Amaca Pty Ltd v CSR Limited

[2008] NSWDDT 18

Dust Diseases Tribunal

of New South Wales

CITATION:	Amaca Pty Ltd v CSR Limited [2008] NSWDDT 18
PARTIES:	Amaca Pty Ltd (Cross Claimant) CSR Limited (First Cross Defendant) Midalco Pty Limited (Second Cross Defendant)
MATTER NUMBER(S):	238 of 2001/1
JUDGMENT OF:	Curtis J at 1
CATCHWORDS:	DUST DISEASES TRIBUNAL :- Cross Claims - Foreseeability - Duty of care - Causation
LEGISLATION CITED:	Law Reform (Miscellaneous Provisions) Act 1946
CASES CITED:	Rose v Abbey Orchard Property Investments Pty Ltd (1987) Aust Torts Reports 80-121 Rentz v Seltsam Pty Ltd [2004] NSWDDT 15 EM Baldwin & Son Pty Ltd v Plane (1998) 17 NSWCCR 434 EMI (Australia) Ltd v BES [1970] 2 NSWR 238 Chapman v Hearse (1961) 106 CLR 112 Bolton v Stone [1951] AC 850 CSR Ltd v Young (1998) 16 NSWCCR 56 Bale v Seltsam Pty Ltd (QLDCA, No 284/95 23 August 1995 unreported) Sutherland Shire Council v Heyman (1985) 157 CLR 424 Donoghue v Stevenson [1932] AC 52 Wyong Shire Council v Shirt (1980) 146 CLR 40 Sullivan v Gordon (1999) 47 NSWLR 319 CSR Ltd v Eddy (2005) 226 CLR 1 Griffiths v Kerkemeyer (1977) 139 CLR 161
DATES OF HEARING:	31/3/08, 1-3/4/08, 2/6/08/, 5/6/08
DATE OF JUDGMENT:	25 June 2008
LEGAL REPRESENTATIVES:	Mr G M Watson SC with Mr J C Sheller instructed by DLA Phillips Fox appeared for the cross claimant Mr B W Walker SC with Ms J Gleeson instructed by Makinson and d’Apice appeared for the cross defendants

JUDGMENT:

Dust Diseases Tribunal of New South Wales

Matter Number 238 of 2001/1

Amaca Pty Ltd

v

CSR Limited

and

Midalco Pty Limited

25 June 2008

JUDGMENT

CURTIS J

Introduction

1. In 1970 and 1971 a plaintiff, Mrs Belinda Dunn, born on 29 December 1967, was at the ages of three and four, exposed to crocidolite asbestos fibres released from asbestos cement roofing sheets removed and broken up in the course of renovations to her parents’ home. The sheets were manufactured by James Hardie & Coy Pty Ltd (Hardies) and fixed to the roof in 1966. In 1998, at the age of 30, Mrs Dunn contracted mesothelioma. She sued Hardies, now Amaca Pty Ltd (Amaca) and recovered, by way of settlement, damages in the sum of $1,500,000 inclusive of costs.

2. Amaca, alleging that the crocidolite fibre used in the manufacture of the sheets was mined at Wittenoom and sold to it by Australian Blue Asbestos Ltd (ABA), now Midalco Pty Limited (Midalco), claims contribution to the settlement from Midalco and CSR Limited (CSR), its parent company, pursuant to s 5(1)(c) of the Law Reform (Miscellaneous Provisions) Act 1946.

3. Midalco and CSR resist the claim upon the grounds that, had they been sued, neither would have been held liable to Mrs Dunn. They assert first, that it cannot be proved that crocidolite supplied by ABA was included in the asbestos cement sheets to which she was exposed (Supply); secondly, that it cannot be proved that Mrs Dunn's mesothelioma was caused by asbestos fibres liberated from the asbestos cement sheets (Causation); thirdly, that they owed no duty of care to Mrs Dunn because her injuries were not reasonably foreseeable (Foreseeability), or, in the event that they were, that the relationship between Mrs Dunn and CSR and Midalco was insufficiently proximate to justify the imposition of a duty of care (Proximity). Further, Midalco and CSR say that Amaca bears a greater responsibility for Mrs Dunn's injuries and in any event imprudently paid too much by way of settlement (Apportionment).

Exposure

Glenys Birks

4. Mrs Birks is the mother of Belinda Dunn. Mr and Mrs Birks purchased a property at 1 Silver Crescent, Grange in early February 1970. Shortly after they moved in, a heavy rainstorm caused the ceiling of the den to collapse. An inspection revealed that the corrugated asbestos cement roofing was unsound and needed replacing. Mr Birks removed this roof, which covered approximately 10 foot by 10 foot.

5. While he did this, Mrs Birks took Belinda, then three years of age, to her mother’s house for lunch. They returned after the asbestos material had been dropped onto a path outside the den. Mrs Birks, accompanied by Belinda, assisted in cleaning up the asbestos cement material and sweeping the path. The sweepings were dusty and fibrous. The path was the thoroughfare between the front and back of the house and Belinda walked and played on that path. The broken asbestos material was placed in a heap on the front lawn where it remained for three or four days.

6. When the builder engaged by the Birks installed the new corrugated iron roof above the den, he pointed out to them that the corrugated asbestos cement roof of the carport also needed replacing. The Birks saved up some money and, the following year, commissioned the builder to replace the carport roof with corrugated iron. Belinda was then four years old.

7. Mr Birks again removed the corrugated asbestos roof himself. The work occupied him over two or three days. He dropped the sheets of corrugated asbestos from the roof to the concrete floor of the carport. The sheets broke up easily and created "a huge mess". Mrs Birks swept up the floor with a shovel, a broom and a dustpan. She placed the broken pieces into a wheelbarrow. Belinda accompanied her and assisted her in sweeping. There was visible dust in the air. The broken pieces were placed in a heap on the front garden.

Robert Birks

8. Robert Birks is Belinda's father. He removed the corrugated asbestos sheeting from the roof of the den and from the roof of the carport. In relation to the den he recalls Mrs Birks and Belinda, on their return from lunch, helping to tidy up. He also recalls that in the case of the carport, Mrs Birks and the three children, including Belinda, cleaned the cement floor of the carport with brooms, creating visible dust.

9. He recalls that broken pieces of asbestos from the carport were placed in a pile on the front lawn where they remained for about one week. During that week he saw Belinda playing games that involved her standing on top of the pile.

10. Mr Birks recalls sandpapering the eaves of the house preparatory to painting when Belinda was young. The eaves were made of asbestos. From time to time the children helped in tidying up. Mr Alan Rogers, an industrial hygienist qualified by Midalco and CSR, did not consider that this work emitted measurable levels of asbestos dust.

Robert Bonner

11. Mr Bonner was a builder who replaced the roofs of the den and the carport with corrugated iron. The roof of the carport was approximately 16 m long by about 3 m wide.

12. Mr Bonner recalls that the remains of the asbestos roof of the carport were piled on the front lawn and that, in the course of fixing the new roof, he saw Belinda climb on to that pile in the course of such games as hide and seek where the pile was used as a base. He also recalls the children playing on the heap, each trying to get higher than the other, and Belinda on top saying "I’m the king of the castle". He has a distinct memory of this occurring on three occasions.

13. Mr Bonner at a later time performed work extending the den of the house in the course of which he cut a single sheet of asbestos cement cladding and fixed it above a window. The sheet was cut with guillotine fibro cutters. On the probabilities this cladding contained no crocidolite, which was withdrawn from the product in about 1967.

Supply

When were the sheets manufactured?

Patricia Dening

14. Mrs Dening made a statement in writing on 18 December 2001. This was prepared for the purpose of admission into evidence in the primary proceedings by Mrs Dunn against Amaca. The cross defendants wished to cross-examine Mrs Dening on the contents of this statement, however she died in the course of this trial before that was possible. Although her evidence is untested, the statement was prepared for litigation in which Mrs Dening had no personal interest and I see no compelling reason why its content should not be accepted at face value.

15. Mrs Dening and her husband purchased the home at 1 Silver Crescent, Grange, South Australia in 1961 from the builder. In 1966 they added the carport and den, the roofs of which were made of corrugated asbestos cement sheets.

Mr Bonner

16. In the course of his work installing the new corrugated iron roof over the carport Mr Bonner recognised the asbestos cement sheets that had been removed as "Deep Six asbestos cement corrugated sheets". It is reasonable to suppose, although Mr Bonner did not say so, that the roof of the den, built at the same time, was also "Deep Six".

Graham Allen

17. From January 1965 to December 1966 Mr Allen was employed by Hardies as the South Australian Field Sales Manager for building products. He said that from about 1956 Hardies were the sole manufacturer of asbestos cement fibro products in South Australia and that "Deep Six" was a Hardies product. He further said that, in his opinion, the average time during which stock was held after manufacture was about two to three weeks. I think his duties qualified him to express that opinion. It is broadly consistent with the minutes of a factory manager’s conference held on the 11 July 1966, in which a manager spoke of the importance of building up stock levels for the Christmas shutdown from the normal level of four to six weeks of supply.

Conclusion

18. We do not know exactly when it was in 1966 that the sheets were installed. Nevertheless, there being 12 months in the year, and calling in aid probability, (see Rose v Abbey Orchard Property Investments Pty Ltd (1987) Aust Torts Reports 80-121), I find that the asbestos cement roofing sheets demolished by Mrs Dunn's father in 1970 and 1971 were probably manufactured no earlier than January 1966.

Did the sheets contain crocidolite from Wittenoom?

19. The Deep Six corrugated asbestos cement roofing sheets were manufactured by Hardies at its Elizabeth plant. They were manufactured in accordance with mix specifications that mandated the proportions of the asbestos blend to be used in the recipe for the particular product.

20. The mix specifications for the manufacture of corrugated sheets at Elizabeth between 10 December 1964 and 22 September 1966 are in evidence. The mix specifications issued between 10 December 1964 and 16 September 1965 required 20 per cent ABA crocidolite. The specifications issued between 21 September 1965 and 19 January 1966, required 18.2 per cent ABA crocidolite. The specifications issued between 17 February 1966 and 22 September 1966 required 18.18 per cent ABA crocidolite.

21. The letters "ABA" in the mix specification refer to Australian Blue Asbestos crocidolite mined at Wittenoom. Midalco admits that in 1965 and 1966 it sold to Amaca crocidolite asbestos mined at Wittenoom, and that it believed that the crocidolite was to be used in the manufacture of asbestos cement building products.

22. Commercial commonsense indicates that neither ABA nor Hardies would stockpile large quantities of crocidolite fibre. I think it probable that the crocidolite included in Hardies products was produced at the mine no earlier than three months before it was included as a component in the manufacture of asbestos sheets.

Conclusion

23. I find that the crocidolite asbestos to which Mrs Dunn was exposed in 1970 and 1971 was crocidolite asbestos mined at Wittenoom after September 1965, and sold by Midalco to Hardies in the knowledge that it would be included in asbestos cement building products.

Causation

Professor Geoffrey Berry

24. Professor Berry is not a medical practitioner. He is a mathematician and an eminent biostatistician and epidemiologist. His report of 28 March 2007 is tendered by Amaca. The substance of his opinion upon which Amaca relies is that epidemiological studies have demonstrated that the potency of crocidolite fibre to cause mesothelioma is between 500 to 750 times greater than that of chrysotile, another fibre included in the manufacture of the asbestos cement sheets, which was not supplied by Midalco.

25. In the course of cross-examination, Professor Berry agreed that in drawing conclusions from epidemiological studies, groups there described as "unexposed to asbestos" may be assumed to have been exposed to some level of "background" exposure to unidentified asbestos fibre, in unknown concentrations. He gave this evidence:

Mr Walker :

Q. If your question of interest is whether a postulated extra bit or increment over and above background has caused the disease, there must be of its nature consideration of the relativities between that increment sought to be implicated and the background? A. Yes.

His Honour:

Q. But that is upon the assumption that it is one or the other rather than a combination of both, is it not? A. Yes.

Mr Walker:

Q. Whereas medically it would be unsafe to proceed on the basis of one or the other, everything rather suggests, because we cannot track fibres being inspired and exhaled harmlessly, that it is the lifetime load, is that correct? A. Yes.

Q. So if you are asking whether an increment to background is to be implicated in causation other than negligibly you do need to know for the reasons His Honour has noted, the relativities of background which is part of the lifetime load, plus the increment, is that correct? A. Yes.

26. Dr Leigh is a consultant occupational physician who was head of the Epidemiology Unit at the National Occupational Health and Safety Commission from 1998 to 2000. He holds a PhD in medicine and an MA in Pure Mathematics. He is a member of the National Health and Medical Research Council Asbestos Working Group, and a consultant to the Australian and New South Wales governments on asbestos issues.

27. Dr Leigh assumed that Mrs Dunn had intermittent bystander exposure to asbestos as a child when repairs to certain asbestos cement parts of her parents’ house were carried out. He said that it was impossible to make any real quantitative estimate of the exposure. Nevertheless he concluded that this exposure made a material contribution to the development of her mesothelioma.

28. Dr Leigh bases his conclusion upon these factors:

(1) All cases of human mesothelioma may be attributed to asbestos.

(2) Asbestos is mutagenic and a complete carcinogen operating as an initiator and promoter of cellular change. It follows that there is no threshold effect for mesothelioma, and all cumulative exposure to asbestos in an individual case plays some part in causation.

(3) Mesothelioma has been recorded by articles in reputable medical journals after very brief exposures, as short as one day.

(4) In the Australian Mesothelioma Register 1986-2000, of 3752 cases of mesothelioma, 70 gave their only exposure as building or renovating an asbestos cement house or fence.

(5) Cases of mesothelioma had occurred in short-term visitors to Wittenoom, not associated with work at the mine.

(6) The latency period of 25-28 years is appropriate.

(7) The composition of the asbestos to which Mrs Dunn was exposed included 18 per cent crocidolite. This is a far more potent fibre than that which may be expected in background exposure.

29. In cross-examination Dr Leigh conceded that, in addition to the childhood exposure the subject of her claim, Mrs Dunn was also exposed to the general background level of asbestos fibre pervading the air in Adelaide, and may have been exposed to other concentrations which she did not recognise or does not recall. He further agreed that in order to conclude that the childhood contribution made a material contribution to Mrs Dunn's mesothelioma it was necessary to make some assessment of the relative importance of each contribution. He agreed that he had not quantified each exposure.

30. When asked:

In order to appreciate the comparative contribution of the assumed facts exposure, compared to the background exposure there does need to be some such work does there not?
Dr Leigh answered:

If you're attempting a quantitative connotation of this.

31. Professor Henderson is the Professor of Pathology at Flinders University in South Australia. He has been published widely on asbestos related diseases, contributing the relevant chapter to the standard textbook Parkes Occupational Lung Disorders. He is a member of the Pathology Panel of the Australian Mesothelioma Surveillance Program.

32. The history assumed by Professor Henderson approximately accords with the evidence in this case. It is an exposure that Professor Henderson describes as "very light to light… but not negligible".

33. Professor Henderson is of the opinion that Mrs Dunn's mesothelioma is attributable to her childhood domestic exposure.

34. Professor Henderson's reasons for this attribution are as follows:

(1) The time lag between the exposure and the subsequent diagnosis falls within the known time lag for asbestos induced mesothelioma.

(2) The asbestos fibre to which she was exposed included crocidolite, which has a greater causal potency than those asbestos cement products produced after 1967 when the dangers of crocidolite were recognised.

(3) Scientific literature records significant increases in the relative risk, or odds ratio, for mesothelioma for comparable low dose non-occupational exposures.

(4) The British Thoracic Society, relying upon case reference studies, adopted as one proposed criterion for the attribution of mesothelioma "Any occupation in which there has been exposure to asbestos, asbestos dust or any admixture of asbestos at a level above that commonly found in the environment at large".

(5) The year 2000 report for the Australian Mesothelioma Register records 70 mesotheliomas as related to "asbestos dwelling/fence-built/renovated" for single exposures only.

(6) Many of the mesotheliomas that Professor Henderson has observed on professional or medico-legal referral related to non-occupational asbestos exposures with histories of light exposure roughly comparable to that for Mrs Dunn.

(7) Professor Henderson had seen several thousand cases of mesothelioma and can recollect having seen only three cases in women about 30 years old. Two were children at Wittenoom and the third was Mrs Dunn. Mrs Dunn's exposure was most unusual, and it is reasonable in her case to make assumptions and extrapolations in comparison with other investigations of very low dose exposures.

(8) At the time of the exposure, when she was only three or four years of age, the asbestos fibres in the lungs of Mrs Dunn from background exposure would have been much less than that of adult persons.

35. In cross-examination Professor Henderson conceded that in the epidemiological studies of low doses upon which he relied, not a single case concerned an exposure so slight as that of Mrs Dunn.

36. For instance, the case-referent study of Iwatsubo et al, upon which he relied, found that the odds ratio for mesothelioma was 4.2 with low-dose exposure in the range of 0.5-0.99 fibres/ml-years. Although in the lower range of 0.001-0.049 fibres/ml-years the study found some increased risk, that risk did not achieve statistical significance. This failure did not deter Professor Henderson from taking comfort from the study, because of the nature of the statistical exercise. He pointed out that statistical significance may be achieved by demanding a 95 per cent confidence level, at which level there is only a 5 per cent chance that the results are explicable by chance. A conclusion of probable causation in an instant case does not require such certainty.

37. Professor Henderson agreed that the Iwatsubo paper did no more than add to a very formidable body of work which suggested a dose response but failed to find a threshold. He also agreed that the studies confirmed that the lower the dose the lower the risk.

38. In explaining his use of statistical and epidemiological material that predicted the odds of causation at low levels of exposure, Professor Henderson maintained that the studies are useful because they indicated a trend of increasing risk even at extremely low levels of exposure. In describing the papers upon which he relied as dealing with comparable exposures he said that they are comparable in that they are in the same ballpark of low-dose exposures.

39. Professor Henderson explained why it is that epidemiological studies, which recorded the excess incidence of disease in a population exposed to a causative agent under investigation compared to an unexposed population and thus predicted risk, were unable to give a definitive answer to the question of causation in this case. He said:

I think once the risk comes home in terms of assigning causation, one brings into account other factors. There is the strength of the association, the specificity of the relationship, the relationship in time, notions of what is the biology of the disease in question and how it is developed, biological plausibility, reasoning by analogy and particular, with papers like this, coherence of the evidence across multiple different studies. So that each one of these studies by itself is flawed, it has its limitations, but when you look at the whole evidence coherently I would then say, when you bring these other factors into account knowing, for example there is a 20 per cent increase in risk I would not attribute lung cancer on that basis to asbestos at a 20 per cent increase in risk because of the multiple different causal factors identified for lung cancer, but for a patient with mesothelioma there is only one known causal factor in practice and that is asbestos. Because of the strength of specificity of the relationship, I'd say, right, that risk has been brought home in this patient, and that coincides with our concepts of the pathobiology of the disease. (T 149.37)
He also said:

[The] relative risk or odds ratio is derived as an average across the group, but we know that humans vary and their risks will vary within that group at any one of those levels of exposure and according to the person's individual susceptibility to the disease in question. One point that I would make is that it is likely that the person within that group with the disease is susceptible and has a high relative risk [at] equivalent levels of exposure than someone who is biologically resistant to the disease. (T 151.48)

40. Professor Henderson's concession that the evidence for biological susceptibility was specifically lacking in Mrs Dunn is to be read in the light of his observation that “it is likely that the person within that group [low-dose exposure] with the disease is susceptible”.

Dr Francis and Mr Alan Rogers

41. Both Dr Francis and Mr Rogers are occupational hygienists who gave evidence as to the probable quantity of asbestos fibre inhaled by Mrs Dunn at the time of her childhood exposure. Their estimates are very different. Having regard to the evidence of Professor Berry, Dr Leigh and Professor Henderson concerning the imprecision of estimates of low dose asbestos exposures, there is little value in determining which of the experts is more correct. The medical opinions do not turn upon any assumption as to the precise quantification of the fibre inhaled.

42. Further, neither expert provided meaningful estimates of the amount of asbestos fibres which for a long time persisted on the path, carport floor and lawn upon which Belinda Dunn played after her initial exposure. Those fibres continued to operate as causative agents in addition to the fibres inhaled as background exposure.

43. On one matter I do accept the evidence of Dr Francis. She estimates the exposure to a person dry sweeping paths at three fibres per millilitre (Mr Rogers makes no estimate). This may be contrasted with her estimate of two fibres per millilitre for hand sawing asbestos cement sheeting, and less than two fibres per millilitre for machine drilling asbestos cement sheets. In general terms this evidence confirms that the exposure of Mrs Dunn when the paths were swept was greater than the exposure considered by Dr McNulty in Rentz v Seltsam Pty Ltd [2004] NSWDDT 15 (Nielsen).

44. I do not accept the evidence of Mr Rogers that the lifetime background risk of mesothelioma may be as high as 260 per million of population. Mr Rogers bases this figure upon those cases in the Australian Mesothelioma Register in which no history of asbestos exposure is recalled.

45. As Dr Leigh points out, an absence of history does not mean absence of exposure. Mrs Dunn denies exposure other than the childhood exposure the subject of the claim. Although this evidence has small weight, because the exposure may have been unrecognised or unrecognisable, it is nevertheless relevant. The dangers of asbestos in low doses have become more apparent in recent years. So also has the realisation in the public consciousness of the extent to which asbestos products were used in the community. More directed questioning has resulted in greater identification of exposure.

Discussion

46. Midalco and CSR have argued that, because on the medical evidence the mesothelioma resulted from both the exposure as a child and the accumulated background exposure, it is necessary that I make a specific finding that the childhood exposure made a material contribution to the whole. So much is unremarkable. The argument further proceeds however, on the basis that, because neither the childhood exposure, nor the background exposure, which may or may not include unremembered or unrecognised exposure, are capable of numerical quantification, Amaca cannot discharge its onus of proving that the childhood exposure was materially causative. I do not accept the submission.

47. This argument was advanced in the cross-examination of Professor Berry and Dr Leigh. Dr Berry, a mathematician, agreed with the proposition, which is unremarkable from the point of view of statistical proof. However as Fitzgerald AJA said In EM Baldwin & Son Pty Ltd v Plane (1998) 17 NSWCCR 434 at 475, “the law does not require the dismissal of a claim because there are no epidemiological studies available which permit the direct comparison considered necessary by an epidemiologist”.

48. Dr Leigh, who has expertise in mathematics and epidemiology, as well as medicine, agreed that the proposition was valid with the proviso: “If you are attempting a quantitative connotation of this”.

49. The law does not require statistical proof. In EMI (Australia) Ltd v BES [1970] 2 NSWR 238 at 242 Herron CJ said:

Medical science may say in individual cases that there is no possible connection between the events and the death, in which case, of course, if the facts stand outside an area in which common experience can be the touchstone, then the judge cannot act as if there were a connection. But if medical science is prepared to say that it is a possible view, then, in my opinion, the judge after examining the lay evidence may decide that it is probable. It is only when medical science denies that there is any such connection that the judge is not entitled in such a case to act on his own intuitive reasoning. It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me that no medical witness states with certainty the very issue which the judge himself has to try.

50. Dr Leigh did not resile from his medical conclusion that in all the circumstances the childhood exposure was causative.

51. Professor Henderson rejected the suggestion put to him in cross-examination that no conclusion could be drawn as to medical causation unless that conclusion was in terms supported by epidemiological evidence.

52. I reject the submission that both Dr Leigh and Professor Henderson failed to reveal their reasoning processes in their evidence. Professor Henderson, in particular, explains how he draws upon epidemiological studies to reach conclusions at reasonable levels of probability that do not satisfy arbitrary standards of mathematical conviction. This is a legitimate reasoning process. The subjects of the epidemiological studies of low-dose exposure from which his conclusions are drawn, were themselves necessarily exposed to background concentrations of asbestos fibre.

53. Mesotheliomas usually do not appear until about 28 years after the first exposure to asbestos fibre. The potency of any particular asbestos exposure to cause mesothelioma is the product of the time between that exposure, and diagnosis, raised to the fourth power. It follows by calculation that if Mrs Dunn were exposed to an (improbably) unrecognised concentration equal to her childhood exposure, at the age of 20, (beyond which all experts say the exposure is irrelevant), that later exposure would be approximately 50 times less potent than the original exposure. The potency of those later exposures, both actual and possible, upon which Midalco relies in an attempt to diminish the significance of the initial exposure, diminish exponentially as time passes after the childhood exposure.

54. Midalco and CSR called no medical evidence to rebut the evidence of Dr Leigh and Professor Henderson. The opinions and conclusions on causation advanced by Dr Leigh and Professor Henderson are persuasive.

Conclusion

55. I find that Mrs Dunn’s mesothelioma was caused by crocidolite fibre released from the asbestos cement sheets removed from the roof of her parents’ home in 1970 and 1971.

Foreseeability

State of Medical Science

56. Before the publication of the article Diffuse Pleural Mesothelioma and Asbestos Exposure in the North Western Cape Province by Wagner et al in the British Journal of Industrial Medicine in 1960, there was no reason to suppose that any cancer, other than lung cancer, may be induced by exposure to asbestos fibre. In the case of lung cancer, the relationship was associated with the presence of asbestosis, a disease contracted after prolonged industrial exposure.

57. Mesothelioma is a very rare form of cancer, the aetiology of which was for a long time unknown. Wagner and his associates studied 33 cases that occurred in South Africa and concluded that their findings were highly suggestive of a relationship between mesothelioma and crocidolite asbestos.

58. The subjects of the study did not all work in the asbestos industry. The histories of exposure included persons who lived for a time near asbestos mines. In only 8 of the 33 cases was evidence of asbestosis demonstrated. The case histories included the following:

Case 4-K. H., a white female, 56 years of age (born 1898), was a social worker, who could only have had a short exposure to asbestos as a child and probably a further slight exposure as a young woman. She may have paid several short visits to the mines with her husband at a later period.

She was born in Griquatown where she lived until she was five years of age. Her family then moved to Kimberley where from 1916 to 1922 she worked as a clerk in an asbestos warehouse. Her husband owned an asbestos mine from 1933 to 1940.

Case 15-S.S.V., a white female, 42 years of age (born 1916), is a housewife, who lived on a mine near Johannesburg ... She spent most of her youth in the asbestos belt.

Case 24-D.G., a white male. 32 years of age (born 1922), by profession an accountant, was born in England but came to South Africa as an infant. He spent his early childhood in Kuruman [a town in the asbestos belt] and left at the age of 7. He later qualified as a chartered accountant in Kimberley. His only subsequent contact with asbestos was the auditing of the books of an amosite mine in the Transvaal.

59. In February 1965 a paper by Newhouse & Thomson, published in the British Journal of Industrial Medicine, drew attention to the incidence of mesothelioma in people living in the vicinity of a London asbestos factory where crocidolite was used.

60. It was then apparent to persons informed by such publications, that, in comparison to those levels required to produce asbestosis and asbestos related lung cancer, lower levels of asbestos in inspired air may cause mesothelioma.

61. The vice of crocidolite, identified by the Wagner and Newhouse articles, was that it was not only an agent of slow change in lung tissue, but also that it may act as a primary carcinogen at very low doses.

Dr McNulty

62. Dr James McNulty was, between 1957 and 1963, a chest physician employed by the Western Australian Department of Public Health as a Mines Medical Officer. During this time he visited Wittenoom and alerted Australian Blue Asbestos to the health hazards presented by blue asbestos.

63. In December 1962 the Medical Journal of Australia published an article by Dr McNulty entitled Malignant Pleural Mesothelioma in an Asbestos Worker. Dr McNulty reported the case of a man who contracted mesothelioma in 1960 with a history of working at Wittenoom as a mill worker between 1948 and 1950. In his discussion of the case Dr McNulty wrote:

There appears to be a relationship between exposure to blue asbestos and the development of the pleural mesothelioma in this case. Pleural mesothelioma is a very rare tumour and the details are known of only three cases in Western Australia. Asbestosis has, regrettably, become less rare, but there are less than 49 cases in the state. The relatively short period of exposure to blue asbestos dust confirms an impression received from Wagner et al (1960, 1961) that these tumours may arise after transitory exposure to crocidolite in susceptible persons.

Experience in Western Australia certainly confirms that blue asbestos is a very harmful and a lethal fibre. The dust is one that urgently requires further experimental study … The interval between exposure and the development of the tumour is much shorter than has been previously reported… (Emphasis added)

64. Dr H Maynard Rennie was a specialist physician, who upon the evidence, acted as a consultant to CSR. It is apparent from correspondence that he was in close contact with the management of CSR and the Australian Blue Asbestos Co concerning conditions at Wittenoom, and advised the company on matters of industrial hygiene.

65. In the period 1961 to 1963, Dr McNulty engaged in correspondence with Dr Rennie concerning the health of men employed at Wittenoom. On 18 September 1961, Dr McNulty wrote to Dr Rennie drawing his attention to the health hazards created by the dust at the Wittenoom mine. He added:

The known hazard is real enough but reading papers on pleural mesothelioma (notably J. C. Wagner, C.A Sleggs & P. Marchand, British Journal Indust Medicine 1960, 17, 260) one is left with a suspicion that a combination of individual idiosyncrasy and minimal asbestos exposure, such as from road surfacing, may be dangerous.

66. On 25 October 1961 Dr McNulty again wrote to Dr Rennie concerning the conditions at the mine. After mentioning that case of mesothelioma the subject of his journal article, Dr McNulty's letter included the following sentence:

I am seriously concerned that these cancers of the pleura which are being reported in large numbers from South Africa, are due to an individual susceptibility and minimal exposure to blue asbestos (crocidolite). (Emphasis added)

67. In yet another letter, of 10 December 1962, Dr McNulty said this:

I am still a little concerned about the carcinogenic effect of crocidolite and wish that the Company would not use its tailings for roads and paths. Tailings were used as fillers at the golf course so that the poor devils inhale asbestos at recreation as well . (Emphasis added)

68. In a letter of 8 March 1963, Dr McNulty forwarded to Dr Rennie a copy of a letter from Dr Wagner. That copy is not in evidence. However in the text of his own letter to Dr Rennie, Dr McNulty said: “The reference [presumably by Wagner] to the possible slightness of exposure especially in childhood is one that has always worried me and why I have always decried the practice of using mill tailings for laying paths etc in the township”. (Emphasis added)

69. Dr McNulty gave evidence in a matter of CSR Limited v Young (1998) 16 NSWCCR 56. In the course of cross-examination he rejected the proposition that the phrase "transitory exposure", which he used in his article in the Australian Medical Journal, was intended to describe the relatively brief exposure of the person the subject of his article. That man worked for two years in an asbestos mill. Further, exposure of Mrs Olson was not transitory in any sense of the word. She lived in a township the atmosphere of which was heavily contaminated with crocidolite fibre.

70. Dr McNulty also prepared a witness statement in the matter of Rentz v Seltsam Pty Ltd (supra). That case concerned a home handyman who contracted mesothelioma. He had, in or about 1975, cut with a handsaw, and fixed to his garage, several sheets of asbestos cement cladding.

71. Dr McNulty's statement read in part:

20. In relation to the handling of and working with asbestos cement products there was a general belief that the asbestos fibres were locked up in the cement matrix of the products and that the asbestos did not represent any real health risk to persons working with the product.

21. For people putting up asbestos fences, for example, on the weekends using hand tools it wasn't thought they were exposed to any real risk of asbestos related disease.

22. It wasn't a belief that working with asbestos sheeting presented a significant health hazard.

72. This evidence of Dr McNulty is to be read in the context of the adoption in his statement of a publication by the Public Health Department of Western Australia that reads in part:

Much criticism and publicity has been given to the health hazards of asbestos but these are largely due to early heavy exposure to asbestos dust and particularly to crocidolite (blue) asbestos. Crocidolite is now no longer mined in Australia and is very little used in this country...

73. It is also to be read in the light of observations by Dr McNulty that the sheets of asbestos cement upon which Mr Nielsen worked in the construction of his garage were manufactured by Seltsam Pty Ltd and "Although James Hardie in Perth did use some crocidolite during the period from about 1963 to 1966 I doubt that Seltsam Pty Ltd would have used it."

74. In giving his evidence Dr McNulty was clearly aware of the significance of small amounts of crocidolite, were that fibre to have been included in the asbestos cement sheets upon which Mr Nielsen worked. Given Dr McNulty's concerns as to susceptibility during childhood, it is also relevant that Mr Nielsen was exposed as an adult.

75. Further, the commonsense assumption that breaking up weathered fibro sheets, and sweeping up the broken pieces and dust would expose a person to a higher respirable concentration of liberated asbestos fibre, (particularly if that fibre were crocidolite) than installing new sheets with hand tools, is borne out by the expert evidence of Dr Francis.

76. While Dr McNulty in communication to Dr Rennie referred to what he saw as an actual danger posed by the use of crocidolite tailings upon paths at Wittenoom, he nevertheless used the term "transitory exposure" in the more general warning contained in his article in the Australian Medical Journal. The duty of Midalco and CSR to Mrs Dunn is postulated upon appreciation of those words in the context of the references by Wagner and Dr McNulty to the especial risks posed to children by slight exposure. In the Shorter Oxford English dictionary the word "transitory" bears the meaning "fleeting".

77. In a letter to Dr McNulty of 29 September 1961 Dr Rennie said: "At the moment I am reading all the articles I can get hold of”. It is improbable in the extreme that he did not read Dr McNulty's article published in the Medical Journal of Australia in December 1962 in which Dr McNulty said that "These tumours may arise after transitory exposure to crocidolite in susceptible persons". He would have read the letter from Wagner to Dr McNulty forwarded to Dr Rennie in March 1963 in which Wagner referred to possible slightness of exposure especially in childhood. It is improbable that he did not read the paper by Newhouse and Thomson published in the British Journal of Industrial Medicine in February 1965.

Discussion

78. Before 1966 no published study reported the occurrence of mesothelioma in circumstances where the exposure was other than environmental, and then in a period measured by years. Dr McNulty was prescient in his use of the words "transitory exposure" to describe the risks of crocidolite. Both he and Wagner appreciated the particular risks of transitory exposure in children.

79. In the course of argument in Chapman v Hearse (1961) 106 CLR 112 Dixon CJ observed at 115 that:

Foreseeability does not include any idea of likelihood at all. I cannot understand why any event which does happen is not foreseeable by a person of sufficient imagination and intelligence.

80. It was not until after 1967 that the uniquely carcinogenic property of crocidolite fibre, and the significance of brief or intermittent exposure in the aetiology of mesothelioma, were generally recognised. Dr McNulty, without the benefit of evidence, but armed with sufficient imagination and intelligence, foresaw this development five years earlier. Although not in 1962 proven in the case of crocidolite, the contraction of cancer by susceptible persons through exposure to an extremely small quantity of a carcinogen was then medically plausible.

81. If Midalco and CSR did not know of the content of Dr McNulty's 1962 article in the Australian Medical Journal then they should have. The subject of the article was one of Midalco’s former employees. If they did not know of the Newhouse and Thomson article published in February 1965 then, the business of ABA being exclusively the production of crocidolite, they should have. If they did not seek to inform themselves by inquiring of their consultant physician, Dr Rennie, as to the content of opinions passing between him and Dr McNulty, an officer of the Western Australian Department of Health who visited Wittenoom in the course of his office, then they should have. In any event they should have informed themselves by speaking directly to Dr McNulty on those occasions when he visited the mine.

Identification of the particular foreseeable risk

82. In addressing foreseeability for the purpose of imposing a duty of care, it is necessary to conceive, at an appropriate level of abstraction, of the class of persons to whom the risk was foreseeable.

83. Relevant to a finding of foreseeability in this case is the circumstance that, at the relevant time, two experts in the field, J C Wagner and Dr McNulty, foresaw that persons who may predictably belong to the class in question, children exposed to low doses, might suffer damage of the relevant kind, and that this belief was communicated to Dr Rennie, a consultant to ABA and CSR. As I have said, if those companies did not seek to inform themselves from Dr Rennie's store of expertise, they should have.

84. By June 1965 CSR and Midalco knew that crocidolite caused mesothelioma. They knew that mesothelioma caused death. They knew or ought to have known that children were susceptible and at risk of contracting this disease from transitory exposure to crocidolite. They knew that certainty of the risks associated with low doses may not emerge for many years, during which time a large number of persons may unknowingly contract the disease. Midalco has admitted that it knew that crocidolite fibre sold by it was used by Hardies to manufacture building products, and that if those products were broken crocidolite dust would be released.

85. Mrs Dunn was a member of a class which may be described as children, susceptible because of early childhood development, who suffer transitory exposure specifically to the crocidolite fibre in the course of home renovation. A remote risk to such a class of persons may nevertheless be foreseeable (Bolton v Stone [1951] AC 850).

86. In 1965 the risks faced by such a class were beyond certain scientific knowledge. However, in my opinion, the test of foreseeability does not depend upon sure knowledge of a risk. It is satisfied if the risk is a reasonable (in the sense of rational) possibility, bearing in mind medical plausibility and the gravity of the consequence of the risk coming home.

87. The resolution of the foreseeability issue in this case depends upon an answer to the question whether foreseeability in disease cases requires a consensus of expert opinion that harm could occur, or whether the test is satisfied by an informed and reasonable conception that, given the uncertain state of knowledge, harm might occur.

88. The former view was adopted by Handley JA in CSR Limited v Young (1998) 16 NSWCCR 56 who held that reasonable foresight of dangerous properties in articles of commerce did not extend beyond the limits of current scientific knowledge [64].

89. This view was not shared by the majority. Giles AJA (with whom Cohen AJA agreed), pointing out [114] that this was the issue that divided the Queensland Court of Appeal in Bale v Seltsam Pty Ltd (QLDCA, No 284/95, 23 August 1995, unreported), preferred the minority view of Fitzgerald P, who said:

The critical question in my opinion, is whether the trial judge was correct in her view that the respondent was not under a duty of care until "the link between exposure to low levels of asbestos dust and malignant mesothelioma had been made", i.e, until the respondent had positive knowledge (actual or constructive) of actual risk, or whether, in the circumstances, the uncertainty which existed concerning the toxic effects of asbestos dust and the level of exposure which could induce illness in susceptible persons, and the risk inherent in that uncertainty, was sufficient to create a duty of care i.e., a duty to implement inexpensive and convenient systems to eliminate the possible risk to, and/or warn, those like the appellant who might be affected.
Fitzgerald P concluded that the trial judge was wrong. He said that at the end of 1962, because of the known toxicity of asbestos dust, the known uncertainty with respect to its effects, and the knowledge that injury or illness might not emerge for many years, a risk from low exposure could not be dismissed as "remote", "slight", "far-fetched", or "fanciful" or otherwise ignored in the circumstances of that case (the wives of asbestos workers). He did not consider that it was open to CSR to assume that the "low-level" exposure to asbestos dust experienced by persons such as the plaintiff was safe until a "link… with malignant mesothelioma had been made out" .

90. Although the notion of reasonable foreseeability of risk does not incorporate concepts of likelihood, the imagination required in contemplation of possible risk should be informed by the magnitude of the possible consequences should the risk come home.

91. In Tame v State of New South Wales (2002) 211 CLR 317, Gleeson CJ, referring to Wyong Shire Council v Shirt said at [12]:

Reference was there made to the rather tendentious description of the requirement of foreseeability as "undemanding"; a description that may be more or less accurate depending upon the context. It is important that "reasonable foreseeability" should be understood and applied with due regard to the consideration that, in the context of an issue as to duty of care, it is bound up with the question whether it is reasonable to require a person to have in contemplation the risk of injury that has eventuated . (Emphasis added)

92. I find that the risk that Mrs Dunn may contract mesothelioma from childhood exposure to crocidolite fibre released in the course of building renovations was foreseeable.

Proximity

93. CSR and Midalco argue that two circumstances militate against the imposition of a duty of care in this case. First, they submit that they had no control over Mrs Dunn (or her parents) of any kind, let alone that which might have enlivened duty of care. Secondly they submit that the class to whom the suggested duty was owed was so large and indeterminate that it was unreasonable to impose a duty to protect all members of that class from the foreseeable harm.

Control

94. The notion of control in relation to the existence of duty is not necessarily directed to control of a person, be that person the plaintiff or of others whose actions may be causally related to the plaintiff's damage. The control may relate to control of a thing or substance. In Sutherland Shire Council v Heyman (1985) 157 CLR 424, Deane J at 497 said this:

The requirement of proximity is directed to the relationship between the parties in so far as it is relevant to the allegedly negligent act or omission of the defendant, and the loss or injury sustained by the plaintiff. It involves the notion of nearness or closeness and embraces physical proximity (in the sense of space and time) between the person or property of the plaintiff and the person or property of the defendant, … and what may (perhaps loosely) be referred to as causal proximity in the sense of the closeness or directness of the causal connection or relationship between the particular act or course of conduct and the loss or injury sustained. (Emphasis added)

95. Proximity in this case is to be found in the relationship between Mrs Dunn's person and the property and actions of Midalco. There is a direct causal connection between the sale of crocidolite fibre by ABA and Mrs Dunn's injuries. This is not a case in which it is suggested ABA was under a duty to prevent harm arising from some extraneous cause. ABA itself created the risk by selling crocidolite for use in building products. In Sutherland Shire Council v Heyman Brennan J. at 479 said:

Thus a duty to act to prevent foreseeable injury to another may arise when a transaction… has been undertaken by the alleged wrongdoer and that transaction… has created... the risk of that injury occurring. Such a case falls literally within Lord Atkin's principal in Donoghue v Stevenson.

96. I have above delineated the class to whom CSR and Midalco owed a duty. It is no more indeterminate than the class to whom the manufacturers were said to owe a duty in Donoghue v Stevenson. In that case it was every person who consumed a beverage manufactured by the defendant. In this case it is each child who, during formative years, was exposed to crocidolite fibre sold by ABA after June 1965, when, as I will later explain, the Wittenoom mine should have been closed

Other factors

97. Other circumstances in this case militate towards the imposition of a duty of care. Mrs Dunn as a child was uniquely vulnerable and without means to protect herself. CSR and Midalco had access to special expertise and knowledge which was not at the relevant time available to the wider community, which included Mr and Mrs Birks. Further, the conduct required in discharge of the duty was conduct required to discharge a concurrent duty owed by CSR and Midalco to the workers employed at the mine.

Conclusion

98. I find that CSR and Midalco owed a duty of care to the plaintiff Mrs Dunn.

Breach of duty

The appropriate response to the risk

99. In Wyong Shire Council v Shirt (1980) 146 CLR 40 at 47 Mason J said this:

In deciding whether there has been a breach of the duty of care the tribunal of fact must first ask itself whether a reasonable man in the defendant's position would have foreseen that his conduct involved a risk of injury to the plaintiff or to a class of persons including the plaintiff. If the answer be in the affirmative, it is then for the tribunal of fact to determine what a reasonable man would do by way of response to the risk. The perception of the reasonable man's response calls for a consideration of the magnitude of the risk and the degree of the probability of its occurrence, along with the expense, difficulty and inconvenience of taking alleviating action, and any other conflicting responsibilities which the defendant may have. It is only when these matters are balanced out that the tribunal of fact can confidently assert what is the standard of response to be ascribed to the reasonable man placed in the defendant's position.

100. Although in The "Wagon Mound" (No 2) [1967] 1 AC 617 at 642-643 Lord Reid said that a foreseeable risk may be so remote that: “A reasonable man, careful of the safety of his neighbour, would think it right to neglect it”.

He also said (at 643-644) that:

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

101. The facts of the present case are extraordinary. Amaca contends that in response to the remote risk posed to Mrs Dunn, ABA and CSR should have in 1965 closed the mine and ceased production of crocidolite asbestos. As it happens, the course proposed by Amaca involved no difficulty, disadvantage or expense to ABA or CSR, nor did it conflict with any other responsibilities which ABA or CSR may have had. To the contrary, it was a course that denied no legitimate commercial advantage to those trading entities and discharged other responsibilities which they bore. The mine was for a long time unprofitable, and its continued operations caused grave harm to many of the workers there employed. It closed in December 1966.

The mine was unprofitable

102. ABA was incorporated on 7 April 1943 by CSR as a subsidiary company to develop asbestos deposits in Western Australia. Mining began in early 1944. The initial mine proved to be unsuccessful. By 1955 ABA had accumulated losses of approximately $1,600,000. A new mine approximately 2 miles distant was opened in 1958. This mine operated profitably until 1961. Thereafter as fibre prices fell and costs increased the mine again became unprofitable.

103. In the year ended December 1962 the company lost $235,000. The losses increased over succeeding years. In the 15 months ended March 1965 the loss was $515,000. In the 12 months ended March 1966 the loss was $820,000. In September 1966 the current rate of loss was estimated to be $850,000 per annum.

104. In a document, apparently a report to the Board, dated 29 September 1966, the author wrote:

In 1954… Hardies would not recognise that blue fibre was worth more than amosite fibre and consequently we could not obtain a market in Australia for the fibre we were producing at a reasonable price. We asked for and obtained a Tariff Board hearing with the object of getting a formal protection which would force the use of blue fibre in Australia at what we believed to be the correct price for its quality. We were turned down by the Tariff Board who accepted Hardies view that the fibre was only as good as amosite and so worth only $100 per tonne approximately as compared to $200 per tonne which we assessed as its proper value.

Later, in 1957, we entered into an arrangement with Hardies whereby we agreed to keep out of the asbestos cement industry as manufacturers and they, in turn, would purchase blue fibre from us at prices keyed to the price of chrysotile fibre. This meant a price of approximately $200 per tonne. It also meant, however, that CSR ceased to have a reason for mining fibre unless it was profitable. (emphasis added)

Over the past 10 years fibre prices have fallen by some 7% despite the fact that the quality of fibre has improved. Our basic costs at Wittenoom, however, have risen sharply, wages and stores have risen some 60 to 70%. For example, in 1956 a tradesman received a total of $36.50 per week. He now receives $59.36 per week, and in addition we had to ensure a six day week to keep such men.

Hardies have continued to pay us more for our fibre than we can obtain on the world market, despite the fact that our grading has not been as good as fibre available from elsewhere (because we could not afford to make it so). Hardies consider that they have been paying us about $10 per tonne more than the fibre is actually worth based on what they could otherwise obtain on the world market and it’s difficult not to agree with this.

105. Later in the document the author informs the board that Cape Asbestos and Hardies had been invited to join in the venture and continues:

The assessment by Cape Asbestos and by Hardies has now been completed and as a result both Cape and Hardies say that they cannot see how they can interest themselves in the venture. They cannot see that the area can be mined economically. They believe that the values of fibre are just too low and, in any case, they believe that on present indications the life of the known ore deposits is so short (a maximum of about five years in their judgment) based on presently available information, that they cannot see that it is worthwhile trying to keep Wittenoom alive.

106. ABA ceased mining operations at Wittenoom in December 1966 because of the continuing losses.

Continued operations caused death and serious injury to employees

107. Dr McNulty visited the mine in November 1959 and again in August 1961. On 18 September 1961 he wrote to Dr Rennie advising him of the serious health hazards confronting the workers because of conditions at the mine. His letter included the following passages:

The primary concern of a company, is to produce a product profitably, but it has been shown, time and time again, that apart from gross exploitation of labour, this is best achieved where the interest and health of the workers is considered. The contrary, where the product is produced at the expense of the health of the worker, cannot be tolerated in a civilised community. If I thought that the state of affairs existed at Wittenoom, and I could not correct it or else close the mine , I would resign. What I do say, is that the dust hazard is not properly appreciated and that the company's attitude is ostrich like. I am certain that working conditions are not ideal and have very grave doubts concerning the statement that everything possible has been done. I have reason to believe that much of the dust extracting machinery is ineffective at times and, further, before extracting the dust, some means of disposing of it away from the workings should be discovered. Increased production should go hand-in-hand with ventilation and not precede it. Frankly, I do not think that the company (CSR or ABA) know how to control the dust.

In a little more than 10 years the industry has produced 20 cases of industrial chest disease (including one proved cancer) and a number of suspected cases. As the years go on I have no doubt that many more will come to light. It should be remembered that many experts in this field claim that the asbestos fibre takes many years to produce significant pulmonary disease. If this is true, the men diagnosed now represent gross pathology and exposure, and the real nature of the hazard, in terms of disease may not become apparent for another 10 years. (Emphasis added)

108. In a further letter of 25 October 1961 Dr McNulty advised Dr Rennie that he was aware of 34 men who had been seriously affected by a mixture of asbestosis and silicosis and whose disease could reasonably be attributed to work at Wittenoom. One of those was dead and at least three were dying. He also said that there were a further 22 men who he suspected were developing disease.

109. In yet a further letter of 10 December 1962, Dr McNulty advised Dr Rennie that the dust counts at the mine were still bad, and that fairly short exposure was causing silicosis and asbestosis, with 42 men now seriously affected or dead.

110. On 6 February 1963 Dr McNulty informed Dr Rennie that a Mines Department Inspector had reported to him that the mill was dirtier than ever.

111. On 25 February 1963 Dr Rennie, in a letter to a Dr Bruce Hunt, said:

It is about a year ago now when I first took this matter up with the company and they claimed that they had made quite a number of alterations which would prove helpful in solving the problem… I gather that the conditions are, in fact, worse than they were and this gives me a tremendous pull.

112. It should not be supposed that Australian Blue Asbestos did nothing to counter the risks of the dust inhalation. Dust control equipment was in operation at Wittenoom from the beginning of ABA's first mine. In a document discovered by CSR, possibly a Board minute, the author provides the following information:

Working from experience gained, and applying advancements in technology, improvements were steadily made to dust control procedures. Multiclones were installed in 1946. At least three Warman dust collectors were installed in 1948. About 1956, at least three rotoclones were installed, following advice by consulting engineers. In about 1964, after further extensive study and advice, an Amerjet bag-house system replaced the rotoclones.

Some of the factors which made dust control difficult were the light floating nature of asbestos particles, its lack of affinity with water in any wet collection process, and the extreme hardness of the rock being crushed which tended to very quickly damage most equipment.

In all the amount spent exclusively on dust control equipment was about $750,000.

In addition about $100,000 was spent in 1956 experimenting with a wet milling process, but this proved unsuccessful.

113. In his letter of 18 September 1961 to Dr Rennie, Dr McNulty, speaking of the dust hazard, had said that alternatives were "correct it or else close the mine". He also said "I do not think the company know how to control the dust".

114. If, despite the attention of management and significant expenditure, the conditions continued to pose the dangers identified by Dr McNulty, it may be concluded that control of the dust at the mine sufficient to protect the workers was beyond the capacity of the managerial skills and technology available to ABA in February 1963 (when the Mines Department Inspector found the conditions to be dirtier than ever). At that stage, given the incidence and gravity of the diseases contracted by some of the workers, there was no reasonable course open to ABA and CSR but to close the mine.

No countervailing responsibilities

115. ABA and CSR tender copies of newspaper articles published between October and December 1966 which deal with issues arising from the closure of the mine. I was not addressed directly as to the conclusions which I should draw from this material, however I assume the intent was to suggest that "other responsibilities" of ABA and CSR militated against closure of the mine. I am not so persuaded.

116. The articles reveal that, because the work at the mine was so onerous, few Australians wanted any part of it and the company directly recruited workers in the cities of Europe. Three quarters of Wittenoom's population consisted of European migrants and their families.

117. In the 12 months before closure the Western Australian government spent a great deal of money on public works. The West Australian reported the opposition leader as saying that it was difficult to understand why the government had spent as much money in the town if it had any idea that Wittenoom's future was in jeopardy. I here observe that government expenditure is not always rational in the face of political expediency, and commercial undertakings are not always forthright in their dealings with governments.

118. In one article the reporter observed that …any experienced businessman in Perth would say the growing losses of the mine made it obvious that it must be closed… The newspaper noted that in the 23 years of its existence ABA had paid only one dividend. It further reported that the people of Wittenoom were bitter at the closure "not so much at the decision itself, as at the shortness of the time they have been allowed to replan their future from such an isolated area".

119. Although the closure of the mine threw about 300 men out of work, in a leading article, published in The West Australian on 2 December 1966, the newspaper predicted that most of the displaced workers were expected to take jobs on the iron ore fields, particularly the Mount Newman project and in mines at Kalgoorlie. On 4 December 1966 the newspaper quoted the Minister for the North West, Mr Court, as saying that "Mount Newman Iron Ore Company has advised us it needs 20 men immediately and within three months could sign on progressively all other Wittenoom men who want work".

Conclusion

120. It follows that there was, certainly by the end of the financial year June 1965, and probably by the end of March 1965, when an account demonstrated losses in the preceding 15 months of $515,000, no impediment to the remedy reasonably suggested by Amaca in response to the real though remote risk faced by that class of persons of whom Mrs Dunn was a member. The mine should have been closed no later than 30 June 1965. In the calculation of utility, the gravity of consequence if the remote risk came home, which was death, infinitely outweighed the burden of obviating the risk, which was zero. Had the mine closed at the end of June 1965, Mrs Dunn would not have contracted mesothelioma. Her injury results from the breach of duty by Midalco and CSR. Had Midalco or CSR been sued by Mrs Dunn, they would have been held liable in respect of her damages.

Apportionment

121. It is appropriate to treat CSR and Midalco as a single unit for the purposes of apportionment.

Causal contribution

122. Mrs Dunn’s injuries resulted from exposure to crocidolite fibre in asbestos cement products. I regard the causal contribution to that exposure by the supplier of the fibre, and by the manufacturer who used the fibre, as equal.

Responsibility

123. Amaca, CSR and Midalco each owed a duty to Mrs Dunn, equally predicated upon the foreseeability of a remote risk arising from the demolition of building products. I am unable to find that the knowledge of any of them in relation to that risk was other than equal. Because in each case the duty could have, and should have, been discharged by the removal of crocidolite from those products, I regard them as equally culpable.

Quantum

124. I accept the submissions by Amaca that the damages and costs recoverable by Mrs Dunn were in the range $1,595,000 to $2,582,500. CSR and Midalco do not submit to the contrary.

125. The matter is complicated because included within those estimates are amounts of $375,000 in the lower estimate, and $1,500,000 in the higher estimate, in respect of Sullivan v Gordon damages. Mrs Dunn was the mother of a child, Nathan, born on 22 November 1997. The decision in Sullivan v Gordon (1999) 47 NSWLR 319 was handed down on 22 September 1999. Amaca settled with Mrs Dunn on 21 January 2002. On 21 October 2005 Sullivan v Gordon was overruled by the High Court in CSR Ltd v Eddy (2005) 226 CLR 1.

126. CSR and Midalco submit that because Amaca chose to settle the proceedings on the basis of a misapprehension as to the common law concerning the availability of Sullivan v Gordon damages, it cannot be just or equitable that they should pay any proportion of this head of damages. I do not agree.

127. Until Sullivan v Gordon was overruled by the High Court, it was a binding precedent to be followed by the Tribunal in the assessment of damages in actions subject to the proper law of New South Wales. Although Mrs Dunn's action was to be determined applying the proper law of South Australia, there is but one common law of Australia. It is true that other jurisdictions are not bound to follow decisions of the New South Wales Court of Appeal, nevertheless appellate courts do not make law, but rather declare what the law was at the time the cause of action accrued. The Court of Appeal in Sullivan v Gordon purported to apply principles of compensation found in the earlier High Court authority of Griffiths v Kerkemeyer (1977) 139 CLR 161. Before the decision in CSR Ltd v Eddy it was a moot point as to whether Sullivan v Gordon was part of Australian common law. I don't think it necessary to decide the question.

128. Section 5(1)(c) of the Law Reform (Miscellaneous Provisions) Act 1946 enables a tortfeasor to recover contribution from any other tortfeasor who is, or would if sued have been, liable in respect of the same damage. Had CSR and Midalco been sued at the same time as Amaca, and the matter not settled, they would have been held liable in respect of the same damage to Mrs Dunn which included a Sullivan v Gordon component.

Conclusion

129. I find it to be just and equitable that CSR and Midalco jointly contribute to Amaca one half of Mrs Dunn’s damages.

130. Verdict for Amaca Pty Limited against CSR Limited and Midalco Pty Limited jointly for 50 per cent of the plaintiff’s damages, plus interest from the date of payment to her.

I direct the parties to bring in short minutes of order reflecting these reasons.

131. I will hear the parties on costs.

Mr G M Watson SC with Mr J C Sheller instructed by DLA Phillips Fox appeared for the cross claimant

Mr B W Walker SC with Ms J Gleeson instructed by Makinson and d’Apice appeared for the cross defendants