samples of the asbestos sheets were examined by Dr G D Pooley whose report of 5 April 2005 is PX3 in the proceedings. Both chrysotile and amosite fibres were easily located in the sample. It was the estimate of Mr G Pickford called for the defendant that 10-15 percent by weight of the fibro consisted of asbestos of which he thought three quarters to ninety per cent or more would have been chrysotile. The remainder would have been amosite. (T141.34-36) Mr Pickford said that amosite was found to be dustier than chrysotile only. (T115.11-12) There was also evidence from Professor Henderson to the effect that the cutting of AC Building materials promotes preferential release of amphibole fibres. (PX2 pg 5; T34.41-48)

12. By any measure, the plaintiff’s exposure to asbestos dust was light.

13. The plaintiff relies on also on the opinion of Professor Douglas W Henderson. The Professor’s report is PX2. He gave evidence in the proceedings and was cross examined.

He expressed the opinion that the plaintiff has a definite malignant mesothelioma of the pleura tubulopapillary epithelial type. That is not disputed.

He also said (pg 12):

Assuming the comprehensiveness and correctness of the asbestos exposure history provided, it is my assessment that Father McNeill’s brief “handyman”-type exposures to asbestos over a period of a few to several days in about 1960 and 1961 in the form of domestic renovation/extension work, made a significant causal contribution towards the induction of his mesothelioma, by way of an incremental causal-contributory effect in excess of and top of any underlying or “background” risk of mesothelioma. ………

Within the totality of Father McNeill’s exposures to asbestos in 1960 and 1961, it is also my opinion that the exposure sustained when he assisted in the installation of a corrugated A-C roof on a rumpus room at his sister’s home in late 1961 made a significant causal contribution to the development of his mesothelioma, “on the balance of probabilities”.

14. Mr Pickford was called by the defendant to provide an estimate as to the plaintiff’s exposure which in the circumstances of the case I have not found helpful. His opinion was based on his own assumptions. At no stage was he able to consider the evidence of the plaintiff about his exposure. His approach has produced for example a scenario relating to the Miranda premises which he described as scenario A in his report and in which the total work occupied 12 hours. Of that non AC work was designated at 5.7 hours. This conflicts with the evidence of the plaintiff the substance of which was that all he did in effect was AC work.

15. Further in his summary of assumed exposure estimates at pg 12 of his report, Mr Pickford assumed exposures at 0.6 and 0.3 fibres per millilitre resulting from the use of a hand saw, rasp and fibro cutter. On its face this appears not to sit comfortably with the exposures set out at pg 11 of the report in the North American Study related to flat and corrugated finishing which involved exposures averaging 2.65 fibres per millilitre and a range of exposures from 0.33 fibres per millilitre to 8.0 fibres per millilitre. Figures from the North American Study correspond reasonably with the report referred to by Professor Douglas W Henderson PX 2 at pgs 4 and 5 taken from the BK report Faserjahre for 1997. From that report figures from 0.5 to 6 fibres per millilitre are quoted. Further, use of a hand saw to cut AC materials is, according to Professor Henderson, known to have yielded fibre concentrations of 2-4 fibres per millilitre. In the light of all of those figures the estimates adopted by Mr Pickford seem to me to be too low.

16. Further in this regard I consider the evidence of Professor Henderson at T38 to be relevant. He was asked:

Q. You have not endeavoured for the purpose of preparing your report to calculate the fibre/ml years to which Father McNeill may have been exposed have you.

A. Well I have not as part of my report, I consider it is likely to have been somewhat greater than Mr Pickford’s estimate but I would emphasise that I try not to develop a cumulative exposure dust simply for the reason that at low dose exposures like this type of exercise, taking into account as it must a variety of assumptions which may or may not be correct, different recorded fibre concentrations in the air can lead to wildly inaccurate and imprecise results whereby a small change in any one parameter of the calculation can lead to a major alteration in the final calculated inhaled dose. All I would say is that in this case there has been a brief but significant episode of above background exposure including amphibolic exposure with an appropriate latency interval and in my opinion it has made a cause or contribution. (T38.16-26)

The Professor’s approach to the calculations of the plaintiff’s exposure seems to me to accord with commonsense.

Foreseeability of Risk of Injury

17. In respect of this matter the plaintiff called Mr Gordon Stewart, an Industrial Hygienist. The defendant called Mr G C Pickford a Consultant in Occupational Hygiene (See part PX9) The defendant also called Dr Ian Gardiner, Respiratory Physician. In addition the plaintiff relied on medical articles tendered pursuant to s25 (3) of the Dust Diseases Tribunal Act.

18. Mr Gordon Stewart worked as a scientific officer in the Industrial Hygiene Department of the Victorian Department of Public Health from 1952 –1965. There was an interruption to that employment between 1959-1961 when he worked at the National Testing Laboratory (T52.20-26) He said that in the course of his work with the Department he learnt that:

…asbestos was a very harmful substance and that if inhaled it was permanently, or those particles which were respirable were permanently attached to the lung and that over a period of time this could give rise to diseases which could be fatal but certainly were disabling and distressing.

19. He said (T54) that after reading the article of Dr Thomas in the Medical Journal of Australia in 1957 (PX9) he came to the view that:

…if you inhaled dust deriving from such a process,(ie cutting asbestos cement sheeting) then you were at risk of contracting a serious disease.

…if the product contained asbestos and then that product was fragmented in some way by grinding, cutting or sawing whatever and was projected into the air, that the dust produced would contain asbestos and those parts of the dust that were inhalable because of their size, would deposit in the lung and would have the effect of putting a person at risk of contacting a serious asbestos related disease….

The advice I would have given would be that they should take measures to minimise the exposure to the dust that might be generated by these processes, and in particular to use a respirator when performing tasks which generated dust in the breathing zone to, if possible, wet down the substance before attempting to do any cutting, to do the cutting in the open air if possible and certainly in a well-ventilated environment and to take any other measures practicable and sensible measure to minimise or avoid the risk of inhaling the dust…

The general view was for all products where people could not reasonably be expected to assess the hazard, then they should be labelled and that included asbestos containing products. If a person could not perceive in picking up an asbestos containing product and commencing to grind, saw and cut in various ways, that the inhalation of dust – any dust generated during that process would be hazardous to their health, then there should be a label and there were many instances where labels were required by the Department on other products where persons expected to have little knowledge would be exposed to hazardous products…

…Given that such label would effectively communicate to the end user that the product contained asbestos, that asbestos was harmful if inhaled, and the following procedures could be used to mitigate or eliminate the risk. Given that the label did all these things, effectively then a label such as that should have been attached in my opinion in 1960

…because there is no control here, external to the factory, you just have a product which arrives unspecified in terms of its content and the implications. I think that for similar reasons a prudent measure, public health measure would be to place on it the composition of the product, what the industrial health or public health implications of it was, and what measures could reasonably be taken to avoid those industrial health or public health outcomes…

20. He was then invited to say what the labels should have said and he gave his version of that.

21. It is important however to remember in respect of this evidence the following:

(i) Dr Thomas’ article in dealing with the topic of asbestos bodies said:

asbestos bodies…have been found in this survey as early as 15 months after exposure commenced.

(ii) There was no regulation which required a warning about asbestos products. (T63)

(iii) Mr Stewart made no investigation of the cutting of asbestos cement sheets during the period 1953 – 1963. (T63)

(iv) He made no investigation of people using asbestos cement sheeting while he worked for the Department of Health. (T64)

(v) The limit of exposure for workers exposed to asbestos dust was at the time 5 million particles per cubic foot. (T66.1-5) That level of exposure was not sustainable for more than a few years or so it was thought. (T66.17-18) It was thought that clear cut cases of asbestosis were not found at dust concentrations below 5 million particles per cubic foot. (T66.26-27)

(vi) It was thought at that time that five years exposure at 5 million particles per cubic foot would produce only between 5 and 10 per cent cases of asbestosis. (T66.29-31)

(vii) The concern in the 1950’s was with asbestosis and after the report of Sir Richard Doll in 1955 with lung cancer. (T67.1-11)

(viii) The focus of the regulation then in force was on workers exposed in occupational settings on a daily basis. (T67.12-15)

(ix) After Dr Thomas’ article there was no change to the regulation.(T67.17-18) Nor was any regulation introduced which required the labelling of asbestos cement sheeting.

22. Dr Ian Gardiner, respiratory physician agreed with the following propositions:

i

a. As a proposition of occupational hygiene it was sound advice to try and ensure that people were not unnecessarily exposed to the dust of asbestos.

b. One of the principal ways of ensuring that would be to inform and educate people as to the potential hazards or dangers of asbestos dust.

c. For those who were large scale producers of asbestos products in the community who were aware or ought to have been aware of the dangers and the nature of the asbestos particle as we have spoken about where that knowledge existed it should have been put out in the public domain. (T87.5-35)

23. Mr Pickford also gave evidence about foreseeability. He was called by the defendant. He did not enter the world of industrial hygiene until he started to work for the defendant in 1972. (T144.13-14) As regards the position pre 1960 he said that he was not able to answer (See for example T147.31; T147.19-20) Further, when asked about the state of knowledge as at 1960 he said “…I’m in no position to argue one way or other.” (T132.24)

24. Mr Pickford’s evidence was severely criticised on credit issues. He was asked about a report he had prepared in a matter of Dunn v Seltsam Pty Limited (PX11). The report was dated 18 May 2005. In that report he had written:

I do not believe that any factory such as Gaythorne (in Brisbane) should have provided warnings to the neighbourhood residents at any time because there was no evidence that asbestos cement factory emissions could lead to any asbestos related disease.

25. This proposition cannot stand with the Newhouse paper DX5 published in the British Journal of Industrial Medicine in 1965 (as to which further reference will be made). Further Mr Pickford confessed he did not read the Newhouse paper prior to writing his report in Dunn.

26. He thought, too, that there might have been another paper which he was unable to identify which touched on the topic but he did not consult that either. (T107.42-45)

27. As has been submitted Mr Pickford attempted to defend his position in respect of the Newhouse paper by saying that the Newhouse paper was

“not actually current. It was not widely distributed in that era and there was no justification or evidence as far as the industry was concerned, in my belief, that they should have warned the community.”

Yet as has been submitted Mr Pickford was not able to describe the distribution of the British Journal of Industrial Medicine. Mr Pickford said further that his evidence that the Newhouse report had not been widely disseminated or distributed in Australia was not based on any research (T109.24-26).

Mr Pickford conceded that the conclusion of the Newhouse paper that there

seems little doubt that the risk of mesothelioma may arise from both occupations and domestic exposure to asbestos.

.

28. Another statement in the Dunn report to attract criticism was the following:

U

ntil the 1980s or 1990s, it was believed that only significant quantities of respirable asbestos fibres for many years would lead to any disease. These conditions only arose when asbestos materials or fibres were being handled or processed and only by people associated with the processes or immediately adjacent to them.

It may be said fairly I think that this statement is contrary to evidence we hear in this Tribunal day after day.

29. Further he was invited to contrast his statement with what appeared in the Newhouse paper. His response was that his statement was intended to be applied only to the Wunderlich situation. (T111.41). As an explanation or excuse this was feeble. A further attempt at justification was given at T111.47-48

I believe the situation is still relatively open…

With great respect to Mr Pickford this is nonsense. He was unable to identify any research upon which he had relied to come to the conclusions that he had expressed in the Dunn report (T112.19-21). Mr Pickford also attempted to wriggle out of his problem by distinguishing the UK asbestos factories from the Australian ones and the amount of dust they produced, notwithstanding that the UK factories were not identified in the Newhouse paper. Mr Pickford was unable to refer to a single paper or commentary to justify what has been described in submissions as this idiosyncratic distinction.

30. Mr Pickford was asked (T113) whether he knew of an article in the British Medical Journal of 6 February 1965 by Elmes entitled Diffuse Mesothelioma of the Pleura and Asbestos. The following was read to him from pg 352:

a study of occupational history suggest (sic) the interval between first exposure to asbestos and discovery of the tumour mesothelioma is often long, it may exceed 40 years and exposure may be light and in some instances very transient. A similar observation was made by Wagner in 1960.

Mr Pickford said he was aware of the opinion. He was asked how that fitted with what he had written in Dunn and at line 30 he eventually answered

I repeat I should have qualified it by the statement that I mentioned a while ago.

Yes well my statement looks global. It was intended to be applying to the Wunderlich situation.

31. Professor Henderson referred to the B K Report Faserjahre for 1997 in connection with measurement of dust exposures for handling A/C products. Mr Pickford did not bother to read the report.

32. Other criticisms have been made of Mr Pickford’s evidence to which it is not necessary to go.

33. Ultimately the submission was made that the report in Dunn can only be explained by way of Mr Pickford being partisan, an apologist for the asbestos industry and as attempt to explain his own failures as an environment control officer at Wunderlich. Further it has been submitted that the report in Dunn demonstrates a witness without independence, a witness who disregards the fundamental obligation of the expert – to be independent. I regret that I must say I think Mr Pickford was being partisan and that for the most part his evidence was unimpressive. Further I accept the submission that his report in Dunn demonstrates a witness without independence. He did not try to be independent.

I accept further the submission that his evidence in this case should be given little weight.

34. The plaintiff however seeks to adopt a number of concessions made by Mr Pickford as he was being cross examined. I set them out hereunder as identified in the written submission delivered by learned counsel for the plaintiff:

(a) That before 1950 asbestos was recognised to be a toxic substance.

(b) The carcinogenicity of asbestos as regards lung cancer was accepted after Doll’s 1955 paper. (T118.6-7)

(c) That during the 1950s there was an appreciation that asbestos exposure was cumulative and additionally dangerous because of its cumulative nature, exposure building up on the fibre content of the lung one after the other. (T118.27-29)

(d) That in the 1950s the injuries recognised as being associated with asbestos were serious and disabling injuries capable of causing death. (T118.43-47)

(e) That asbestos related disease often presents many years after exposure to asbestos. (T118.48-49)

(f) That the injuries once in place could not be corrected. (T119.1-2)

(g) That because of the nature of the injuries, precautions were more important. (T119.3-4)

(h) That he expected by 1950 any large–scale producer of asbestos goods in Australia to be well aware of the potential dangers of asbestos dust. (T118.1-3)

(i) That when dealing with substances known to be dangerous or toxic a basic tenet of occupational hygiene is to minimise or limit exposure to such substance whether or not there be a standard in force. (T117.18-20)

(j) That the aim of reducing and minimising exposure to asbestos was in place from the early decades of the 20th century there was a constant push to lower concentrations and be more and more careful about exposure to asbestos. (T119.21-23)

(k) That because asbestos dust had the ability to accumulate in the lungs, one exposure after the other, a prudent person would avoid or minimise such exposure (T118.32-34) irrespective of whether he knew of the risk of mesothelioma or not. (T118.41-42)

(l) That in the 1950s the Dreesen standard was subject to criticism (T119.7-8) and that any reasonable reading of the Dreesen study showed there was a proved hazard of asbestos at lower levels than the Dreesen standard. (T119.16-18)

(m) That as at 1930 there was a great deal of uncertainty concerning the asbestos fibre and the potential for even low concentrations, as then understood, to cause disease. (T123.17-19)

(n) That no one really knew the level of fibre that could cause the asbestos diseases prevalent amongst those working with asbestos. (T119.9-11)

(o) That any easy change of process of material to a safer one is a very desirable, good principle. (T114.38-40)

(p) That it was appreciated in 1930 that persons with the responsibility for sawing to size asbestos cement sheets were potentially at risk of asbestos disease. (T123.1-4)

(q) That from the 1950s there was an acceleration in the use of asbestos cement material in the building industry (T132.42-44) and that AC sheets were used as internal and external claddings on anything from domestic residences through to factories and large buildings, (T1.56.15-16) asbestos cement being a cheap alternative which spread through lower cost housing. (T1.56-27-28)

(r) That he would have anticipated in 1960 or 1961 that asbestos cement sheets produced by Wunderlich after leaving the factory would have been machine sawed for preparing various ingredients for kit homes. (T133.27-33)

(s) That power saws and bench saws were reasonably common in the 1960s. (T133.34-36)

(t) That once the sheets left the factory one did not know what happened to them. (T133.40-41)

(u) That the defendant did not know how much exposure an individual would have from sawing or trimming or machining a sheet after it left its p remises. (T133.45-48)

(v) That the defendant did not know whether the user of the sheet would be a handyman/home renovator or a full-time carpenter who built asbestos cement cottages. (T134.1-2)

(w) That the defendant did not know how much asbestos would be used by one carpenter as compared to another. (T134.3-5)

(x) That he could not point to any tests carried out in relation to asbestos cement sawing in the field in the 1960s. (T134.9-28)

(y) That the defendant did not know how much exposure to asbestos fibre a person would have who used a sheet in the manner anticipated after it left its factory. (T134.6-8)

(z) That a basic tenet of occupational hygiene is to inform or educate those working with or using a dangerous or toxic substance so that the person using the dangerous or toxic substance can take precautions to avoid exposure to it. (T117.21-24)

(aa) That persons working with or liable to be exposed to asbestos dust should as far as possible be informed and educated about the risk. (T118.15-16)

35. In addition to the evidence called in the case the plaintiff has tendered medical evidence in the form of articles published during the twentieth century in medical and industrial journals dealing with the dangers of exposure to asbestos. The material has been tendered pursuant to s25(3) of the Dust Diseases Tribunal Act 1989 (NSW). It is necessary to refer to some of that material.

36. In 1898 the Inspector of Factories report (UK) (PX12 1.1) included:

Of all the dusty occupations which specially came under observation in 1898 three, in addition to china scouring, stand out on account of their easily demonstrated danger to the health of the workers, and because of ascertained cases of injury to bronchial tubes and lungs medically attributed to the employment of the sufferers. These occupations were asbestos sifting and carding, silk opening and combing, and hemp spinning. Although the dust inhaled in considerable quantities was necessarily injurious in a greater or less degree according to the constitution of the persons in question, it was found that with properly applied ventilation in some factories the occupations could be rendered comparatively innocuous.”

Miss Deane reports on the abundant evidence she has had of the evil effects of dust:-

In the majority of cases the evil is very insidious, and the general symptoms produced by dust on the various respiratory organs are to the lay mind so similar to those produced by other causes that it is not always easy to trace the connection. The incessant ‘sore throat’ the irritation of the bronchial passages, the frequent ‘colds on the chest.’ And ‘hoarse voice’ and ‘morning cough’ from which girls employed in dusty processes suffer are all symptoms which to casual observers might be easily accounted for in other ways. One or two sad cases of phthisis medically certified to be seriously aggravated, if not induced, by work in rope factories which came under my notice have emphasized in my mind the grave possibilities arising from work in these places.

Such instances can seldom be fully traced except with infinite labour and patience. The worker falls into ill-health, and sinks away out of sight in no sudden or sensational manner so that attention is seldom attracted to the ultimate source of the trouble.

The evil effects of asbestos dust have also attracted my attention, a microscopic examination of this mineral dust which was made by H.M. Medical Inspector clearly revealed the sharp, glass-like, jagged nature of the particles, and where they are allowed to rise and to remain suspended in the air of a room, in any quantity, the effects have been found to be injurious, as might have been expected.

As in china-scouring, so in a still greater degree in other dusty trades, the worker may continue for a very long time apparently unaffected, before the symptoms of the evil become marked.

It is often impossible to bring positive proof of definite injury solely attributable to working in a dusty atmosphere, for except in extreme cases the symptoms are similar to those attributable to other causes: but the certainty of the danger can be clearly demonstrated, as, for instance, by examination of the dust particles. Even when the evil reaches such grave proportions as to be capable of easy and tragic proof as in the case of china scouring or flax preparing, there is always a certain proportion of “old workers” – the survivors of their mate – who are to be found in every unhealthy industry, and who, like the Circussian poison-eaters appear to thrive on their unhealthy calling.

In less obviously unhealthy conditions the only convincing proof of actual injury, viz. reliable comparative statistics of mortality, or of health-standards, is practically unattainable in the case of any given factory, at any rate with the time and opportunity at present at our disposal.

37. All dust was recognised as a threat to health. Kober in Industrial Health 1924 (PX12 tab 1.7) stated interalia:

The injurious effect of dust in all its forms cannot be questioned and is made sufficiently apparent by a study of tuberculosis in relation to dusty trades. Fortunately only about 25 per cent of the dust inhaled actually reaches the lungs, the bulk, according to Lehmann and his pupil, .Saito and others, is sneezed or coughed up or swallowed. But this does not imply that the dust which has found its way through the stomach remains harmless, for it may reach the lungs by ways of the lymph channels, and certainly all poisonous, dusts can be absorbed in the gastrointestinal canal.

In addition to the mechanical, irritant and toxic character of dust, Haldane very properly points out that “it inevitably tends to lower the social status and self-respect of the work people.

38. The next document referred to was an article by Cooke reported in the British Medical Journal in 1924 (PX12 tab 1.8). At 147 the following appears:

Medical men in areas where asbestos is manufactured have long suspected the dust to be the cause of chronic bronchitis and fibrosis, and Professor J.M. Beattie has a theory that the dust causes fibrosis in guinea-pigs………

39. Reference was then made to the report of the Director General of Public Health New South Wales for the year 1927 (PX12 tab 1.12). The paper is headed (at pg 102) Notes on a Fine Type of Fibrous Pneumonokoniosis produced by Silicates and other Minerals. Asbestosis is specifically mentioned at pg 102. It is described as follows:

Asbestosis a fibrosis of the lungs due to asbestos which is a silicate of magnesium. It is a fine fibrosis with characteristic, microscopic stigmata. There is no comparative account of radiographic appearances.

These dust fibroses of the lungs are found either simple or complicated with tuberculosis or other infective processes which add a tuberculous or infective fibrosis to the already existing dust fibrosis.

At pg 106 there is a section of the report devoted to asbestosis. The types of asbestos are described ie chrysotile, crocidolite and amosite. Amosite was described by the author as a comparatively recent discovery. The chemistry has not been completely worked out but it appears to be somewhat similar, the author said, to crocidolite in composition. The summary at pg 110 contains a reference to asbestos and cement workers.

40. The next document referred to in submissions was that published in 1930 by the International Labour Office under the title of Occupational and Health. The sub title is Encyclopaedia of Hygiene, Pathology and Social Welfare . (PX12 tab 1.17). There is a section of the work devoted to asbestos (p189). Under the heading Dangers and Hygiene the following appears (at p190):

The worker engaged on the extraction and manufacture of asbestos is constantly exposed to danger from dust more especially, however, in the operations of spinning and weaving.

The weaving of asbestos has only developed importance during the last twenty years. Now that it is widely practised the application of local exhaust systems during such processes as that above described is called for.

All processes from extraction onwards unquestionably involve a considerable hazard, and American and Canadian life insurance generally refuse asbestos workers on account of the assumed deleterious conditions in the industry.

The lack of more accurate and detailed data in medical literature regarding this industry in various branches, including the utilization of by products, is to be deplored in view of the self-evident importance of asbestos dust as a predisposing cause of pulmonary tuberculosis, more especially since the rapidly increasing development of industries utilising asbestos adds greatly to the urgency of studying the conditions with a view to their amelioration.

41. PX 12 (Tab 1.20) contains a copy of the report of by E R A Merewether MD, HM Medical Inspector of Factories published in 1930. The title of the report is the Occurrence of Pulmonary Fibrosis and Other Pulmonary Affections in Asbestos Workers. The work is 60 pages long. At 255 the summary of the article commences with the following:

Summary. 1. There is a definite risk of the development of the diffuse pulmonary fibrosis in persons exposed to the inhalation of asbestos dust……

4. With continued exposure to high concentrations of dust the disease may be fully developed in seven and nine years and may cause death after about thirteen years, exceptionally in a shorter period.

42. The next document referred to in submissions is the report on Effects of Asbestos Dust on the Lungs and Dust Suppression in the Asbestos Industry by E.R.A. Merewether and C.W. Price published on 14 March 1930 (PX12 tab 1.21). It was published by the British Home Office and interestingly Crown Copyright was reserved in respect of it. At pg 5 the following appears:

2. – Effects of Irritant Dust Upon the Lungs

The most important local effects which may follow the inhalation of dust include pulmonary and bronchial catarrh, asthma, bronchitis, fibrosis of the lungs, and secondary changes, such as emphysema, local or diffuse. These changes in the lungs, which may be looked upon as a measure of the efforts of the living tissues to repel or incarcerate the irritant particles of dust, necessarily cause interference with the general efficiency of the lungs. The impairment of functional capacity may be slight or severe, and temporary or permanent, depending on the variety of dust, and on other factors, such as concentration of dust and length of exposure.

Asbestosis – the Pulmonary Fibrosis of Asbestos Workers. – It is helpful to visualise fibrosis of the lungs as it occurs in asbestos workers as the slow growth of fibrous tissue (scar tissue) between the air cells of the lung wherever the inhaled dust comes to rest. While new fibrous tissue is being laid down like a spider’s web, that deposited earlier gradually contracts. This fibrous tissue is not only useless as a substitute for the air cells, but with continued inhalation of the causative dust, by its invasion of new territory and consolidation of that already occupied, it gradually, and literally, strangles the essential tissues of the lungs.

In common with other essential organs of the body the lungs have a large reserve of tissue for use in emergencies and to permit of a diminution of functional capacity due to advancing age or disease. For this reason, and because fibrosis of the lungs is essentially a local disease, it is only when the fibrosis progresses to the extent of obliterating this reserve that undue shortness of breath on any extra effort draws the worker’s attention to the fact that his health is not what it should be. The other symptoms of the disease such as cough are equally unassuming, and are readily ascribed to some common and trivial cause.

From this point the progress of the disease is more rapid, since it is now encroaching on the remaining sound tissue of the lungs, already only just sufficient to maintain him in his ordinary daily activities. Ultimately, if no acute respiratory infection has precipitated a fatal termination, a stage is reached when the lungs can do little more than maintain life, and the shortness of breath becomes extreme.

In its main clinical features, therefore, the disease resembles silicosis, as might be expected. It differs from silicosis, however, in the mode of distribution of the fibrous tissue in the lungs, in its more rapid development, in its radiological features, and there is some reason for believing, in a lessened susceptibility to the supervention of pulmonary tuberculosis, the liability to which disease is so definitely an added hazard in silicosis.

Finishing processes on asbestos-cement sheets include sawing to size, corrugating, pressing and drilling, carried on in some factories with the material so moist as to prevent dust, and this practice should be adopted generally. Otherwise much dust is produced in sawing owing to the rapid cutting speed and localised exhaust is necessary, though not applied.

One may observe that the sawing of asbestos cement sheeting was even then a matter for concern for the authors of the report.

43. The submission goes on to point out at pg 31 under the heading Summary and Recommendations the following:

The appropriate methods for suppression of dust may only be fully determined when the harmful effects of comparatively low concentrations of asbestos dust are duly appreciated.

The asbestos manufacturers are clearly confronted with the necessity of attaining conditions in their industry which will ensure much less dust in the atmosphere than can safely be tolerated in many comparable trades not using asbestos.

44. The next document referred to in submissions is an article published by Frederick Willson, M.D. in the magazine Safety Engineering published in November 1931. The title of the article is The Very Least an Employer Should Know about Dust and Fume Diseases. The article appears under tab 1.29 in PX12. The article commences:

The harm wrought in industry by diseases due to inhalation of dust and fumes is, as yet, not so well recognized as are those visible injuries caused by industrial accidents. Nevertheless, the employer who has at heart the welfare of his workmen and the best monetary interests of his company should wish to have some information on this subject, that he may nor err through ignorance of the danger of dust and fumes or of the liability under the law which he must always fact.

Scientific knowledge of the results of dust exposure has not progressed far enough to exactly predicate the degree of danger in every kind of dust and fume. The only safe way for an employer is to regard all dust in industry as a hazard. Under best conditions it cannot help but be harmful to a degree, while under adverse conditions the shortening of life is almost inevitable. We do know, however, that breathing of dust under the following conditions is seriously harmful:……………

Asbestos and every operation in which it is used.

45. The next article referred to in submissions is the article entitled Silicosis and Asbestosis appearing in the magazine The Quarry and Roadmaking published in October 1932. (PX12-tab1.30) At pg 422 a section of the report is devoted to asbestosis. In the second column at 422 the following appears:

Processes involving exposure to asbestos dust which are known to give rise to asbestosis or in which the conditions are such as to be liable to produce the disease are the breaking, crushing, disintegrating, opening and grinding of asbestos and the mixing or sieving of asbestos or any mixture of asbestos, the manufacture of asbestos textiles, the making of insulating slabs or sections and the making or repairing of insulating mattresses composed wholly or partly of asbestos, and the sawing, grinding and turning in the dry state of articles composed wholly or partly of asbestos such as motor car brake and clutch linings, electric conductors and packings and jointings.

46. The next matter the subject of submissions was the article by Dr Shiels, the Director of the Department of Health of Victoria in a Health Bulletin published in 1932 (PX12 – also under tab 1.30) in which he said (pg 1914.4-6)

All workman should be told something of the dangers of the material with which they come into contact and not be left to find out for themselves sometimes at the costs of their lives.

This statement was accepted by Mr Pickford as being sound in principle and from his point of view mandatory. (T124.25-26)

47. That there was concern about hazards from short exposures to asbestos dust emerges from the article published in 1933 by Donnelly in the American Journal of Public Health. The title of the article was Pulmonary Asbestosis. (PX12 tab 1.31) At pg 1281 the following appears:

That exposure to and the inhalation of this dust for even a comparatively short time is a definite and serious industrial hazard, has been too frequently indicated to be open to doubt. The fact that the condition once acquired is permanent and more or less rapidly progressive, is most important from a public health view point.

48. I note in passing in PX12 under tab 1.35 a publication entitled Safety Engineering published in August 1934. Under the heading asbestos dust the following appears:

a potential asbestosis hazard is to be looked for whenever asbestos dust is created. Possible sources are the mining and milling of asbestos and the weaving, machining and mixing of asbestos and asbestos compounds. Industries included in the latter group are the manufacture of asbestos textiles and clothing, brake linings, cement and roofing material.

49. A copy of the Dreesen study of asbestosis in the asbestos textile industry published by the United States Government printing office in 1938 appears under tab 1.47.

50. Under tab 1.45 of PX12 is a copy of a paper entitled Dangerous Dusts published by John B Hawes in 1937. His views are very strongly expressed. At pg 162 he speaks out about inter alia:

The crooked and mercenary attorney.

The truth of the matter is that tobacco dust is not dangerous but that the work involved in this industry called for little or no physical exertion and, therefore, invited weaklings, while, in addition, the hygiene of the workers was notoriously low.

At pg 164 the author wrote:

Asbestosis is a relatively new disease, concerning which we know remarkably little except it does not seem to correspond to the laws governing silicosis in general. There is not the slightest doubt, however, in my mind at least that asbestos dusts is the most dangerous of all dusts. Asbestosis is able to produce total and permanent disability in a remarkably short length of time, even after only two or three years of exposure and occasionally less compared to the much slower and more gradual action of pure silicon and the great majority of silicates.

51. It is pointed out in submissions by Counsel for the plaintiff that Mr Pickford agreed that this comment of Hawes was a sound warning for those concerned with the manufacture of asbestos products and agreed that the description of asbestos as highly dangerous was something that was appreciated in the late 1930s (T124.48-T125.5).

52. The Annual Report of the Chief Inspector of Factories United Kingdom 1938 was the next document referred to in submissions. The document appears in PX12 under the tab 1.50. At pg 63 the following appears:

Moreover dust that is thought today to be harmless may following in research be viewed in another light tomorrow. It is not many years ago when the dust of asbestos was regarded as innocuous while today it is recognised as highly dangerous.

Mr Pickford did not disagree (see T125.15).

53. The next document referred to is an article published in Industrial Medicine in April 1942. The author was Warren Cooke. A copy of the document appears under the tab 1.53 in PX12. In the second full paragraph on the second page of the article the following appears:

In the case of the asbestos dust condition our evaluation of the exposure should be based on the knowledge that the present toxic limit for asbestos is 5 million particles per cubic foot of air. This is a very small concentration, so small in fact the condition may look good even to a critical eye and still present an exposure greater than this low limit.

In the case of asbestos dust however and this holds with even more certainty for dusts free in high silica content, the toxic limit is so low that the only safe procedure is to have recourse to actual dust determinations.

54. The submission next points to several articles which associate asbestos with the development of carcinoma of the lung. Those pointed to are articles by Gloyne, in Tubercle, 1935 (PX12-1.39) Lynch and Smith, American Journal of Cancer, 1935, (PX12-1.42)

55. Hueper in 1942 in his text Occupational Tumours and Allied Diseases (PX12 – 1.54). writes at pg 400 the following:

Conditions and types of exposure. The chief health hazard consists in the inhalation of asbestos dust, which is produced abundantly during the preparation of the mineral for the spinning process (purification and removal of stony impurities) and during various other phases of the production and manufacturing processes of asbestos and asbestos containing goods.

The development of a pulmonary asbestosis depends according to Bauer, upon the duration and degree of exposure of asbestos dust and on a certain personal disposition.

Asbestosis usually develops after an exposure of three to fifteen years (Martz), but may not produce subjective symptoms until many years after the cessation of exposure to asbestos material.

There is an incidence of lung cancer in asbestosis of the lung which is definitely excessive. The relatively small number of necropsies on which this conclusion is based represents an urgent indication for more intensive post mortem examinations in cases of asbestosis; …………

56. Counsel for the plaintiff also points out that Mr Pickford agreed that at the time of the Hueper publication there was huge amount of literature concerning the association between asbestos and lung cancer. (T125.31-34)

57. Under tab 1.55 is a copy of an article published in Industrial Medicine in April 1943. The title of the article is the Minimal Requirements for Safety and Industrial Health in Contract Shipyards. At pg 262 para 313.7 the author deals with asbestosis. He wrote:

Asbestosis –

Sources: In general any job which asbestos dust is breathed for example

Job When material is

Handling,

sawing, Asbestos

cutting,

moulding, Asbestos mixtures

welding rod salvage

Mr Pickford agreed that this would apply to any asbestos material. (T125.44-45).

58. Under tab 1.65 is a report of the Director General Department of Health in New South Wales published in 1948. At the foot of the second column the following appears:

To reduce the loss of heat from molten metal held in a crucible one firm covered it with a coarse asbestos, the finer particles of which spread throughout the building when it was shovelled onto the metal. The exposure to asbestos was intermittent and of short duration, about five minutes at each pouring, and as at the time, asbestos was only being used two or three times a week, the dust hazard was considered to be small. However, in view of the dangers associated with asbestos dust it was advised a substitute such as magnesia…should be used.

The plaintiff points to this passage as evidence of concern at that time about even short exposure to asbestos. The defendant replies by saying the asbestos being used would almost be certainly have been pure asbestos and hence that differentiates the circumstance being considered from the plaintiff’s circumstances.

The plaintiff’s counsel submits that Mr Pickford agreed that the cautious attitude shown in the article was wise (T126.5-13).

59. The submission refers to an article published in the Medical Journal of Australia in 1950 by Dr Smith (PX12 –1.71). The publication of the document followed the Third International Conference of Experts of Pneumonokoniosis held in Sydney under the auspices of the International Labour Organisation (1950). Under the heading The Composition of Dust (P778) the following appears:

Asbestos which contains no free silica produces a severe pulmonary disease, but the mode of action of the asbestos fibre differs from that of the silica particle.

Asbestosis apparently occurs after a shorter exposure. Thus Wyers (1949), who investigated 115 fatal cases of asbestosis, found the average exposure had been 10.4 years.

Under conditions of intermittent exposure it is more difficult to predict the likely effect on the lungs than if the exposure was continuous, but the severity of any dust hazard is usually lessened in such circumstances. This however might not apply with very high intermittent exposures.

In regard to asbestosis which is a very infrequent occurrence in this country all the evidence from overseas indicates that it is much more common in workers engaged in the processing and fabrication of asbestos in factories (textile work) than in asbestos miners.

They also refer to reports by various investigators which indicate that workers in chromite factories and those exposed to arsenic and asbestos have a high incidence of pulmonary cancer.

60. In 1952 an article was published by the Editorial Board of the American Medical Association in Archives of Industrial Hygiene and Occupational Medicine (PX12-1.74). At pg 262 is a table of cases of carcinoma of lungs detected among 4,000 asbestos workers in the period 1940-1950. The table includes reference to two cases of pleural mesothelioma. In respect of the first the asbestosis was described as minimal; that person is said to have had 10 years of exposure to asbestos. The second person had no asbestosis and no years of exposure according to the table although he had 28 years in the industry.

If asbestos is carcinogenic, I would not expect to see it produce only one type of tumour I am interested in your observation of two cases of pleural mesothelioma. This is a rather rare tumour. In examining pathological material sent us from England by Dr Hinson, we found among six cancerous asbestotic lungs two presenting alveolar cell carcinoma. These tumours are often diagnosed as “pleural mesothelioma”. I should very much like to exchange slides with you.

61. On July 11 1953 an article was published in the Lancet. It was entitled The Prevention of the Dust Diseases. The author was A I G McLaughlin (PX12-tab1.76) He was the Medical Inspector of Factories. The article contains an entertaining historical review commencing with Hippocrates (about 400BC) going through Paracelsus also known as Bombast, Georgius Agricola (1556), a translation of whose work was undertaken in 1912 by Herbert Hoover a mining engineer from America (later President Hoover), Bernardino Ramazzini (1700), Thackrah (1831) and others. Thackrah had noted that bricklayers and lime workers were long lived and that sandstone masons usually died before they reached the age of 40. He was not clear in his mind how much the taking of alcohol had to do with these pulmonary diseases. The author went on:

He was against alcohol (in the same way that President Coolidge was against sin) and no doubt he had good reason to be, because it was quite cheap in those days.

The concentration of dust which can be inhaled without danger varies according to the nature of the dust and also to the length of time that a man is breathing it. Again, the intermittent exposure to high concentrations of dust may be more dangerous than exposure to lower concentrations over a longer period. The harder the job is, the more deeply will a man have to breathe and in consequence he will breathe more dust. Individuals vary greatly in their capacity to deal with dusts and if two men who have been working at the same job for the same length of time one may get a disease of the lung and the other may be unaffected. This is one reason why I am not greatly impressed by the validity of what are known as the maximum allowable concentrations of dust (M.A.C.) of which lists have been drawn up in various countries. The MACs seem to be based on the assumption man is a standardised machine which clearly he is not. The reasons for the differences in individual reaction to dust are not accurately known but it is likely that they depend on anatomical psychological and biochemical variations from one person to another.

62. The next matter adverted to in submissions is the publication in 1955 in the British Journal of Medicine (PX12 1.77) of the paper by Sir Richard Doll entitled Bronchial Carcinoma: Incidence and Aetiology. The paper was published on 5 September 1953. At pg 526 the author noted:

The classical method leading to the isolation of chemically pure carcinogens is the observation of specially high cancer risks in specific occupations. With lung cancer, exceptional risks have been recognised in several unrelated industries. These are: mining of various ores in Schneeberg (Germany) and in Jachymov (Czechoslovakia); chromate production; nickel-refining (in Clydach, S. Wales); asbestos manufacture; and the production of gas.

I

n the manufacture of asbestos and arsenical sheep dip the risk is more likely to have been of the same order as that involved in the production of gas. For example, Gloyne (1951) found that of 52 men dying with asbestosis about 20% gave evidence of the presence of a primary lung cancer, whereas among men with other forms of pneumoconiosiss the proportion was 7%. As is shown later, there are reasons for believing that the incidence among men with pneumoconiosis is generally close to the average.

63. The next material referred to in submissions is an article published in the magazine Manufacturing and Management on 10 July 1956. The title of the article is Dust Hazard in Industry. (PX12-tab 1.82) It is an editorial staff article. There is a section on asbestosis. In the second column at pg 21 the following appears:

People prone to the disease are those handling asbestos in its raw state or processing it to make lagging materials; also operatives sawing and cutting any finished product containing asbestos such as brake linings asbestos sheeting and various insulating materials. Dismantling old dry lagging is a hazardous occupation.

Once established, asbestosis constitutes a grave threat to life and health………

Industrial equipment available for protection against dust includes gas masks and respirators of various kinds. Filter respirators are used for protection against silica dust and toxic dusts………

64. An article published in the Medical Journal of Australia on 19 January 1957 is the next material referred to. It appears under tab 1.85 in PX12. The title of the article is Pneumonokoniosis in Victorian Industry, the author is D L Gordon Thomas. It was this article which caused Mr Gordon Stewart to say, once he had seen it, that asbestos cement sheeting should have had warnings fixed to it. A survey of 300 asbestos workers is referred to at pg 76. In the first column the procedure for the survey is there described. If the subject demonstrated the presence in his system of asbestos bodies he was radiologically examined. Later all workers the subject of the survey who were exposed to dry asbestos were radiologically examined (Ibid). The author then went onto say:

The following occupations are involved: handling the substance in its raw state; grinding the substance prior to its use in some process; mixing with diatomaceous earth or kaolin to form lagging materials; sawing, cutting and finishing any product containing asbestos – for example brake linings, asbestos sheeting and various insulating materials; tearing down old lagging – this a very dangerous process, even in the open air; spraying asbestos on walls and ceilings as an insulator.

During the running of the case the defendant sought to submit that the occupations thus described simply designated those occupations from which the subjects of the survey were taken. I do not think that is a reasonable reading of the material. The clear intent of the author it seems to me, is to say that the activities described involve risk.

65. The next material the subject of submissions appears under the tab 1.86 PX12. It is an article entitled Toxic Agents - in the Factory by Dr W F Cooper, Medical Director of General Motors Holden Limited. It was published on March 1 1958. At pg 37 the following appears:

Asbestos is another destroyer of lung tissue and the maximum permissible concentration is two and half million particles per cubic foot that is 87 particles per cc.

The prevention of silicosis and asbestosis revolves itself around the suppression of dust and exhausting it plus personal protection of workers by respirators.

It is to be noted that the author was proposing a maximum permissible concentration of asbestos dust at one half of that tentatively put forward by Dreesen in 1938.

66. Reference is made also to the report of the proceedings of the Pneumoconiosis Conference held in the University of Witwatersrand, Johannesburg on the 9-24 February 1959. (PX12 1.87) There is a copy of a paper by J C Wagner entitled Some Pathological Aspects of Asbestosis in the Union of South Africa provided. The paper discusses the emergence of diffuse mesothelioma in some of the subjects. Some of the mesothelioma sufferers were not employed in mines. It is, for present purposes, sufficient to go to the conclusions drawn by the author. They are expressed in these terms:

Conclusions

In conclusion it would appear from the examination of human material and preliminary animal experiments with chrysotile and amosite that the lesions caused by exposure to amosite and crocidolite dust are essentially similar to those caused by chrysotile.

The problem requiring most urgent investigations is the high incidence of mesotheliomas on the Cape asbestos fields, where a very serious hazard may exist.

67. A paper (PX12 1.90) by J C Wagner, C A Sleggs and Paul Marchand was published in the British Journal of Industrial Medicine in 1960. The title of the paper Diffuse Pleural Mesothelioma and Asbestos Exposure in the North Western Cape Province. It is submitted and I accept that the paper is noteworthy because it described case histories of people being diagnosed with mesothelioma who did not work in the asbestos industry.

68. PX12 1.91 contains a paper entitled Complications of Asbestosis published on April 30 1960 in the British Medical Journal. At pg 1351 the following appears:

Carcinoma of the lung is a serious and well-recognized complication in asbestosis. Its frequency in asbestosis is difficult to determine, for it is now a common condition in the general population. Moreover exposure to asbestos may have occurred many years before the cancer develops. Nevertheless, the paper by Doll makes it fairly clear that a patient with asbestosis has a risk about 10 times that of the general population of getting carcinoma of the lung. Another hazard is mesothelioma of the pleura. This rather rare tumour may draw attention to the fact that a patient has worked in asbestos dust. Finally, in women who work with asbestos there is a high incidence of cancer of the ovary.

Asbestosis was first described in this country by M. Murray in 1907. After that, in 1930, Mereweather (sic) and Price reported the dangers of asbestos dust in the lungs and made recommendations for dust suppression. Thereafter there was a great improvement. In the factory where our patient worked the utmost precautions are now taken to prevent asbestosis occurring. It is a disappearing disease. Nevertheless, asbestos dust is most toxic, and the amount needed to cause asbestosis is not known, so constant vigilance and new preventive methods are needed if this disease is to be abolished.

Unhappily it appears that the idea that asbestos is a disappearing disease has proved to be wrong The other matters at the end of the passage quoted seem to me however to be of significance.

69. It is submitted that the articles referred to thus far were available in libraries throughout Australia at the time of the plaintiff’s exposure to asbestos from the defendant’s product. In this regard reliance is placed upon PX17, the report of Anne Cameron Batt, Librarian. That may well be so. There are some copying deficiencies in the copy of the report tendered in evidence which make it difficult to demonstrate the accuracy of the submission. It can however be said firstly that most of the publications referred to one would expect to be widely available, for example the Lancet, the British Journal of Industrial Medicine or the British Medical Journal. Secondly it is plain enough from the statement of Anne Batt that many of the articles therein set out were widely available throughout Australia.

70. Against the background of that material it was submitted that by 1950 it was well recognised exposure to asbestos in any concentration should be avoided. In as much as this means that it was prudent or desirable to minimise exposure to dust generally including asbestos dust, I do not think there is any dispute. In this regard the plaintiff relies on the evidence of Mr Stewart in these proceedings and in earlier proceedings. As Mr Stewart said in this case (T73.41-74.14) in cross examination:

In my opinion in minimising (sic) exposures has been the mantra of industrial hygiene. That applies more particularly to carcinogenic toxic products than any other. There are some where it doesn’t really matter, like carbon monoxide flows in and out of the blood unless you get heart failure during an episode but products like silica, asbestos, radiation exposures are fully cumulative and accumulate over your whole life time. Specifically focusing if you wish on these products, irrespective of what the standard of the day is, then the criteria of good hygiene is to use every endeavour to minimise the exposure. In my opinion that is the criteria. You can still get dust diseases at whatever level if you are exposed long enough or if you re exposed sufficiently heavily, or if you got a type of accumulation which finally reaches a critical level and you don’t really know what that s going to be.

Q. And that because there can be an accumulation over time, or an effect over time, you see it as prudent to minimise exposure to the particular substance is that correct.

A. Prudent, indeed yes.

71. Reliance is also placed upon evidence given by Professor Ferguson in various cases. As Professor Ferguson said in McCusker v James Hardie & Coy Pty Limited DDT 176 of 1996 (PX15):

……all the precautious have merit and are desirable, they are desirable as a matter of good practice, in our field of occupational health our attitude is not to permit exposure up to the limit current to the day but rather to reduce exposure to all airborne substances to as low as is reasonably practicable.

72. Great care has been taken in the preparation of this submission but, as I say, I do not really understand that the proposition is contested at all. It is related to the proposition that as a matter of industrial hygiene it is a basic principle that people should be made aware of the risks associated with materials with which they worked. I do not think anybody in the case disputes that this is so. In the circumstance I do not propose to go through the various cases in which it is said that evidence to this effect has been given previously. In the way this case has been presented both parties accept the substance of those two propositions.

73. The defendant’s response to the welter of evidentiary material is most conveniently seen in the submissions made by learned counsel. I will point to them in due course. One submission was that the evidence of Mr Pickford demonstrated that the plaintiff’s exposure was slight. Even if it be accepted that Mr Pickford’s evidence was unsatisfactory in many respects there is no gain saying the proposition that the plaintiff’s exposure was very light.

74. It is relevant to note one part of Mr Pickford’s evidence at (T98 and 99) which was not the subject of challenge. It was to the following effect: 5 million particles per cubic foot is equivalent to about 30 fibres per millilitre. Those two measurements were undertaken by different machines; the former by a midget impinger (T98.16-18) the latter by the membrane filter method. The hygiene standard for chrysotile asbestos was based on the concept of one hundred fibre/ml/years. In Britain a standard was adopted based on a working life of 50 years. The standard specified was 2 fibres per ml based on an exposure of 8 hours per day. In Australia the workforce was thought to be more mobile. The same basic idea underpinned the Australian standard: that is exposure should not exceed 100 fibre/ml/years over a lifetime. Because workers were not likely to stay longer than 25 years in the industry the standard adopted in Australia was 4 fibres per millilitre based on a shift of 8 hours per day. This was the standard said to be adopted by the National Health and Medical Research Council in Australia. Mr Pickford said that the standard was adopted in 1976. A question put by learned counsel for the defendant at T152.18-19 suggests that the standard was established in 1968. The letter of 22 September 1971 (part of PX9) from the Division of Occupational Health and Pollution Control to the Ship Painters and Dockers Union confirms that at that time the accepted standard for asbestos in air was 4 fibres per cc. Further in this regard in T128.38-39 Mr Pickford said that those in industry accepted that if you were under 4 fibres per ml on an 8 hour day that was satisfactory.

75. Evidence was adduced in reply from Mr Pickford about some of the documents tendered by the plaintiff (see T150-155). He described the exposures referred to in the documents under the following tabs in PX12 as heavy exposure: 1.2, 1.17, 1.29, 1.21. With regard to the document under tab 1.31 the exposure was over 18 months in the card room of an asbestos plant. This was, he said, huge exposure. The documents under tabs 1.50, 1.55 contained reference to exposure which he said was heavy. The exposure described in the document under tab 1.65 was large exposure by comparison with the plaintiff (T154.31-37). The exposure referred to in the document under tab 1.82 related to people employed in industry (T155.1-3). In respect of the document under tab 1.91 he said that it was thought that large exposure was needed over a long period to cause cancer (T155.29-35).

76. Reference was also made to some further documents by the defendant.

77. DX3 is a copy of an article published in the Medical Journal of Australia on 15 December 1962 by Dr J C McNulty, Chest Physician from Kalgoorlie. It was a report about a man who had worked as a mill worker relevantly in an asbestos mine from 1948 to 1950. He was referred to the chest clinic on 13 December 1959. The patient refused to attend the hospital thereafter and went bush. On 25 October 1960 he was again referred to the chest clinic for examination. Pleural biopsy was eventually undertaken and pleural mesothelioma was diagnosed. The patient died in June 1961. The author wrote that the material in the report was believed to be the first case of pleural mesothelioma reported in an asbestos worker outside South Africa.

Under the heading Discussion the author wrote:

There appears to be a relation between exposure to blue asbestos and the development of the pleural mesothelioma in this case. Pleural mesothelioma is a very rare tumours and details are known of only three cases in Western Australia……

Experience in Western Australian certainly confirms that blue asbestos is a very harmful and lethal fibre. The dust is one that urgently requires further experimental study (Barnes 1961).

78. DX4 is a paper published by Dermott O’B. Hourihane in the medical journal Thorax in 1964. The title of the article is The Pathology of Mesotheliomata and an analysis of their association with asbestos exposure. At pg 276 the author wrote:

I think it is possible to be reasonably certain of mesothelioma when only a small piece of tissue is available (biopsy).

While many of the cases were known to have had asbestosis before death the majority were not, and asbestos bodies were an unexpected finding on histological examination. Several cases gave no history of exposure to asbestos dust and some of these had very few bodies in the lungs…………and it is possible that a temporary perhaps trivial exposure to asbestos dust had occurred, not necessarily related to industrial contact.

the association of these tumours with asbestos bodies in lung tissue is confirmed. Many of the cases gave no history of industrial exposure and it is possible that temporary or relatively trivial exposure may have occurred.

79. DX5 was a copy of the article by Newhouse and Thompson published in the British Journal of Industrial in 1965 which has been referred to above.

The significance of the paper is that it drew attention to the occurrence of mesothelioma in household members and people who lived in the neighbourhood of asbestos factories not only asbestos workers.

The article was published about four years after the plaintiff’s exposure at Miranda.

80. Exhibit DX6 is a copy of a letter to the British Medical Journal from Wagner and others published on 3 November 1962. In the body of the letter the following appears:

More information is required on this subject to establish what proportion of these uncommon tumours occur in people who have been exposed at sometime to asbestos dust………

81. DX7 consists of a letter written by Eva Francis, Scientific Officer in the Division of Occupational Health and Pollution Control to an Officer of the Health Commission of New South Wales which letter bears date 27 April 1977. In the body of the letter the following material appears:

In the use of asbestos cement products in the building industry, the levels of exposure to asbestos dust of the workmen have been found to be quite low. At these exposures, which are still below maximum exposure of 4 fibres per ml of air recommended by the National Health and Medical Research Council in Australia, the health risks are minimal. Also blue asbestos is not used in asbestos cement products now and is not to our knowledge presently used in the building industry in Australia, so that the risk of contracting mesothelioma from present exposures to asbestos dust would be very low indeed in building workers………

There is much information on the biological effects of asbestos published in Health and Engineering literature, including specific reports on seminar proceedings devoted to this subject. New information is being presented very frequently as a result of the intense interest being taken in asbestos related disease. Any of the larger, or medical, libraries would have this information.

82. The defendant relies also on the contents of PX14: extracts from notes on factory managers conference held July 11 1966. Paragraph F, J and K are in evidence. The document is in a very truncated form. Its provenance suggests that it would be supportive of the defendant’s interests notwithstanding the fact that it was tendered by the plaintiff. Paragraph K is in these terms:

Therefore possible that in the future strictures will be placed on siting of asbestos using factories. It is inevitable that much tighter dust control will be insisted on.

Heaviest exposures cause asbestosis, lighter exposures cause cancer. Therefore, as dust levels reduce, more cancer will become apparent. It can be said that with better control those being exposed are now living long enough to develop cancer.

83. The defendant then points to some evidence given by Mr Stewart commencing at T74.43:

Q. If you were advising someone in 1961 the nature of the disease that was then understood to arise from asbestos exposure was either asbestosis or lung cancer was it not.

A. That’s probably fair enough.

Q. (At75.14) In 1961 the risk of asbestosis was understood as arising in circumstances of heavy occupational exposure to asbestos dust, is that not correct.

A. There was a formula, exposure concentration time years of exposure. It was seen as figuring the risk. Over the above that there was the general fuzziness of any piece of data and that where the opinion of Dr Badham came in that at between five and 10 million particles per cubic foot the risk of contracting asbestosis was about 5 to 10 per cent over 5 years.

The point of the evidence appears to be that the witness was agreeing that the thinking in those times was that more than occasional exposure was required to constitute a risk of injury.

84. In re-examination the plaintiff’s counsel led from Mr Stewart the opinion that Dreesen’s standard was not concerned with time weighted averages but with the sampling of dust in air. (T77-78)

85. The defendant sought further support for its contention that in 1960 or 1961 the concern was with extended exposures to asbestos by pointing to Mr Stewart’s report in the matter of Banno (PX16 at pg 19.2). The author was conducting an historical review of published material. When summarising the Wagner paper he wrote:

The conclusion from this study was that extended exposure to asbestos on this mining field apparently even at very low level, was sufficient to produce a risk of contracting a fatal asbestos related cancer.

As was submitted, the exposure of those about whom the report was written, or some of them, may have been of a low level but by comparison with the plaintiff the exposures were very high.

86. Reference was also made in the PX16 (at pg 18.6) to an article published in the Melbourne Age in 1956. It there referred to:

………disturbingly high incidence of asbestosis among works regularly handling asbestos………

87. The next matter relevant to this topic appears from annexure B to the statement of Dr McNulty (DX11tab 8). The document was a statement prepared for Dr McNulty in a case of Nielsen v Seltsam Pty Limited DDT280 of 2003. The defendant points to paragraphs 20-22 the thrust of which was that:

……asbestos did not represent any real health risk to persons working with………asbestos cement products.

88. The author is criticised as being pro the asbestos industry which fact is evidenced it is submitted by annexure A to the statement which is laudatory of the properties of asbestos. It think the criticism has substance. But annexure B to the statement is in a different category. It is a document published by the Commonwealth Department of Health under the auspices of the National Health and Medical Research Council. The document was published in 1982. It contains a brief historical review of the growth of knowledge about asbestos. The second paragraph of the foreward is in the following terms:

In 1965 the British Occupational Hygiene Society established a committee to examine available evidence and propose hygiene standards for chrysotile asbestos. The committee estimated that occupational exposure to asbestos fibres in air of 2 fibres per cm3 for 50 years or 4 fibres per cm3 for 25 years or 10 fibres per cm3 for 10 years, as measured by methods used at that time, would create a 1% risk of the earliest demonstrable lung changes due to asbestos.

89. We are concerned in this case with exposure to a mixture of chrysotile and amosite (an amphibole form of asbestos). But the material quoted lends support to the view advanced by the defendant that exposure over considerable periods of time is what was being considered when risks related to asbestos were being assessed.

The other obvious matter to observe is the British Committee reported several years after the plaintiff’s exposure.

90. The defendant points out that the Wagner report was preliminary and the problem it disclosed was to be further investigated.

The paper of Hourihane (DX4) was then published in 1964 confirming the link between asbestos exposure and mesothelioma.

Newhouse and Thompson (DX5) followed in 1965.

The picture is one of knowledge increasing over time.

91. The defendant relies also on evidence given by Professor D A Ferguson in the matter of Olsen tendered in these proceedings pursuant to s 25(3) of the Dust Diseases Tribunal Act. The evidence is in DX11 under tab 1. At pg 765 Professor Ferguson said:

In 1960, the only concern of occupational physicians would have been with people who – what I call, primary asbestosis workers who worked in some sort of asbestos process, whether from mining or milling or transport or manufacture or installation or removal of asbestos products, day in day out eight hours a day, in conditions of asbestos dust and in those days, the sort of conditions that gave rise to asbestosis were reasonably well worked out.

And a little later:

………and so there was a realisation that it was heavy exposure over some years, that gave rise to asbestosis.

The Dreesen standard was de facto – the accepted standard of exposure limit for asbestos workers in New South Wales. (ie in 1960)

The 1960 paper of Wagner and colleagues created little immediate public reaction, until the conference of experts on the biological effects of asbestos in New York in 1964, the proceedings of which were published in the Annals of the New York Academy of Sciences in December 1965………

The defendant submits that it would be unrealistic to expect it to be on notice of any risk of injury in the circumstances described in the Wagner report. (T198)

92. The next matter pointed to is the report of Professor Ferguson bearing date 16 June 1997 prepared in the matter of CSR Limited v Wren behind tab 2 in DX11. At the foot of the first page the Professor wrote:

As I have made clear in the report of Murray, there was in the 1950s in Australia scarcely any infrastructure in occupational health and almost no trained private consultant advice in this area was available to employers, even if they had been aware of any need to inquire. There was further in those times no epidemiology knowledge of chronic lung disease, nor was there any ready differential diagnosis of interstitial lung disease, of which asbestosis is only one of many types. The International Labour Office did not produce a standard set of chest xrays defining the changes of asbestos disease and distinguishing them from those of silicosis until 1970. Radiological diagnosis of asbestosis was frequently in error.

As a general physician I received no instruction in occupational lung disease when studying for membership of the Royal Australasian College of Physicians in 1954; and I am aware that in the 1960s trainee chest physicians received no instruction in occupational lung disease. Chest (respiratory, thoracic) medicine was not organised in Australia until 1962, when the Thoracic Society of Australia was formed; previously, chest physicians specialised in tuberculosis, and only one or two chest physicians in Australia specialised in occupational lung disease. ………

93. In the matter of Peter Bradley v James Hardie and Coy Pty Limited and Ors DDT58 of 1995 Dr Maurice Joseph gave evidence. See DX11 tab 3. He was referred to an article in the British Journal of 1965. Dealing with certain recommendations in the paper the witness said of one of them (at the top of pg 91):

Yes, it shows that there was a body of opinion which was worried about the possibility of asbestos related diseases in people who were handling asbestos apart from those involved in the manufacture and working in asbestos factories. That was the conference 1964, and these were the recommendations of the International Union Against Cancer. So that in 1965 there was a beginning of awareness of these dangers but it wasn’t – no special recommendations regarding precautions were as yet propagated.

94. Professor Ferguson gave evidence in McCusker under tab 4 DX11. At pg 569 the following appears:

Q. Do you agree that anyone with a modicum of knowledge of the risks of inhalation of asbestos knew by the mid-60s that there was risk to health from sawing of asbestos cement boards containing crocidolite?

A. By the mid-60s, as far as I can recall, I don’t believe there was concern about people sawing asbestos cement products in building construction. It’s a different matter from a person who did nothing else all day long to sit at a machine cutting up dry pieces of asbestos cement in the factory.

Q. I suggest to you that by the mid-1960s anyone with a modicum of knowledge had concern about the risk to health of anyone who was sawing up asbestos cement boards containing crocidolite. Do you agree or not.

A. No, I don’t agree.

I certainly recall being concerned that people in - who were working substantially full-time in asbestos cement factories sawing up asbestos cement products, I was concerned about that, because those people, unless the product was wet or unless there was ventilation, might take in large quantities of dust. But I didn’t translate that concern to und-users of asbestos cement products.

If Professor Ferguson was not concerned, the defendant says, how could it be expected that we should be.

95. At pg 573 of the same transcript Professor Ferguson said:

In the mid 1960s when I talk of situations where people were sawing up asbestos cement for – dry asbestos cement in factories, full-time, the risk was largely of asbestosis in those days. There had been no reported occupational cases of mesothelioma before 1965. The case of McNulty was clearly not occupational, because the induction period was only 11 years and the first serious report in Australia was that by Dr Milne in ’69 in the Medial Journal of Australia and that included no people working induced (?) with asbestos cement products. There had been nothing to raise concern at that stage.

When was it first that you were concerned at the prospect of a risk of mesothelioma from crocidolite dust out of asbestos cement sheets.

Professor, I am asking you when, if ever were you concerned at the risk of mesothelioma from cutting or handling the formed boards containing crocidolite.

In the same matter at 594 Professor Ferguson was asked:

96. In a statement prepared for a matter of David Scutt v James Hardie and Coy Pty Limited DDT199 of 1996 (DX11 tab 5) at paragraph 2.16 the following appears:

It was not until the early 1970s that any concern was felt by specialists in occupational health generally about he risk of asbestos disease in the construction industry in terms of the handling and treatment of asbestos cement products, as distinct from asbestos insulation or other asbestos fitted in buildings.

There is remarkably little to find in the occupational health literature before 1985 on the occurrence of mesothelioma among people in the construction industry handling new asbestos cement products. In Australia, this observation may be related to the long latency period………

In the late 1960s and 1970s, it was reasonable to believe that with the removal of crocidolite from asbestos cement building products there would be no risk of mesothelioma developing in the end-users of the products. While in that period there was still uncertainty as to the possible contribution to risk of the disease from amosite and chrysotile, the risk from such fibres was considered to be far less than that from crocidolite (Wagner 1991 [76]), so that when one took into account the small proportion of asbestos in asbestos cement and the bonding of the asbestos fibres to the cement in the products, no hazard to end-users could reasonably have been perceived.

After the mid-1970s, provided exposure was kept below the standard and warnings on asbestos products were followed, there was not even remotely a question that exposure to dust from asbestos cement building products would put a worker such as the plaintiff at risk of asbestosis asbestosis-related lung cancer or mesothelioma.

We found a relatively high occurrence of mesothelioma among carpenters (56 cases out of 456? subjects in whom a valid occupational history of exposure to asbestos was taken), carpenters being the occupational group most likely to be exposed to asbestos as end-users of asbestos cement products (Ferguson et al, 1987). I recall that at the time we were surprised not to be able to find other reports in the literature of such occurrence. Our cases did of course arise out of exposure first sustained on average in the 1940s.

To the best of my recollection, occupational physicians were of the opinion in the 1960s and 1970s that there was no convincing medical literature showing any respiratory problem arising from the end-use of asbestos cement building products.

The relevance of these opinions is self evident. The issue is whether they should be accepted in the light of the bulk of other material available.

97. The next material referred to is the statement of Dr Bryan Gandevia prepared for the matter of McCusker v James Hardie and Coy Pty Limited DDT179 of 1996 (DX11 tab 7). At para 2.7 of the statement the following appears:

The existence of mesothelioma as a specific entity was not accepted by the world’s leading cancer authority, Professor Rupert Willis, (a former Melbourne pathologist), nor was its relationship to asbestos appreciated prior to the mid-1960s, with the exception of a few deeply involved experts.

Finally, in regard to attitudes to asbestos and its problems in the 1950s, stress must be laid upon the sense of false security engendered by the evident success of the 1931 British Regulations in reducing the frequency and severity of asbestosis, with a concomitant decline in lung cancer risk. The complacency was accentuated by difficulty in early diagnosis as outlined above. When I was in England in the early 1950s, it was generally considered that asbestosis was a disease of the past as a result of these Regulations. This turned out to be untrue largely because of the improved methods of diagnosis of relatively early or mild cases. Nonetheless, it gave the industry a considerable sense of security which was ultimately misplaced. My information is based on personal experience in industry and in discussion with UK experts at the time as well as the literature.

It was only in the early to mid 1970s, that a question was beginning to arise as to whether the use of asbestos cement products might conceivably pose a hazard of mesothelioma. I am confident that this concern would not have amounted to a widely held view, certainly if there was no crocidolite in the product. By 1975, I believe there was certainly no crocidolite in the products.

I was present at a Symposium on Asbestos by invitation held at Johannesburg in 1978. There were nearly 50 distinguished contributors to a very comprehensive review of asbestos and asbestos-related disorders. There was no mention at that conference of end-product users.

To develop asbestosis requires a very large dose. Even allowing a concentration of 5 fibres/ml in the breathing zone of a carpenter, it would be surprising if he ever approached a threshold level. Most asbestos cement products were handled with hand tools, often in the open air, giving fibres in the breathing zone at a lower level than quoted. It is true that power tools were coming into use increasingly from about 1960, but they were required only for certain purposes and, I believe, a limited range of products. Most of the ordinary asbestos sheeting was still better handled by manual methods.

It was not foreseeable in 1960 that there could be any risk in using asbestos cement products. By 1970, some doubts were being expressed regarding the possibility of mesothelioma from cement materials containing crocidolite, but to my recollection, there was no dogma on this issue.

The submission developed in the light of these materials is to the effect that if the defendant had sought the advice of Professor Ferguson or Dr McNulty or Dr Gandevia about the risk of injury in 1960 or 1961 to an end user of asbestos cement products they would have been informed that there was no such risk. It is submitted that such a risk of injury to the plaintiff or indeed to any end user of the products was not foreseeable at that time.

98. I read carefully the evidence of Professor Ferguson and the material from Dr Gandevia and Dr Joseph. In respect of Professor Ferguson’s evidence in particular it seems to me that there is simply too much other evidence from all over the world published over many years to permit Dr Ferguson’s evidence to be accepted without qualification. The material set out above from the Professor does not seem to sit comfortably with the concessions made by Mr Pickford about the state of knowledge generally.

99. From the defendant’s point of view there is simply too much material demonstrating the known risks of asbestos for it to be permitted to comfortably rest behind the bulwark provided by Professor Ferguson’s view. More especially is it so when there is no evidence from the defendant itself about its knowledge or attitude to the articles published both here and overseas or about its attitude to risks undertaken by users of its products. None of its records has been produced.

100. The observations of the author of the article published under the auspices of the National Health Medical Research Council seem to pay no heed to the vast body of other material to which I have referred. A similar comment may be made about Dr Francis in DX7.

101. Dr Gandevia’s opinion supports the defendant’s position, and so does, to some extent, the view of Dr Joseph.

They are, however, to be read against the background of the other material referred to above. They are not sufficient, in the light of that material, to carry the day for the defendant.

102. Having come to these conclusion, I note that I have said nothing, or nothing much, about the evidence of Mr Stewart.

103. Much of what he had to say was corroborated by the concessions made by Mr Pickford. I have reached the view I have expressed without placing great reliance on Mr Stewart’s evidence. In some respects, he is the other side of Mr Pickford’s penny. They have been giving evidence on the opposite sides of cases for years. I note however that the view I have reached is in accordance with and supported by Mr Stewart’s opinion.

His evidence is not criticised as lacking independence or probity. Further, he was engaged in industrial hygiene in the years leading up to the plaintiff’s exposure, and after it.

104. I find that the matters conceded by Mr Pickford which are enumerated above and which are substantially confirmed by the evidence given by Mr Stewart set out in a convenient form the state of knowledge which the defendant had or should have had in respect of its asbestos products.

105. As regards whether or not a duty of care existed owed by the defendant to a class of persons of whom the plaintiff was one I turn firstly to the defendant’s written submission para 17 where the following appears:

It is generally accepted that a manufacturer owes a duty of care to an end user – cf Donoghue v Stevenson [1932] AC562. Lord Atkin in Donoghue:

“The rule that you are to love your neighbour becomes in law, you must not injure your neighbour; and the lawyers question, who is my neighbour? Receives a restricted reply. You must take reasonable care to avoid acts or omissions which you can reasonably foresee would be likely to injure your neighbour. Who, then, in law is my neighbour? The answer seems to be – persons who are so closely and directly affected by my act that I ought reasonably to have them in contemplation as being so affected when I am directing my mind to the acts or omissions which are called in question” (at 580)

106. There is a convenient statement of principle in the judgment of Powell JA in CSR Limited v Wren (1997) 15NSWCCR 650 at 655. In relation to the cross appeal (about which His Honour dissented as to causation) the following statement of principle appears:

I accept that, as a general rule, the manufacturer of a product which is known, or believed, or suspected, to be hazardous owes a duty to a prospective user of the product, at the least, to make that user aware of the hazardous, or potentially hazardous, nature of the product, and to advise such a potential user of the precautions which ought to have been taken to avoid, or at least, to reduce, the risks to which a potential user might be exposed by the use of the product, as also do I accept that that duty extends to warning potential purchasers of the product of the risks to which potential users of the product – such as the employees of such a purchaser – if using the product in such a manner as might be known, or might reasonably be expected as normal and proper, to be used (see, for example, Wright v Dunlop Rubber Co Ltd [1972] 13 KIR 255).

107. Further in this regard I note the following passage from Wright v Dunlop Australia Co Ltd quoted with approval by the Full Court of the Supreme Court of Victoria in Thompson v Johnson and Johnson Pty Limited (1991) 2 VLR 449 at 490:

If the manufacturer discovers that the product is unsafe, or has reason to believe that it may be unsafe, his duty may be to cease forthwith to manufacture or supply the product in an unsafe form. It may be that in some circumstances the duty would be fulfilled by less drastic action: by, for example, giving proper warning to persons to whom the product is supplied of the relevant facts, as known or suspected, giving rise to the actual potential risk. Factors which would be relevant would be the gravity of the consequences if the risk should become a reality, and the gravity of the consequences which would arise from the withdrawal of the product.

108. Given that as Mr Pickford conceded:

(a) That before 1950 asbestos was recognised as toxic.

(b) After Doll’s paper in 1955 it was recognised that it caused cancer.

(c) During the 1950s it was appreciated that asbestos exposure was cumulative and additionally dangerous because of its cumulative nature.

(d) The injuries it caused were serious and disabling and capable of causing death.

(e) That the asbestos related disease often presented many years after the exposure of asbestos.

(f) That the injuries once in place could not be corrected.

(g) The above known factors meant that precautions were more important.

(h) That it was known that it was prudent to minimise exposure to such substances.

(i) No one knew the level of fibre that could cause asbestos diseases.

(j) That it was appreciated in 1930 that persons sawing asbestos cement sheets were potentially at risk.

(k) That power saws and bench saws were reasonably common and could be used to cut the asbestos sheeting.

(l) That once the asbestos cement sheets left the factory one did know what happened to them or how they would be used.

(m) The defendant did not know, indeed could not know, how much exposure any individual would have from sawing or using asbestos cement sheets after they had left the defendant’s premises,

then in those circumstances I find that the defendant owed any users of its product a duty of care. That duty was to prevent harm from the foreseeable risk of injury arising from the use of the asbestos cement sheets in the fashion contemplated at the time they were sold.

109. I accept that the law as to foreseeability is as set out in Wyong Shire Council v Shirt (1979-1980) 146 CLR 40. A submission was made in this case, and later withdrawn, that doubt now attached to the authority of that decision as a result of comments made by McHugh J in Tame v New South Wales (2002) 76 ALJR 138. That this submission is incorrect may be seen from the following:

(i) The judgment of Spigelman CJ in Julia Farr Services Corporated v Hayes (2003) 24 NSWCCR 138 at 142.

(ii) The judgment of Gummow J in Swain v Waverley Municipal Council (2005) 79 ALJR 565 at 108.

(iii) The decision of the Victorian Court of Appeal in Berrigan Shire Council v Ballenini and Ors (2005) VSCA 159.

110. I observe in passing that Mr McHugh, as he then was, was Counsel for the unsuccessful appellant in Shirt.

111. In Shirt the existence of duty of care was conceded. The argument about foreseeability took place in the relation to the question of whether there had been breach of the duty. At 45 Mason J said speaking of Bolton v Stone (1951) AC 850:

The examination was designed to show that the case raised a new problem, the problem being that posed by a risk of injury which was foreseeable, notwithstanding that “the chance of its happening in the foreseeable future was infinitesimal”,so infinitesimal “that it was only likely to happen once in so many thousand years”.

The House of Lords held that there was no breach of duty, not because the risk of injury was not foreseeable but because the risk, though foreseeable was so small that a reasonable man would have been justified in disregarding it and taking no steps to eliminate it. Lord Reid then went onto observe that a reasonable man would only neglect such a small risk if he had some valid reason for doing so, “eg that it would involve considerable expense to eliminate the risk”.

Following the critical sentence which I have quoted above Lord Reid said:

What that decision [Bolton v Stone] did was to recognise and give effect to the qualification that it is justifiable not to take steps to eliminate a real risk if it is small and if the circumstances are such that a reasonable man, careful of the safety of his neighbour would think it right to neglect it.

In this sentence his Lordship characterises the risk in Bolton v Stone, earlier described as “infinitesimal” yet one which could not be described as “a fantastic or far fetched possibility” as nonetheless constituting “a real risk”.

The “Wagon Mound”

If a real risk is one which would occur to the mind of reasonable man in the position of the defendant’s servant and which he would not brush aside as far-fetched, and if the criterion is to be what the reasonable man would have done in the circumstances, then surely he would not neglect such a risk if action to eliminate presented no difficulty involve no disadvantage, and required no expense.

In essence its correctness depends upon a recognition of the general proposition that foreseeability of the risk of injury and the likelihood of that risk occurring are two different things………

112. In this case I find as a fact that what was foreseeable was the development of a lung disease from exposure to asbestos dust, liberated from asbestos cement sheeting.

113. I wish to say something about Dreesen. Dreesen (PX12-1.47) was concerned with exposure of workers in asbestos cloth making factories. They were exposed day in and day out. His recommendation for those workers was that (p 43) dust should be controlled at the point of origin by means of local exhaust hoods so designed and operated that no dust is permitted to reach the breathing zone of workers or to contaminate the general air.

It was in that context that he recommended that dust levels be kept to a level of 5 million particles per cubic foot or lower.

Because clean-cut cases of asbestosis were found only in dust concentrations exceeding 5 million particles per cubic foot, and because they were not found at lower dust concentrations, 5 million particles per cubic foot may be regarded tentatively as the threshold value for asbestos-dust exposure until better data are available.

114. It has been said many times in the Tribunal that if dust is visible it is probably at a greater concentration than 5 million particles per cubic foot.

115. In a circumstance in which no safe level of exposure was known, this surely should have alerted the manufacturers to a possible risk of injury.

116. Further, it was an insufficient response to say in effect, Dreesen was concerned with workers in factories – we do not have to worry about light exposures.

To approach the matter this way was to turn one’s back to the risk.

117. Similarly the defendant submitted (T178) that to ignore dose and duration of exposure is to look at only half the story.

The unspoken corollary of that submission appears to be that unless you have major exposure for a long period a manufacturer is entitled to disregard risk arising from exposure to asbestos dust.

Once again such an approach seems to me to involve turning one’s back on the possible risk.

That is not the conduct of a reasonable man.

118. The issue of foreseeability in this case is different from that issue in Seltsam Ltd v Minahan (1996) 13 NSWCCR 410. In that case the question was whether one of the employers should have known of a risk of exposure to small amounts of asbestos well below the exposure standard. In this case, the plaintiff was a member of a class, namely the end users of asbestos of cement sheeting. Those members might be exposed to very light exposures or heavier exposure if they used power tools day in and day out. It was the class that was exposed to the risk. To do nothing in the circumstances identified earlier, when a warning was a simple thing to attach to the sheets, was unreasonable.

119. The defendant was already placing a stamp on the A/C sheeting advertising the product as Wunderlich Durabestos. It seems to me to require very little to add another stamp warning people not to breathe in the dust generated by working the product, because if they did they might become very sick and even die. It may be to affix such a stamp would adversely affect sales. It is not hard to imagine that this might occur. It is a relevant consideration. On balance, however, it could not be the deciding factor for a reasonable person.

120. I conclude that the defendant could easily have fixed a warning to its asbestos cement sheets against the dangers of breathing in the dust. I find further that having regard to the well known dangers a reasonable person in the defendant’s position would have given such a warning. The failure to give such a warning constituted a breach of the duty owed by the defendant to the end users of its product to take care to prevent them suffering harm from a risk of injury which was foreseeable.

121. In coming to this view I have repeatedly cautioned myself against, the obvious danger of looking back over 45 years or so and assessing the defendant’s position with the benefit of hindsight. It is an easy mistake to make. The matter which keeps recurring in my mind is the sheer volume of the material emanating from a number of countries warning about the dangers of asbestos, particularly when no one knew what a safe dose was.

122. In Rolls Royce v James Hardie and Coy Pty Limited (No 4) (1999) 18 NSWCCR 653 at 685 Curtis J found, in respect of Mr Hay who was exposed to asbestos dust from products of James Hardie between 1958-1961:

……that James Hardie owed to Mr Hay a duty to protect him by placing warning labels on its products and by bringing to the attention of his immediate supervisors the dangers to which he was exposed……

123. Foreseeability does not require foreseeability of the precise of injury suffered. See Mt Isa Mines v Pusey (1970) 125 CLR 383, Julia Farr Services Incorporated v Hayes (2003) 24 NSWCCR 138 at 176-177. It is sufficient that it was foreseeable that the inhalation of asbestos could cause an injury of the kind which the plaintiff suffered. (See for example Beazley JA in Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307 quoted with approval by Giles JA in Julia Farr Services Incorporated v Hayes (2003) 24 NSWCCR 138 at 177. Or as Windeyer J said in Pusey at 482:

Nor does it suppose foresight of the particular harm that occurred, but only some harm of a like kind.

124. As regards causation I accept the evidence of Professor Henderson supported as it is by that of Professor Bryant. Dr Gardiner concedes that causation is possible. In light of all of the evidence I am satisfied that more probably than not the plaintiff’s exposure to asbestos emanating from the defendant’s product at the Miranda job in 1961 made a material contribution to the contracting of mesothelioma from which he now suffers. As to whether a warning would have eliminated the risk, the plaintiff said if there had been a warning he would never have used the A/C sheeting. I accept his evidence. Further, at the very least, the failure to warn contributed to the risk of injury to which the plaintiff was exposed and succumbed. See CSR v Wren (1997) 15 NSW CCR 650 at 695 A-B.

125. The plaintiff is entitled to a verdict.

126. As regards damages the parties have reached agreement on a number of heads.

127. I turn to assess general damages. The plaintiff was born on the 7 June 1927. He is 78 years old. He has undergone the following procedures in relation to his mesothelioma:

(i) On 20 July 2003 he was admitted to Hornsby Hospital for a total hip replacement unrelated to this claim. The procedure could not be undertaken until he had fluid drained from his right lung. 300 mls was drained on this occasion.

(ii) On 19 August 2004 at Hornsby Hospital Dr Harris drained 1.9 litres from his right lung. He had one day in hospital.

(iii) On 6 December 2004 at Hornsby Hospital Dr Harris drained 1.3 litres from his right lung. He had one day in hospital.

(iv) On 6 January 2005 he was admitted to Sydney Adventist Hospital under Dr Richard Chard. He underwent thoracoscopy, pleural biopsy, talc pleurodesis and 1.5 litres of fluid was removed from his lung. He was in hospital from 6 January 2005 to 13 January 2005.

128. After his discharge from Hospital the plaintiff was told that he had cancer. He was upset that he was not told what his diagnosis meant.

129. He suffers from breathlessness on exertion.

He has lost weight and is now frail. He is not able to walk long distances without becoming tired and breathless and he must walk slowly. He used to be able to walk for a kilometre but he has stopped doing this.

His life is now much reduced. He finds this frustrating.

130. He has been, thus far, apart from the procedures which he described, relatively free of pain. This cannot be expected to continue. It is likely that the plaintiff will gradually develop increasing evidence of pleural and pulmonary involvement because of his condition causing breathlessness, tiredness, weight loss and cough (Dr Bryant). He is likely to require gradually escalating treatment from a palliative care physician to assist in the alleviation of these symptoms and he will gradually require increasing assistance with the activities of daily living.

131. Death from mesothelioma has been described many times in this Tribunal. It is not necessary to recount the details here. It is most unpleasant and demeaning. I find the appropriate award for general damages is one of $150,000.

132. As regards interest on general damages, symptoms set in in mid 2003. I notionally apportion the damages so that $80,000 is referrable to the period up to date. Interest should be allowed on that sum for 2 years at 2 per cent ie $3,200.

133. As regards of loss of expectation of life Dr Bryant thought when he wrote on 19 April 2005 that the plaintiff might hope for a further 12 months of life from that time. I accept that evidence. Damages under this head are conventionally awarded in a modest sum. They are intended to compensate for loss of prospective happiness. I allow $7,500.

134. As to future medical treatment there has been agreement reached about expenses other than chemotherapy. As regards chemotherapy the plaintiff did not seem to know what it was. When it was proposed to him that a course of chemotherapy might prolong his life he said words to the effect that if that were so he would take it as gift from God and undertake the treatment.

The cost of the treatment is approximately $30,000 for 6 cycles.

Dr Bryant thought that whether or not he had the treatment was a matter to be sorted out by the plaintiff and his oncologist.

Dr Gardiner thought that because of his age it was unlikely that he would be given the treatment.

Further it seems that alimta is administered either to alleviate symptoms (Dr Gardiner) or to delay the onset of the more difficult symptoms associated with mesothelioma (Dr Bryant T46). At present the plaintiff is untroubled by the major symptoms generally associated with the disease although his breathlessness is serious and his lifestyle has been disrupted. The treatment has side effects. In effect the plaintiff would have to trade feeling not too bad for dealing with the side effects of the treatment in the hope that the major symptoms associated with mesothelioma might thereby be deferred. It seems to me that it is far from certain to happen. There is however a chance that it might. Pursuant to the principles in Malec v J C Hutton Pty Limited (1990) 169 CLR 638, I allow $5,000 as compensation for that chance.

135. The damages then are as follows:

Interest on general damages $ 3,200

Loss of expectation of life $ 7,500

HIC reimbursement $ 8,054.45

HCF reimbursement $ 8,928.50

Nursing aids and equipment $ 5,423.00

Reimbursement of nursing home bond $ 1,000

Future medical expenses (excl chemotherapy) $ 16,010.00

Future chemotherapy $ 5,000

136. Verdict and Judgment for the plaintiff in the sum of $205,115.95.

137. I order the defendant to pay the plaintiff’s costs.

Mr J Rush, QC instructed by Turner Freeman appeared for the plaintiff.
Mr J Fernon, SC instructed by Makinson and D’Apice appeared for the defendant.

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Citations

Father Robert McNeill v Seltsam Pty Limited [2005] NSWDDT 43

Most Recent Citation

Seltsam Pty Ltd v Mcneill [2006] NSWCA 158

Cases Citing This Decision

1

Seltsam Pty Ltd v Mcneill [2006] NSWCA 158

Cases Cited

10

Statutory Material Cited

1

Equuscorp Pty Ltd v Glengallan Investments Pty Ltd (No 2) [2005] HCA 5

Berrigan Shire Council v Ballerini [2005] VSCA 159

Mount Isa Mines Ltd v Pusey [1970] HCA 60

CITATION:	Father Robert McNeill v Seltsam Pty Limited [2005] NSWDDT 43
PARTIES:	Father Robert McNeill (Plaintiff) Seltsam Pty Limited (Defendant)
MATTER NUMBER(S):	84 of 2005
JUDGMENT OF:	Duck J at 1
CATCHWORDS:	Damages :- Light exposure Foreseeability of risk of injury Duty of manufacturer to end users of the product Duty to warn Damages
LEGISLATION CITED:	Dust Diseases Tribunal Act s 25(3)
CASES CITED:	- McCusker v James Hardie and Coy Pty Limited DDT 176 of 1996; - CSR Limited v Wren (1997) 15 NSW CCR 650 at 655; - Peter Bradley v James Hardie and Coy & Ors DDT58 of 1995; - David Scutt v James Hardie and Coy Pty Limited DDT 199 of 1996; - Wyong Shire Council v Shirt (1979-1980) 146 CLR 40; - Tame v New South Wales (2002) 76 ALJR 138; - Julia Farr Services Corporated v Hayes (2003) 79 ALJR 565 at 108; - Swain v Waverley Municipal Council (2005) 79 ALJR 565 at 108; - Berrigan Shire Council -v Ballenini and Ors (2005) VSCA 159; - Bolton v Stone (1951) AC 850; - The "Wagon Mound" [No2] 1967 AC 617 at 643-644; - Seltsam Ltd v Minahan (1996) 13 NSW CCR 410; - Rolls Royce Industrial Power (Pacific) Ltd v James Hardie and Coy Pty Limited (No 4) (1999) 18 NSW CCR 653 at 685; - Mt Isa Mines v Pusey (1970) 125 CLR 383; - Bendix Mintex Pty Ltd v Barnes (1997) 42 NSW LR 307; - Malec v JC Hutton Pty Limited (1990) 169 CLR 638; - Nielsen v Seltsam Pty Limited DDT 280 of 2003; - Wright v Dunlop Australia Co Ltd (1972) 13 KIR 255; - Thompson v Johnson and Johnson Pty Limited (1991) 2 VLR 449 at 490
DATES OF HEARING:	2, 3, 4, 5,16 and 18 August 2005
DATE OF JUDGMENT:	09/05/2005
LEGAL REPRESENTATIVES:	FOR PLAINTIFF: Mr J Rush, QC instructed by Turner Freeman FOR DEFENDANT Mr J Fernon, SC instructed by Makinson and D'Apice