Nawaf Hawchar v Dasreef Pty Ltd

[2009] NSWDDT 12

Dust Diseases Tribunal

of New South Wales

CITATION:	Nawaf Hawchar v Dasreef Pty Ltd [2009] NSWDDT 12
PARTIES:	Nawaf Hawchar (Plaintiff) Dasreef Pty Ltd (Defendant)
MATTER NUMBER(S):	7323 of 2007
JUDGMENT OF:	Curtis J at 1
CATCHWORDS:	DUST DISEASES TRIBUNAL :- Definition of dust disease - scleroderma
LEGISLATION CITED:	Workers’ Compensation Act 1987 Workers’ Compensation (Dust Diseases) Act 1942 Workplace Injury Management Act 1998 Evidence Act 1995 Civil Liability Act 2002 Dust Diseases Tribunal Act 1989 Uniform Civil Procedure Act 2005 Uniform Civil Procedure Rules 2005
CASES CITED:	Mahoney v J Kruschich (Demolitions) Pty Ltd (1985) 156 CLR 522 Quazi v Quazi [1980] AC 744 Frost v Amaca Pty Ltd [2004] NSWCA 358 JLT Scaffolding International Pty Ltd (In Liq) v Silva, New South Wales Court of Appeal, 30 March 1994, unreported Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 282 Adelaide Stevedoring Co Ltd v Forst (1940) 64 CLR 538, Ramsay v Watson (1961) 108 CLR 642, E.M.I. (Aust) Ltd v Bes [1970] 2 NSWR 238 Malec v J.C Hutton Pty Ltd (1990) 169 CLR 638 Planet Fisheries Pty Ltd v La Rosa (1968) 119 CLR 118 Berowra Holdings Pty Ltd v Gordon (2006) 225 CLR 364 The Ritz Hotel Ltd v Charles of the Ritz Ltd (No 8) (1987) 12 IPR 75 Wattyl Australia Pty Ltd v McArthur [2008] NSWCA 326
DATES OF HEARING:	27,28,29,31 October 2008, 3,4,5,6,7, November 2008, 26 Februrary 2009, 2,4,5, March 2009, 16 April 2009, 13 and 15 May 2009
DATE OF JUDGMENT:	22 May 2009
LEGAL REPRESENTATIVES:	Mr A J Bartley SC with Mr F Tuscano instructed by Keddies Lawyers appeared for the plaintiff Mr T G R Parker SC with Mr D T Miller instructed by Moray and Agnew appeared for the defendant

JUDGMENT:

18

Dust Diseases Tribunal of New South Wales

Matter Number 7323 of 2007

Nawaf Hawchar

v

Dasreef Pty Ltd

22 May 2009

CURTISJ

JUDGMENT

Introduction

1. Mr Nawaf Hawchar worked as a labourer and stone cutter for Dasreef Pty Ltd (Dasreef) between 21 October 1999 and May 2005. In this occupation he was exposed to silica dust generated by the application of angle grinders, hammers, chisels and abrasives, to cut and shape sandstone. He suffers from the diseases of silicosis and scleroderma and claims damages from Dasreef, asserting that his injuries were caused by the inhalation of excessive quantities of silica dust, and would not have occurred had Dasreef exercised reasonable care for his safety, and discharged its statutory duties to protect him from the dangers of excessive dust.

2. In answer to the claim, Dasreef says that Mr Hawchar cannot prove that his diseases were caused by his employment, that Dasreef exercised reasonable care in protecting him from the dangers of silica dust, that it complied with its statutory duties, and that, in any event, the silicosis from which Mr Hawchar suffers is not disabling.

A preliminary issue

Is Mr Hawchar's claim for damages in respect of scleroderma subject to the modified common law damages regime established by Division 3 of the Workers’ Compensation Act 1987?

3. Mr Hawchar's claim in respect of scleroderma is subject to the provisions of that Act unless:

(a) He was not a worker within the meaning of the Act, or;

(b) His disease of scleroderma is "a dust disease" within the meaning of the Workers’ Compensation (Dust Diseases) Act 1942, which diseases are, pursuant to s4 of the Workers CompensationAct, excluded from the operation of that Act.

4. Because silicosis is a dust disease within the meaning of the latter Act, Mr Hawchar is entitled to damages at common law in respect of that condition, if he can establish that the silicosis results from a breach of duty by Dasreef.

Was Mr Hawchar a worker within the meaning of the Workers’ Compensation Act 1987?

5. The Workplace Injury Management Act 1998 applies to a person who is a worker, defined by s4 as "a person who has entered into or works under a contract of service…" or a person who is deemed a worker pursuant to Schedule 1 cl 2 which relevantly provides that:

(1) Where a contract:
(a) to perform any work exceeding $10 in value (not being work incidental to a trade or business regularly carried on by the contractor in the contractor’s own name, or under a business or firm name), or

(b) [repealed]

is made with the contractor, who neither sublets the contract nor employs any worker, the contractor is, for the purposes of this Act, taken to be a worker employed by the person who made the contract with the contractor.

6. Mr Hawchar worked under a contract of service with Dasreef between 21 October 1999 and 30th June 2000. Thereafter, pursuant to the instructions of Dasreef, he registered a business name, Nasso Stone Construction, for a business that he then conducted as a partnership between himself and his wife. From that time he provided invoices to Dasreef, claiming labour charges which included GST, and paid his own tax. He says that "Otherwise, nothing changed between when I was an employee and a contractor". Mr Hawchar continued to work under the direction and control of Dasreef, Dasreef provided all tools, materials and equipment, and told him what time to start and finish work each day. He was paid for the hours worked, and not fixed sums for the products of his labour.

7. On occasions between 2002 and 2005, Mr Hawchar independently contracted to perform private stone masonry work on weekends. Sometimes he employed labourers to assist him and paid them wages. The cost of stone used in this work was claimed as a tax deduction against the income generated by the partnership Nasso Stone Construction.

8. Mr Bartley SC for Mr Hawchar submits that after 30 June 2000 the work performed by Mr Hawchar for Dasreef was not work pursuant to a contract of service, but was work incidental to a trade or business regularly carried on by him as a contractor in his own name.

9. If the work with Dasreef did not bear the lineaments of a contract of service that argument may be persuasive. There is, however, no inconsistency in Mr Hawchar’s providing his labour to Dasreef pursuant to a contract of service during the week, yet offering private clients contractual rates for work performed on weekends. Even if the contract with Dasreef was not characterised as a contract of service, the work performed pursuant to that contract was not work incidental to the trade or business carried on, irregularly, by Mr Hawchar on weekends.

10. I find that, pursuant to his contract with Dasreef, Mr Hawchar was a worker within the meaning of the Workplace Injury Management Act 1998.

Is scleroderma a dust disease within the meaning of the Workers’ Compensation (Dust Diseases) Act 1942?

11. Section 3 of the Workers’ Compensation (Dust Diseases) Act 1942 relevantly provides that:

Dust disease means any disease specified in Schedule 1 and includes any pathological condition of the lungs, pleura or peritoneum, that is caused by dust that may also cause a disease so specified.

12. Silicosis is a disease specified in Schedule 1. Scleroderma is not. Although scleroderma may directly affect lung tissue, Mr Hawchar's lungs have not yet been affected.

13. Mr Bartley submits that Mr Hawchar’s scleroderma is a pathological condition of the lungs…caused by dust because:

(a) The inability of Mr Hawchar to completely inflate his lungs, because of scleroderma reducing the elasticity of the skin around his chest wall, constitutes a pathological condition of his lungs; and/or

(b) The sceleroderma results from derangement or aberration of the immune system within the lungs caused by dust, which disorder constitutes a pathological condition of the lungs that may, and did in Mr Hawchar's case, concurrently cause a disease so specified, that is, silicosis.

14. In developing his first contention Mr Bartley argues that the words pathological condition of the lungs should be given the widest meaning, so as to include any abnormality of the lung caused, even indirectly, by dust. Although the scleroderma has caused no change to the substance of Mr Hawchar’s lungs, if dust caused the scleroderma, and if his ability to inflate his lungs is compromised by the scleroderma reducing the elasticity of the skin around his chest wall, then he suffers from a pathological condition of his lungs caused by dust.

15. It may be accepted that the words "caused by dust" include not only a direct cause, but also an indirect cause (see Mahoney v J Kruschich (Demolitions) Pty Ltd (1985) 156 CLR 522 at 528-30). The question raised by this submission is what work the words of the lungs do in assisting interpretation of the definition.

16. Schedule 1 of the Workers’ Compensation (Dust Diseases) Act lists 14 diseases, each of which is a disorder characteristic of, and confined to, the lung. Scleroderma is a disorder of the immune system that may be manifested in multiple organs, only one of which is the lung.

17. The Class Rule (Ejusdem Generis) applies:

to cut down the generality of the [final expression]… where it is preceded by a list of two or more expressions having more specific meanings and sharing some common characteristics from which it is possible to recognise them as being species belonging to a single genus and to identify what the essential characteristics of that genus are. The presumption then is that the draughtsman's mind was directed only to that genus and that he did not, by his addition of the [general word] to the list, intend to stray beyond its boundaries, but merely to bring within the ambit of the enacting words those species which complete the genus but have been omitted from the preceding list either inadvertently or in the interests of brevity ( Quazi v Quazi [1980] AC 744 at 807 per Lord Diplock LJ).

18. In context, the words "pathological condition of the lungs" must be read as confining the pathology in question to the substance of the lung. Mr Hawchar’s scleroderma has not yet affected the substance of his lung. I am not persuaded by Mr Bartley's first argument.

19. Assuming the medical evidence bears out Mr Bartley's second argument, the question remains whether the words pathological condition of the lungs mean a pathological condition or process which causes a disease, or a pathological condition which is a disease.

20. Both meanings are available. Blakiston’s Gould Medical Dictionary (4th Ed) provides these definitions:

(1) The failure of the adaptive mechanisms of an organism to counteract adequately the stimuli or stresses to which it is subject, resulting in a disturbance in function or structure of any part, organ, or system of the body. A response to injury; sickness or illness.

(2) A specific entity which is the sum total of the numerous expressions of one or more pathological processes. The cause of a disease entity is represented by the cause of the basic pathological process in combination with important secondary causative factors.

21. The question is not without difficulty. Because the words includes any pathological condition of the lungs, follow the words, means any disease I tend to think that the draughtsman intended the meaning to accord with the second definition.

22. The correct interpretation of the definition of dust disease is of great importance, not only to Mr Hawchar, but also to the proper exercise by the Tribunal of its exclusive jurisdiction. I regret that I do not have jurisdiction to state a case for the opinion of the Court of Appeal (Frost v Amaca Pty Ltd [2004] NSWCA 358).

23. As a matter of construction, I rule that the words "pathological condition of the lungs…caused by dust" do not encompass diseases or pathological conditions existing elsewhere in the body caused by dust, which adversely affect lung function, or pathological conditions existing elsewhere in the body which result from a pathological process or condition in the lungs (caused by dust) which process or condition is not itself a specific disease entity.

24. Because I may be wrong in these conclusions I will address the medical evidence that bears upon the issue.

Questions for determination

25. The following questions arise:

(1) Was the silicosis caused by Mr Hawchar's work at Dasreef?

(2) Was the scleroderma caused by that work?

(3) Did the silicosis, or other pathological condition of the lungs caused by dust, cause or materially contribute to the development of the scleroderma?

(4) Did the injuries result from a breach of duty by Dasreef?

(5) What is a proper sum to award as damages for silicosis?

(6) What is the appropriate order to make in respect of the claim for damages for sceleroderma?

Mr Hawchar

26. Mr Hawchar is not fluent in the English language and much of his evidence was confusing and difficult to understand. I nevertheless formed the opinion that, with one exception, prior exposure to sandstone dust, he was attempting to tell the truth. Such other inconsistencies as appear in his evidence arise because the nature of his duties changed over the course of his employment, or he did not entirely understand the questions. With one exception, where his evidence differs from that of Mr Hayek, I prefer the evidence of Mr Hawchar, because it is corroborated in material respects by the evidence of independent witnesses.

27. Mr Hawchar was born in the village of Asoun in Lebanon on 1 March 1971 and educated until the age of 18 when he completed high school. Although he enrolled in university he did not attend. He said that, other than working without pay in his family orchard, he was unemployed until about 1991 or 1992 when he commenced teaching at a primary school. He did this for about three years and was again unemployed before migrating to Australia in 1996.

28. In cross-examination, Mr Hawchar admitted that an uncle of his conducted a stone masonry business in Asoun, although he denied working as a stonemason in that business. He denied telling Mr Hayek, one of the proprietors of Dasreef, that he worked as a stonemason for his uncle before coming to Australia. He also denied that he told Dr Leon Le Leu that he had worked for his brother in stone masonry work for one or two days a week in Lebanon and that his brother used a large saw for cutting stone.

29. In his affidavit Mr Hawchar said that he started working with Dasreef on 21 October 1999 and usually worked five or six days per week commencing work at 7 a.m. and finishing at 3:30 p.m. He started work at the beginning of each day at the yard at Richmond Street at Flemington. Large slabs of sandstone were brought to the yard by truck. Mr Hawchar’s task was to take a grinder to where the slabs were stored and cut them into smaller pieces. These pieces were then taken to the water saw where they were cut into still smaller pieces, or their edges trimmed.

30. The stones were cut initially by the angle grinder, which incised a 3-5mm deep groove on the surface of the stone. A bolster was applied with a hammer to cleave the stone along the line of the groove.

31. This work in the yard would take about one hour each morning, although sometimes it continued throughout the day with usually two men, on occasions three men, performing similar cutting work in close proximity to Mr Hawchar.

32. Mr Hawchar estimates that he did cutting work on sandstone in the yard for at least eight hours each week.

33. Most of Mr Hawchar's work was away from the yard on-site. Although the stones on site were generally pre-cut, about 30 per cent of them needed further cutting or grinding. On some sites the percentage was much less than this, on some sites much more. When working on the construction of a "crazy" wall or floor, where each piece was deliberately of a different size, he would use the grinder throughout the day.

34. Mr Hawchar said that although there were three to four men working on each site, it was he who did most of the cutting.

35. Although he was supplied with a mask, the mask did not form a proper fit over his mouth and the dust would get through the sides and into his mouth and nose. He wore the mask, as instructed, only when he was operating the angle grinder. He was not instructed to wear it at other times.

36. In cross-examination, Mr Hawchar agreed that some cutting was done without the angle grinder but simply with a bolster and hammer. He also said that before 2003 or 2004 there was a lot of work done in the yard, and it was then that he, and sometimes others, would cut stone all day in the yard on perhaps one or two days each week.

37. In addition to his work with sandstone in the employment of Dasreef, Mr Hawchar cut and laid sandstone at his own home, at his sister's house, and pursuant to occasional part-time work on weekends for private customers. In this work he also used an angle grinder, although he also wore a mask while grinding.

38. In various statements to doctors and others, Mr Hawchar described working in a plastic tent supplied by his employer to reduce neighbourhood pollution. In giving evidence he readily conceded that this tent was used on only two or three occasions. I am at a loss to understand how it is that the tent figured so largely in his history before the trial. No mention of the tent was made in the history given by Mr Hawchar to the case manager of the Dust Diseases Board or to Dr Englert. Perhaps there has been some misunderstanding or perhaps it was an exaggeration on his part. I do not think it necessary to decide the point because of my conclusion that even without the presence of a tent, Mr Hawchar was exposed to excessive concentrations of silica dust.

Mr Bilal Mohammed Yousef

39. Between 2002 and 2005, Mr Yousef worked with Mr Hawchar, both on-site and in the yard. Mr Yousef said that Mr Hawchar's main job was cutting and preparing the stone both on-site and in the yard, and that this work occupied him for between four and six hours each day.

Mr Ralph Buono

40. Mr Ralph Buono is the owner of factory premises in Richmond Rd adjoining the Dasreef yard. Mr Buono said that from the time he occupied the factory in about 2000, on three or four occasions each week, for about four hours each time, visible clouds of dust were generated by stone cutting in the Dasreef yard. This dust coated the cars parked at his premises, and affected his staff and his machinery. He saw that the dust was generated by the use of angle grinders and other saws.

41. On three separate occasions Mr Buono complained to the council about this nuisance and eventually the cutting was reduced to maybe once or twice a week, the dust problem then being greatly reduced. That reduction is consistent with Mr Hawchar's evidence that it was before 2003 or 2004 that a lot of cutting work was done in the yard, and that this cutting involved the use of an angle grinder, and evidence from a principal of Dasreef that the use of the angle grinder in the yard ceased in 2005.

Dr Le Leu

42. Dr Le Leu gave evidence on one issue only. Dr Le Leu, a specialist physician, examined Mr Hawchar in July 2005 for CGU. The history he recorded included this passage:

Note that when he was in Lebanon he used to help his brother, also a stonemason, on two days a week. However, he was not cutting. His brother had a big floor saw, a handsaw. There was no grinder. He says there was not much dust around. He may have helped his brother for one year, but just in the summer after stopping university. (He was at university for two years.)

43. Mr Hayek is a principal of Dasreef. He trained as a stonemason with his father in Lebanon and came to Australia in 1989 at the age of 19. In 1991 he established the business of Dasreef with his partner, Tony Taouk. In 1999, when Mr Hawchar commenced, the business employed six or seven persons, usually two professional tradesmen and four labourers, and occupied a yard at 14 Richmond Rd Homebush where stone was stored and cut.

44. Most of the stonework undertaken by Dasreef was on domestic building and renovation sites in wealthy Sydney suburbs. The average job took about four to six weeks to complete. The work involved laying sandstone pavers and flagging stones, facing walls with sandstone blocks, and building stone retaining walls.

45. The company used about 85 per cent new stone purchased from Gosford Quarries, and about 15 per cent second-hand stone, purchased from demolition contractors, or available on the site of renovations.

46. The amount of cutting involved in the work on new stone depended upon whether the stone required was purchased pre-cut from Gosford Quarries for delivery to the site, or whether a job lot of sandstone was purchased on advantageous terms from Gosford Quarries, delivered to the yard, cut there, and then transported to the job site.

47. The amount of additional cutting on pre-cut sandstone was essentially limited to creating curved paving, cutting capping stones on walls, and cutting those stones placed at the boundaries of paving or walls.

48. Second-hand stone required far more cutting, with some stones requiring cutting on all four sides. It is for this reason that Mr Hayek preferred using new stone.

49. During the period of Mr Hawchar's employment, Dasreef owned two hand-operated wet saws, and five or six angle grinders used for cutting. Because the wet saw was big and heavy it could not perform accurate cuts, with nice sharp edges. Accurate cutting required use of the angle grinder.

50. On some sites there was very little cutting required. On other sites a worker may be engaged in continuous cutting for five or six days. On those occasions the angle grinder would be actually cutting for approximately 30 to 40 minutes, the balance of the time being occupied with resting, measuring, marking, and work with a bolster and hammer.

51. Although Mr Hayek denied that it was usual for one person to be assigned exclusively to cutting duties, in this respect I prefer the evidence of Mr Hawchar and Mr Yousef. The evidence of Mr Hawchar and Mr Yousef is consistent with other evidence from Mr Hayek that usually three or four men would be on each job, and that neither the qualified stonemason nor the labourers would cut the stones. After 12 to 18 months of employment Mr Hawchar was promoted to work as a stone cutter.

52. Mr Hayek said that a wet table saw and angle grinders were used at the Flemington yard to cut stone in circumstances where there was no room to cut on site. He did say that, very rarely, "probably once a year", he left one or two men at the yard cutting stone. This evidence cannot stand with that of Mr Buono, whom I accept as a disinterested witness of truth.

53. Mr Hayek conceded that in 2001, 2003 and 2005 Strathfield Council directed Dasreef to cease cutting stone in the yard because the work created considerable nuisance dust, and that this dust came from angle grinders. He said that "when you're cutting, you’re cutting a lot". Mr Hayek said that, in response to the complaints, Dasreef did cease all cutting with angle grinders in the yard.

54. Mr Hayek gave evidence that in the course of a conversation in about 2002, Mr Hawchar said that he had worked with his uncle in a stonemasonry business in Lebanon. Although Mr Hawchar denied this conversation, I accept the evidence of Mr Hayek on this matter because it is corroborated by that of Dr Le Leu.

Findings on exposure

55. Before coming to Australia, Mr Hawchar worked part-time with stonemasons for a period of one year. In this work he was exposed to the inhalation of respirable silica generated from work by hand tools upon sandstone.

56. Between 1999 and 2005 Mr Hawchar was exposed to the inhalation of respirable silica particles in the employment of Dasreef. He spent most of each day cutting and dressing sandstone with either a hammer and bolster, or an angle grinder. He frequently worked on five consecutive days cutting with an angle grinder. On each of those days the cumulative time operating the angle grinder exceeded 30 minutes. On many occasions he worked in close proximity to other men operating angle grinders. Mr Hawchar wore a mask supplied by his employer when he was operating an angle grinder but not otherwise.

57. Between 2002 and 2005 Mr Hawchar was occasionally exposed to the inhalation of respirable silica particles on weekends when he dressed sandstone with angle grinders and chisels in the course of private work.

58. Having regard to the duration and concentrations of exposure, I assess the relative contributions to Mr Hawchar's total silica burden as one part the Lebanon exposure, two parts the exposure in the course of his private work, and 20 parts the exposure in the employment of Dasreef.

Expert evidence

59. Mr Parker SC raised over 70 objections to the plaintiff’s expert evidence given in this case. The basis of those objections were variously that the opinions were not wholly or substantially based on the expert’s training, study or experience, that the opinions did not satisfy the conditions laid down in Makita (Australia) Pty Ltd v Sprowles (2001) 52 NSWLR 705, and that the experts purported to express legal opinions. Rather than address the merit of each objection, I have recited the qualifications of each expert and attempted to summarise in each case his reasoning process.

Dr Kenneth Basden

60. Dr Basden graduated as a Bachelor of Science in Applied Chemistry from the University of New South Wales in 1954. In 1960 he was awarded his PhD. He is a founding member and fellow of the Clean Air Society of Australia and New Zealand and a fellow of the American Industrial Hygiene Association. He is an associate member of the American Conference of Governmental Industrial Hygienists and of the Australian Institute of Occupational Hygienists.

61. Between 1954 and 1987, Dr Basden lectured in Mining Engineering and related topics at the University of New South Wales. He established a dust laboratory, and taught subjects which included "Mining Hygiene and Dust Control" and "Practical Aspects of Air Pollution Measurement and Control". His many publications include "Air Pollution Measurement and Control", "Measurement of Fugitive Particulate Emissions from Mining Operations”, "Air Pollution Guide-Particulate Matter", "International Standards and Legislation on Dusts", "Characterisation of Fugitive Particulate Emissions from Industrial Sites", "Monitoring of Fugitive Dust From Industrial Sites” and "The Rapid Measurement of Airborne Particulate Concentrations and Applications to Evaluation of Source Emission Factors".

62. Dr Basden has supervised candidates for Masters degrees in studies that include The Physical Characterisation of Ambient Atmospheric Particulates, and The Generation and Properties of Airborne Particulate Matter from Industrial Grinding Operations.

63. From 1987 until the present time, as an Engineering and Environmental Consultant, Dr Basden has conducted many field and laboratory investigations into air pollution, and workplace atmospheric contamination. He is experienced in the measurement of respirable dust concentrations, and familiar with Australian/New Zealand Standard 1715 entitled "Selection, use and maintenance of respiratory protective devices".

64. The deleterious effects of the inhalation of dusts containing free silica have been known for many years. Sandstones of the Sydney region contain almost 100 per cent free silica, and in consequence, cutting, sawing, chipping and grinding of this stone has produced many silicosis casualties over the years.

65. The Australian National Health and Medical Research Council from about the 1960s adopted the guidelines of the American Conference of Governmental Industrial Hygienists which limited the "permissible concentration" for airborne dusts containing more than 50 per cent silica at 5 million particles per cubic foot of respirable particles of between 0.5µm, and 10µm, in diameter. In 1996 WorkSafe Australia adopted 0.2 mg/m³ as the maximum time weighted average (TWA) to which a person may be exposed in industry. This is the average airborne concentration calculated over a normal eight-hour working day for five working days. (The evidence does not spell this out, but I assume that this standard relates to particles of respirable size.)

66. Australian/New Zealand Standard 1715 is directed towards precautions necessary to achieve reduction of inspired particles to below harmful levels. The standard states that as a general principle "No person should be exposed without suitable protection to an atmosphere that is or may be injurious to health", and that "If efforts to prevent or control the hazard at the source are unsuccessful, suitable respirators should be provided and used".

67. The standard requires that a person exposed to an atmosphere containing excessive concentrations of harmful dust be provided with a respirator capable of filtering those particles to concentrations below the acceptable standard.

68. Pursuant to the standard, respirators are denoted as P1, P2, and P3, indicating increasing efficiencies of filtration. In general terms, P1 respirators reduce the concentration of respirable particles by a factor of 10, P2 by a factor of 50 and P3 by a factor of 100.

69. The necessary protection factor in a given environment is defined as the ratio between the concentration of the contaminant outside the respirator to the concentration inside the respirator, ie breathed by the wearer.

70. The standard states that: "The required minimum protection factor for any given situation is that factor necessary to reduce the exposure of the wearer to below an accepted level or exposure standard or to minimise the potential exposure."

71. The protection factor and required minimum are expressed in the following equations:

72. In accordance with this standard the concentration of airborne particulates inhaled by Mr Hawchar from inside his mask should not exceed the proclaimed concentration standard of 0.2 mg/m³ of respirable particles. Dr Basden says that the actual dust concentrations generated in Mr Hawchar's breathing zone generated by the cutting wheel of the angle grinder "Most certainly would not be from half to two ten-thousands of a gram per cubic metre of air, but more realistically would be of the order of a thousand or more times these values [0.2g] or even approaching one gram, or thereabouts, per cubic metre."

73. Dr Basden says that the minimum protection factor required by the standard in order to protect Mr Hawchar was well in excess of 100 plus, and could realistically approach 1000, and that the only suitable type of respirator would be a Powered Air Purifying Respirator fitted with a PAPR-P3 filter. He says that there are a many such respirators available in Australia.

74. In cross-examination Mr Parker SC for Dasreef established that while Dr Basden had experience in measuring the atmospheric concentration and respirable fractions of a number of dusts, he has not measured the respirable fraction of dry ground sandstone. He has measured respirable concentrations of dust in the vicinity of wet cutting of sandstone and of silica on construction sites. On one occasion he observed the dust generated by the application of the grinding wheel to sandstone, and he has seen a video of this process tendered in evidence by the defendant. He said that from his experience in observation and measurement he was able to form an opinion based on those observations alone, within general parameters.

75. Mr Parker further elicited from Dr Basden admissions that he could not express a numerical opinion about Mr Hawchar's exposure to respirable silica, that he could not express an opinion about the amount of dust that Mr Hawchar would have inhaled during his time with Dasreef and could not express a numerical opinion about the time-weighted average of Mr Hawchar's exposure to silica.

76. These admissions are to be seen in the context of these further questions:

MR PARKER

Q.Dr Basden, you are not in a position to say based on specialised knowledge based on your study, training or experience what the concentration of respirable silica would have been in Mr Hawchar's breathing zone when it was cutting stone with an angle grinder at Dasreef?

A. That's correct.

Q. You would not claim, would you, to be able to express an opinion based on specialised knowledge that you have as a result of your study, training and experience, that the existence of a visible dust cloud when one cuts with an angle grinder enables one to quantify the amount of respirable silica in the air in that cloud?

A. That's correct, the actual figure couldn't be given.

Q. Did you say "couldn't be given", the actual figure?

A. The actual figure.

HIS HONOUR

Q. Could a range be given?

A. It'd be difficult to say, your honour, precisely. I mean there's a lot of dust and a visible cloud and it has a long probability spread part of which of cause is going to be in the respirable size [range] but as for amounts, no, without actually taking measurements it would be difficult to quantify exactly.

77. After these exchanges, when asked upon what basis did he express the opinion that the dust in Mr Hawchar's breathing zone was in the order of a thousand or more times that permitted by the standard as a time weighted average, Dr Basden said:

Well, general knowledge of being in this area of dust for quite some time, your Honour, being used to the amounts of dust when seen on a microscope slide when dispersed in the air, what the clouds look like, the 0.10 milligrams of dust is not a very big amount. I’ve written some reports which actually have a photograph of 10 mg on a microscope slide sitting on the balance showing it is 10 mg that's there. It's a very, very small amount and that dispersed in one cubic metre of air would be virtually invisible but would show up in a very large room, but therefore when there are clouds of visible dust within an area of a metre or so of the source the concentrations are going to be very high.

78. Dr Basden also gave this evidence in re-examination:

MR BARTLEY
Q. Having viewed what you see on the DVD and assuming that it was using a grinder of that type that the plaintiff was involved in, what effect, either by strengthening or weakening your opinion about the view that the actual dust concentrations that Mr Hawchar was exposed to would have been in the order of a thousand or more times these values, what does the viewing of that do to your opinion?

A. I'd leave it exactly the same, unaltered.

79. The video watched by Dr Basden is in evidence. At 15 minutes 39 seconds it demonstrated that the visible cloud of dust generated by the angle grinder enveloped the head of the worker.

80. Dr Basden's position is made abundantly clear in later evidence:

MR PARKER

Q. You have expressed an opinion, a numerical opinion, as to the amount of dust of respirable silica in Mr Hawchar’s breathing zone, have you. A---In this statement here.

Q. Yes. . A---Yes, that's right.

Q. By that statement are you or are you not expressing an opinion as to what numerically you think the concentration of respirable dust in Mr Hawchar’s breathing zone would have been when he undertook the task that you saw depicted in the photograph. A---I couldn’t give a precise figure, that's only just a general ballpark estimate type of figure because you wouldn’t get a precise figure unless an actual measurement were made with the instruments.

Q. You were expressing the opinion that the level of dust in that cloud of dust produced by the grinder during the time that the grinder was operating would have greatly exceeded the level of point 2 milligrams per cubic metre. A---Yes.

Q. But you were not seeking to be precise as to whether it would have exceeded it by five times or 500 times. A---More like 500 or a thousand times is what I stated there. There would have been in those clouds that I witnessed at that time something of the order of a fraction of a gram, point something of a gram, not point 0-something or other, or point double 00-something of a gram.

Q. I do not understand that that particular statement that you have made about it ranging between 500 times or a thousand times. A---There again, it's only a ballpark to justify the reason I was recommending the protection factor of about a thousand for the use of a VAPR respirator. That was the purpose of it.

Q. That figure or that range of figures or that ballpark figure, as I think you have described it. A---Yes.

Q. That figure, I think we have established, is not based on any comparison with any measurements that you have undertaken of respirable silica, correct?

Q. Yes. A---I have undertaken work in the past to determine the amount of dust and clouds in the air over lots of situations and it's just the sort of opinions that I have come up with. I’ve measured dust clouds from time to time and weighed the filters afterwards.

81. Concessions by Dr Basden that the atmospheric concentration of silica particles to which Mr Hartcher was exposed "could be" less than 1000 times the prescribed concentration constitute no more than an admission that he may, possibly, be wrong in his judgment that the concentration was, more probably than not, "realistically…in the order of a thousand or more times these values [0.2 mg/m³] or even approaching 1 gram or thereabouts, per cubic metre”.

82. A simple calculation may be made upon the basis of Mr Hayek's evidence that a man engaged in cutting stone through the course of one day would use the angle grinder for approximately 30 to 40 minutes, and Dr Basden's opinion that during this time he would be exposed to dust concentrations at least 1000 times greater than the permissible limit of 0.2 mg/m³ per cubic metre. Accepting for the moment that the P2 mask provided to Mr Hawchar fitted perfectly and provided a protection factor of 50, the concentration of respirable particles within the respirator when cutting was 1000 ÷ 50 × 0.2mg/m³ = 4 mg/m³.

83. The standard TWA of 0.2mg/m³ permits the accumulation of 40 hours × 0.2mg/m³ = 8mg/m³. If a man is exposed for 30 minutes on each of five days to a concentration of 4mg/m³ his cumulative weekly exposure is 2.5 hours × 4 mg/m³ =10 mg/m³. The TWA of this exposure over 40 hours is then 10 mg/m³ ÷ 40 = 0.25mg/m³. This exceeds the permissible limit. If he were exposed for 40 minutes each day his TWA rises to 0.33 mg/m³.

84. This exercise assumes that the atmospheric concentrations of respirable silica completely disappear the instant the grinder is turned off, and that no other grinders were being used by men working beside him. Dr Basden, who has conducted studies on the dispersion rate of respirable silica particles, said that the finer particles, below 10µm, (the respirable fraction) remain almost permanently suspended in the air until removed by contact with a solid surface or by rain. On windless days the respirable particles remained in and about Mr Hawchar's breathing zone to be inhaled by him without the protection of the P2 mask that he wore, as instructed, only when cutting. Mr Buono has described the clouds of dust that, for several hours, surrounded the men cutting sandstone in Dasreef's yard.

85. Further, the additional activities of cutting, splitting and dressing sandstone with a hammer and bolster also generated dust that does not feature in the calculation. The first study that showed a relationship between scleroderma and silica, by a Dr Bramwell in Scotland early in the 20th century, related to stonemasons working on stone with hammers and chisels but without respirators. Dr Helen Englert, the defendant's expert, when asked whether persons working with hammers and chisels on sandstone without respirators were at risk, replied "Absolutely".

86. The video to which I earlier referred, at five minutes 39 seconds, demonstrated that visible dust was liberated by the application of a hammer and bolster to sandstone placed within 50 cm of the worker’s nose and mouth. This video, filmed for, and tendered by, the defendant, confirmed that masks were worn when cutting stone with an angle grinder, but not when using a hammer and bolster.

87. Of greatest significance is the fact that Mr Hawchar suffers from silicosis. The Dust Diseases Tribunal is a specialist jurisdiction and I am permitted to take into account my experience that this disease is usually caused by very high levels of silica exposure (JLT Scaffolding International Pty Ltd (In Liq) v Silva, New South Wales Court of Appeal, 30 March 1994, unreported).

88. Dasreef has admitted that it qualified Mr Alan Rogers, an occupational hygienist, for the purpose of giving evidence in this case. He is not called. I draw the inference that his evidence would not advance the defendant's case that, in the absence of measurement, no conclusion may be made as to the probable concentration of respirable silica dust in the breathing zone of a person cutting sandstone with an angle grinder.

Findings on expert evidence

89. Mr Hawchar, when using an angle grinder in the employment of Dasreef, was frequently exposed to high concentrations of dust, which exceeded the maximum time weighted average of 0.2 mg/m³ for one week mandated by the WorkSafe Australia standard. He was also, when cutting with a hammer and bolster without wearing a mask, or in the vicinity of persons cutting with hand tools or angle grinders, exposed to sufficient concentrations of dust to create the risk of contracting a silica-related disease.

90. The P2 mask provided by Dasreef to Mr Hawchar was adequate to protect him from silica inhalation when cutting with a hammer and bolster. On the evidence of Dr Englert, stonemasons were at risk of contracting silica-related diseases if such a mask was not worn while performing this work.

91. The P2 mask was inadequate to protect Mr Hawchar from silica inhalation when working with an angle grinder. A suitable mask, a Powered Air Purifying Respirator fitted with a PAPR-P3 filter was reasonably available for purchase by Dasreef.

The Medical Evidence

Was the silicosis caused by Mr Hawchar's work at Dasreef?

92. Silicosis is a diffuse pulmonary fibrosis caused by the inhalation of excessive quantities of silica-containing dust. The sole cause of silicosis is the inhalation of excessive quantities of silica particles. Dasreef admits that Mr Hawchar suffers from silicosis. There is no suggestion that Mr Hawchar was exposed to silica particles other than in Lebanon, in the employment of Dasreef, and in his private building work. His disease has been caused by the cumulative effect of all three sources.

93. Professor Henderson says that short latency intervals are unusual, but not unknown, and that latency intervals of about 5-10 years characterise accelerated silicosis, suggesting that Mr Hawchar's silica exposure was intense. Professor Henderson atttributes Mr Hawchar’s silicosis to a history of exposure to silica dust over a period of six years beginning in 1999.

94. It is now apparent that the exposure in Lebanon is also a contributory cause, although, being far less intense, I believe it to be a minor cause.

Findings on silicosis

95. Silicosis is a divisible disease. In accordance with my earlier findings as to relative concentrations of exposure, I find that as to 20 parts in 23 the silicosis was caused by Mr Hawchar's work at Dasreef.

Was the scleroderma caused by the work at Dasreef?

96. Scleroderma is a disease of the immune system that results in increased deposition of fibrous tissue in the skin. This causes tightening of the skin, stiffening of the joints, and gradual wasting of the muscles. The pathology may be systemic and involve the gastrointestinal tract, and the small blood vessels with resultant ischaemic manifestations (Raynaud's phenomenon). It is common ground that Mr Hawchar suffers from each of these manifestations. In such cases the disease is called Progressive Systemic Sclerosis (PSS).

97. There is universal agreement among the doctors who have given evidence in this case that silica is a causal determinant of PSS in a population. Mr Hawchar relies upon the opinions of Professor Douglas Henderson, Dr Harry Patapanian, Dr Anthony Frankel, and Dr Ali El Jaam, that in his particular case, the disease was caused by silica particles released from the sandstone upon which he worked. The defendant relies upon the sole opinion of Dr Helen Englert, not that Mr Hawchar's disease was not caused by his work at Dasreef, but that "it is not possible to say in any scientific way" that it was.

Professor Douglas Henderson

98. Mr Parker SC for Dasreef submits that the opinions of Professor Henderson are not opinions based on specialised knowledge within the meaning of s79 of the Evidence Act 1995 because the opinions are not based on Professor Henderson's training, study or experience. I do not accept this submission.

99. Pathology is that science which deals with the causes of, and changes produced in the body by, disease. Professor Henderson has held the chair of Professor of Pathology at the Flinders University of South Australia since 1994. He has by himself and in conjunction with others, published over 300 books, monographs, papers and letters on pathological topics including silicosis. Titles include Diagnosis of Non Neoplastic Lung Disease by Ultrastructure, The Morphogenesis and Classification of Diffuse Interstitial Lung Diseases, and Pathology of Non Neoplastic Disorders of the Respiratory System.

100. Professor Henderson has been a member of the editorial boards of various international medical journals including Ultrastructural Pathology (based in New York), the Journal of Pathology (United Kingdom) and the Journal of Submicroscopic Cytology and Pathology (based in Bologna, Italy). Cytology is the study of changes at cellular level caused by disease. His evidence in the present case draws upon his training, study and experience over 40 years in this particular field.

101. Professor Henderson's evidence also draws upon his training, study and experience relating to epidemiological evidence. He concedes that he is not a professional epidemiologist, and that the detailed analysis and design of epidemiological studies lies outside his real areas of expertise. Nevertheless, in collaboration with expert epidemiologists, he has reviewed many epidemiological studies related to lung diseases, and has co-authored articles in peer reviewed journals, which articles include epidemiological content. He has also personally reviewed epidemiological data before submitting the review to a co-author who is an expert epidemiologist for comment, correction and discussion. He states that he is able to read an epidemiological study and, taking into account the cogency and design of that study, detect flaws that lie within it. He is also able to assess the coherence of the evidence across multiple epidemiological studies.

102. In Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 282 at 287, Spigelman CJ said: "I have no difficulty with a medical practitioner drawing on and assessing epidemiological studies."

103. I am satisfied that, on the basis of his study of many epidemiological reports, the training he has received in discussion with epidemiologists, and his experience in evaluating the probative value of particular epidemiological findings, Professor Henderson has acquired sufficient specialised knowledge to form and express an opinion as to the reliability and cogency of the epidemiological studies upon which he relies.

104. Professor Henderson relates Mr Hawchar's disease of scleroderma to silica exposure for, in summary, these reasons:

(1) Mr Hawchar was extensively exposed to silica dust for a period of about six years beginning in 1999.

(2) Medical literature contains many individual case reports of an association between the inhalation of silica dust and the development of scleroderma

(3) Epidemiological studies confirm that association.

(4) A causal relationship is biologically plausible. Scleroderma is an autoimmune disease. A causal relationship between inhaled silica and disruption of the immune system has been demonstrated in human subjects where silicosis is present, and experimental studies on mice have found that silica inhalation accelerated the predisposition of these mice to develop auto immune disease.

(5) Mr Hawchar suffers from silicosis. Studies in Germany have found that the probability of developing scleroderma is 110 times higher for patients with silicosis than for the normal male population.

105. Mr Parker for the defendant suggested to Professor Henderson that, because no epidemiological study establishes a dose response, Mr Hawchar cannot establish that his inhalation of silica dust in the defendant's employment was sufficient to cause his disease.

106. In rejecting this contention, Professor Henderson said that although the epidemiological studies have not defined dose relationships in numerical terms, the risk appears to be related to the intensity of cumulative exposure, and that if the exposure in a particular case is well above background it is unnecessary to quantify that exposure numerically to attribute the disease to the exposure. He gave this evidence:

One can say on the basis of epidemiological studies that where there has been intense above background exposure, especially if there is silicosis, that there is a strong causal - there is a strong statistical relationship between the two, and that one can draw causal inferences from the consistency of that strong statistical association.

107. In cases in which the disease occurs after several discrete exposures to silica dust, Professor Henderson attributes the presentation of the disease to the sum of the cumulative exposures because: "You cannot fractionate, all you can say is that it is attributable to the total cumulative exposure".

Professor Henderson then gave this evidence:

I would agree then in the absence of dose response data, when there are multiple episodes of exposure I cannot attribute or exculpate any one particular exposure. All I would say is that the man has had above background significant silica exposure and that is the factor which has been identified in multiple epidemiological studies as a causal contributory factor for scleroderma. But one cannot, - this is a very broad brush non numerical approach.

108. Dr Patapanian is a Consultant Physician and Rheumatologist. He relates Mr Hawchar's PSS to his work because, and I summarise:

(1) He has a history of very significant silica exposure.

(2) Epidemiological studies establish silica as a causal determinant of the disease.

(3) Mr Hawchar exhibits all the classical phenotypic features which are referred to in the epidemiological literature that relate the scleroderma to silica exposure, including the particular antibody pattern and antibody response.

(4) Mr Hawchar has silicosis and scleroderma, two diseases which are very rare in the general population, both of which share a similar aetiology from the viewpoint of epidemiological studies. The incidence of scleroderma in the general male population is around 1 in 10,000.

(5) The epidemiological literature relates the manifestation of scleroderma more closely to dose rather than duration. Silicosis is an indication of dose, because the majority of people who are exposed to silica do not get get pulmonary silicosis.

109. Mr Parker's contention that, without reference to epidemiological studies that are directly comparable to Mr Hawchar's exposure, no conclusion as to causation was possible, was addressed in the following evidence:

MR PARKER:

Q. So far as you are aware the dose response relationship, if any, between silica exposure and scleroderma has not been defined by any epidemiological study. A---I’m not sure if it's been quantified but reference has been made to the fact that because, in general, it's considered that a high inhalation or burden results in silicosis and the silicosis patients exposed to silica are at increased risk of scleroderma in comparison with their work mates who don’t have silicosis there is, I understand – and I qualify my response that I’m not a thoracic physician – but there is a dose response relationship from the viewpoint of silicosis that they’re the patients who are more likely than their non silicosis colleagues to develop scleroderma. That's the only relationship that I could come to but not in terms of the actual quantification of exposure. I can't recall that.

………

Q. So that you would agree with me that if the cases described in the epidemiological studies had much higher exposure to silica than Mr Hawchar did, then you could not draw any proper conclusion from those studies about causation in Mr Hawchar’s individual case. A---I don’t think that would exclude it.

….

Q. Could you explain to us how, if you have a study which shows an association among cases who have much higher levels of exposure than Mr Hawchar that allows you to draw any valid scientific inference as to what the cause was in his individual case. A---Purely on the base of the epidemiological studies with non quantifiable risk and exposure to silica, that's all.

…………

Q. Did you attempt to analyse the studies and to ask yourself whether they were comparable to Mr Hawchar’s circumstances. A---No, I didn't. From the history that I took from Mr Hawchar, from what he described to me, I thought he’d had very significant silica exposure and the majority of the epidemiological studies that I read, there was no reference to quantification. There is the problem of the lag time, and I can’t explain that, the latency interval, that he doesn’t fall into the typical latency interval, which as you indicated is decadal, but there are cases which, in very high exposure, the diseases, silicosis, in particular, has occurred more quickly.

Q. But those are only individual cases. A---That's right.

Q. They do not allow any generalised medical conclusion to be drawn from that, do they. A---We depend on case reports when we are confronted with difficult clinical problems for which there is no other clinical precedent on which to base our formulation of disease and how to approach treatment. For example, if somebody is particularly ill with a very rare disease on which there has been no controlled prospective study from treatment, and we feel that that patient needs treatment, we have to go to case reports and we cite case reports and the outcome of those case reports as the basis to conclude that that’s a reasonable approach to take.

….

Q. Did you not tell me a little while ago that you could not tell by looking at Mr Hawchar’s physical characteristics or the particular disease that he had, what the cause of that was in terms of silica exposure or not. A---Well he’s got silicosis so that’s easy. He has got florid silicosis of his lungs.

Q. But that tells us that he has got exposure to silica, it does not tell us that that exposure or some other exposure to silica is the cause of his scleroderma. A---But if on the basis of our epidemiological studies which we've been discussing, that silicosis is related to silica exposure, and that the workers who are exposed to silica and who develop scleroderma are more likely to have silicosis, he has got two diseases which are very rare in the general population, and they both share a similar aetiology from the viewpoint of epidemiological studies. So I though it was a reasonable conclusion to arrive at on clinical grounds.

Q. Sorry to repeat things but I am going to just put this to you again and can you please either agree or disagree. It is not possible to tell from looking at Mr Hawchar or the way his disease has manifested itself whether his particular condition of scleroderma is caused by silica or something else. A---I would agree.

Q. That being so the only proper basis for expressing an opinion as to the causation of his condition in his case is to try to reason from epidemiological evidence. A---As well as his silicosis.

Q. Do you agree with me or not. A---No. I disagree. I mean he's got silicosis, he's got pulmonary silicosis which is evidence of an unusual reaction to an environmental stimulus to which he has been exposed and we know that the minority of people who are exposed to silica get pulmonary silicosis so he is in that group anyway and we know from - I don't have any other patients with scleroderma in 20 years of my practice who have silicosis. He is the only patient that I have who has pulmonary silicosis and scleroderma so I can't agree with you. So there are clinical factors in Mr Hawchar's case which clearly distinguish him from other patients in my practice.

….

Q. You did not attempt to carry out an investigation into whether the exposure circumstances of the people - of the cases referred to in the epidemiological studies on which you say you relied were or were not comparable to Mr Hawchar's exposure circumstances, true or false. A---True.

Q. Would you agree with me therefore that to the extent that you have sought to rely upon the exposure circumstances disclosed in those epidemiological studies and to apply them to Mr Hawchar your reasoning is missing a step and is invalid. A---No.

……………

Q. When you say - what I wanted to put to you was when you used the word significant you are not in a position to relate that word to any particular epidemiological study. A---In terms of quantitative, no.

……

Q. In conclusion, you cannot say that it was significant in an epidemiological sense, can you, that is Mr Hawchar's exposure. A---I disagree. I think he did have significant exposure.

110. Dr Frankel is a Consultant Respiratory Physician to whom Mr Hawchar was referred by Dr Patapanian. Dr Frankel believes that Mr Hawchar's exposure has, "On the balance of probabilities" contributed to his sceleroderma. He relies upon the history of exposure, and three references, which he cites. Frazer and Pare’s Diagnosis of Diseases of the Chest (Volume IV) states that: "The association of progressive systemic sclerosis with silicosis and with exposure to high concentrations of silica dust is well established". The interim report of the Compensation Board on Scleroderma, Industrial Disease Panel report of findings No 8, Toronto March 1992 reported that: "in reaching a conclusion on this uncommon disease, the Panel is satisfied that the evidence is supportive of a causal relationship between silica exposure and scleroderma". A case reference study conducted by M Bovenzi et al confirmed the occupational role of silica in the aetiology of scleroderma.

111. Dr Frankel responded to Mr Parker's case that nothing is knowable without numbers in this evidence:

Q. My question was in terms of reasoning process. Do you agree that, given that you cannot tell the cause in Mr Hawchar’s case from any physical examination that you carried out, the only way to determine cause in his case is to seek to do so by looking at the epidemiological evidence about populations generally and seeing if that can be extrapolated or applied to his particular circumstances. A---I think it is not necessarily only epidemiological evidence, I think it is evidence that is, not evidence, it is when people who are experts in the field write about conditions that they are expressing an expert opinion because they have studied the disease, they have a number of patients with the disease and they gather a number of facts and have written a statement about that disease process. It is the same with any disease process, just coming back to lung cancer. If I examine a patient with lung cancer, I have no idea that it is associated with smoking. There is nothing generally on most people that says they are smokers. So it is taking a history which is in medicine where you get 90 per cent of our facts and can make most diagnoses just from history, and the history is going to be based on other facts that are around in coming and making our decision.

….

Q. I want to suggest to you that before you reason in that way, you would need to satisfy yourself that the silica exposure in the cases described in the studies was really comparable to the silica exposure that Mr Hawchar has. Would you agree. A---I mean, the silica exposure in the studies we may not know the exact details. We know they have been exposed to silica. There are variable time periods they have been exposed and because there are a whole number of patients in there who may have had variable exposure to silica, one can I believe only make an assumption that they have been exposed to silica, variable amounts over variable times. He has been exposed to silica over a shorter period of time and what I assume to be fairly extensive exposure in that time, and that exposure to silica in the one group has been shown to be causally related to scleroderma and in his case exposure, from my reasoning, I would assume, would be a factor in causing his scleroderma.

Q. I would like to ask about your reasoning process, or the logic of your reasoning process. Do you or do you not agree that before you can use the results of particular studies to reason in Mr Hawchar’s case, you need to be satisfied that those studies related to exposure that is in some way comparable to Mr Hawchar. A---I think one can assume that even though you can't compare them exactly, that there has been exposure in both, assuming there has been exposure, and in his case there has been exposure and one would just say from the likelihood of the probability is that it is there. One cannot say a hundred per cent definite they are the same, and we can never say a hundred per cent definite if they are not being exactly compared to each other. If that was the case, then in many things we could not say anything happens.

…….

Q. That is the point of my question. You do not know what the exposures were that were being referred to in this text book when they spoke of high concentrations of silica. Correct.

A. I don't know the exact exposure, but I would suspect that there was a significant amount of silica exposure, because they would not have used high, I presume, if it was just a tiny little amount….I would assume that a high amount of exposure means that they have been exposed to a considerable amount and if they are using the word “high” as in English high, I would assume that that’s the case.

Q. If Fraser and Pare, in talking about high concentrations, are talking about that sort of mining exposure, then any conclusion that they reached would not be translated to Mr Hawchar’s circumstances at least unless you were satisfied that his exposure really was comparable to that sort of mining exposure. Correct. A---Reading through it and reading what his exposure was, I would be comfortable that he had high exposure and that potentially they would have also had high exposure.

Q.Because you had not looked at the studies in the text book, you were in not position to understand in any quantitative or scientific sense whatsoever, what Fraser and Pare meant by high concentrations of silica dust. True. A---The exact amounts are, I do not know, but from a clinical context, I would be quite comfortable in comparing what they say is high exposure to what I know he had high exposure.

112. Dr El Jaam is Mr Hawchar’s treating general practitioner. He is also from Lebanon. His opinion that Mr Hawchar's scleroderma has been caused by his work with sandstone is based upon what he has was told by Dr Patapanian and what he read after receiving that opinion. He does not claim any specialised knowledge in the area of epidemiology but did inform himself from reading articles in the epidemiological literature. He relevantly said that: "Mainly scleroderma affects women and mainly Caucasian more than our race".

Dr Helen Englert

113. Dr Englert is a Physician and Rheumatologist with particular interests and expertise in the treatment of scleroderma and in epidemiology. She has been awarded a Doctorate of Philosophy in Medicine for her work in the latter field. She is the author and co-author of many original articles on male systemic scleroderma, and conducted a population based study on male systemic sclerosis and occupational exposure to Sydney sandstone. This study identified an odds ratio of four.

114. In December 2005 Dr Englert was asked by CGU to furnish an independent medical opinion regarding the necessity of certain treatment for Mr Hawchar's systemic scleroderma.

115. Dr Englert examined Mr Hawchar and reported to CGU on 15 December 2005. Her report records that he worked for Dasreef as a stonemason between December 1999 and May 2005, and that:

He both cut and built with stone (presumably sandstone), and sometimes mixed sand and cement. Stone was cut either by using a grinder (90% of the time) or with a saw. The latter required lifting the rock on to a saw table. It employed water and so was not very dusty. However the "stones" were too heavy to lift to this saw table and in these instances a grinder was used. The latter was very dusty and no water was used to minimise dust. He wore a white surgical mask but it was "no good" - he got sand in his mouth, between his teeth, and spat out "dirt". He also noted cement dust settling on the skin which caused pruritis until washed off.

116. Dr Englert diagnosed diffuse systemic scleroderma and wrote:

Although systemic scleroderma must be multifactorial in its aetiology, one environmental factor for which there is increasing evidence as a causal determinant is silica exposure. Mr Hawchar has had considerable exposure to silica as part of the stonemason occupation (presumably largely using sandstone which has a high silica component, and also using sand to mix the cement) and this exposure predated his scleroderma onset. Therefore in Mr Hawchar's instance, occupational silica exposure must have causally contributed to scleroderma onset." (Emphasis added).

117. Dr Englert has now changed her mind.

118. After several lengthy conferences with a solicitor and barristers acting for Dasreef, Dr Englert swore an affidavit of 20 pages which was written entirely by those lawyers, but which, she says, fairly represents her present opinion. The affidavit explains why she changed her mind in these paragraphs:

15 In the broad there were four stages to my reasoning.

15.1 I considered that the epidemiological evidence established that silica exposure was a causal determinant of scleroderma in humans.

15.2 Based on what Mr Hawchar had told me, I proceeded on the basis that he had had significant exposure to silica dust whilst employed by Dasreef.

15.3 No other agent, and no silica exposure, had been suggested as a possible cause of his scleroderma.

15.4 I thought that it followed that his silica exposure with Dasreef was the likely cause of his scleroderma, although I noted a relatively short latency.

16 Since preparing that December 2005 report, an argument consisting of the following propositions has been put to me by the lawyers acting for the defendants in this case:

16.1 Epidemiological evidence necessarily relates to causation on a population level. The conclusion that silica is a causal determinant of the sceroderma in the human population does not necessarily establish that where any particular individual has been exposed to silica and has contracted scleroderma, that the silica exposure is a universally causal determinant of that particular individual scleroderma.

16.2 A valid scientific conclusion about causation of the scleroderma in an individual by any particular exposure to silica could only be reached as a matter of mathematical probability from population based data. This would only be possible if those data defined the dose-response relationship in numerical terms.

16.3 The existing epidemiological data concerning the association between silica exposure and scleroderma does not allow the dose response relationship to be stated in numerical terms, or indeed to be defined at all, and accordingly,

(a) It is not possible to say in any scientific way that Mr Hawchar's exposure to silica, as distinct from some other agent(s), was the cause of his scleroderma; and

(b) Still less is it possible to say that, assuming the cause of Mr Hawchar's scleroderma was silica exposure, it was his exposure while employed by Dasreef, or some part of that exposure, as distinct from some other silica exposure he might have had that was a cause or contributing factor in his case.

119. In cross-examination, Dr Englert said that whereas her initial opinion expressed in the report of 15 December 2005 proceeded on the basis that Mr Hawchar had significant exposure to silica dust whilst employed by Dasreef, her revised opinion proceeded upon the assumption that this was not so.

120. Dr Englert said that she was asked by the defendant's solicitors to assume, and did assume for the purpose of expressing her present opinion, that the majority of Mr Hawchar's cutting work was undertaken using a water dampened table saw that did not create respirable dust, that he used a mask specifically designed for stonemasons, and that his exposure to silica dust during the five years of work on Dasreef sites at no time exposed him to a time weighted average concentration of silica dust in excess of the standard of 0.2 mg/m³. Further inquiries by Dr Englert led her to assume that a concentration at or below 0.2 mg/m³ was a concentration below which there was no risk to health.

121. It appears that Dr Englert's change of mind was no more than the result of a perfectly sensible conclusion that if Mr Hawchar's Dasreef exposure was de minimis, then the cause of his disease was to be found elsewhere, either in other exposures, or idiopathically. Because of the history of earlier silica exposure, and the unusually short latency period, Dr Englert tended to believe that the exposure in Lebanon was the cause to the exclusion of the exposure with Dasreef.

122. Dr Englert, resiling from her earlier opinion that "Therefore in Mr Hawchar's instance, occupational silica exposure must have causally contributed to scleroderma onset" did not go so far as to say that the employment at Dasreef was not a cause of Mr Hawchar's scleroderma.

123. In her affidavit she said this:

Had I been informed of a possible exposure to silica dust more closely proximate to the mean latency I would have expressed the opinion that that possible exposure was more likely to have been causative of Mr Hawchar's scleroderma.

… had I been informed on December 2005 that in around 2002/2003 Mr Hawchar had been exposed to silica dust while undertaking private stonemason work in Sydney not connected to his Dasreef employment I would not have expressed the unqualified opinion that I did on page 3 of the 2005 Report. That is, I would have said no more than that Mr Hawchar's employment exposure to silica dust with Dasreef could not be excluded as a cause of his scleroderma, and that equally other exposures to silica dust in Sydney not connected with Dasreef employment could not be excluded as a cause of his scleroderma. (Emphasis added)

124. In cross examination Dr Englert agreed with the proposition that if the exposure both in Lebanon and at Dasreef was excessive, it was not possible to say that neither had a causal effect because the causal contributions were not divisible. In this respect her evidence accords with that of Professor Henderson who said that "You cannot fractionate, all you can say is that it is attributable to the total cumulative exposure".

125. I am not persuaded that the opinion expressed by Dr Englert in a report of 15 December 2005, predicated upon heavy exposure in the employment of Dasreef, is vitiated by her reconsideration of the short latency period. In the course of conferring with Dasreef's lawyers Dr Englert remarked that, notwithstanding the short latency period, it was still possible to link Mr Hawchar's development of scleroderma with his exposure at Dasreef.

126. I find that Mr Hawchar's exposure to silica dust in the employment of Dasreef caused or materially contributed to his disease of Progressive Systemic Sclerosis.

Did the silicosis, or other pathological condition of the lungs caused by dust, cause or materially contribute to the development of scleroderma?

Professor Henderson

127. In a report of 10 October 2008 to Mr Hawchar's solicitors, Professor Henderson wrote:

Silicosis itself contributes to scleroderma. In a condition such as silicosis the body responds to the pathological changes in the lung by generating auto antibodies. These auto antibodies have an adjuvant effect to the development of scleroderma. Thus, the scleroderma has two causes to varying degrees. The first is the direct exposure to silica. The second is the development of silicosis with its own autoimmune implications also contributing to the scleroderma.

128. In oral evidence, Professor Henderson explained that he used the word adjuvant to indicate that the antibodies enhanced the biochemical changes which led to the development of scleroderma. He bases this opinion on pathological and epidemiological grounds.

129. The Professor said, that process by which silica particles may lead to the development of the disease was aptly described by Benvenuto Pernis in an article entitled Silica and the Immune System published in ACTA Biomed 2005; Suppl 2; 38-45. The abstract is as follows:

This Article collects the evidence that shows that the biological reactions to silica are due to the stimulation of the immune system. Both innate and adaptive immunity are involved. The following sets of events take place sequentially: (1) Silica is recognised as a PAMP (pathogen associated molecular pattern) by the receptors of innate immunity: (2) this causes the stimulation first, and then the death, of T-cells of innate immunity (the macrophages): (3) While stimulated, macrophages produce cytokines (IL-1 and TNF) that stimulate fibroblasts [connective tissue cells]; (4) The same and possibly other cytokines produced by silica-activated macrophages induce the maturation of the dendritic cells, which are the connecting elements between the innate and the adaptive (lymphoid) Immune Systems; (5) It follows a polyclonal activation of the Adaptive Immunity; (6) The end result is the formation of fibro-hyaline tissue. In view of a double involvement of the Innate and the Adaptive Immune Systems and their cooperation in the stimulation of fibrosis, Silicosis can be considered as a "Collagen" Disease, related to other diseases of that group like Rheumatoid Arthritis, Lupus erythematosus and Scleroderma. Not surprisingly the incidence of these diseases has been shown to be significantly increased in humans exposed to Silica.
Pernis summarised the process in these terms:
The whole process reflects the effort of the vertebrate immunity to eliminate what is sensed as a potential pathogen, but of course the silica particles are indestructible and the only final solution is to bury them inside collagenous tissue.

130. In evidence, Professor Henderson explained that autoimmune sequelae are known to be a feature of silicosis and they are also known to be a driving factor for the development of scleroderma. The development of fibrosis in silicosis is associated with the production of various auto antibodies including the inflammatory mediator called Interleukin-1 (IL-1) which is causally relevant to the development of scleroderma. In this manner, those aberrations of immune responsiveness, which are part of silicosis, contribute to the immune derangements responsible for deposition of similar collagen-containing tissue in the skin and other organs as part of scleroderma.

131. This explanation by Professor Henderson accords with the description by Pernis of that same mediating cytokine, IL-1, also being produced when macrophages are stimulated by silica particles, leading to the creation of fibroblasts in the development of both silicosis and scleroderma.

132. The authoritative text Harrison's Internal Medicine, 16th edition states that:

Existing evidence indicates that cell mediated immunity plays a central role in the development of fibrosis in SSc (Systemic Sclerosis (Scleroderma)). T cells, macrophages, endothelial cells, and other cells along with cytokines and growth factors interact in a complex matter to stimulate fibrosis.…

Macrophages are present in increased numbers in the infiltrates of SSc lesions, including the pulmonary alveoli. Activated macrophages secrete several important products involved in the pathogenesis of SSc including IL-1, IL-6, tumour necrosis factor (TNF α, TGF-β, and PDGF.

133. Anderegg, Saalbach & Haustein (Arch Dermatol Res (2000) 292) demonstrated in vitro that silica is able to directly activate cytokine expression. Fubini and Hubbard (Free Radical Biology and Medicine, Vol 34, number 12, pp 1507-1516, 2003) demonstrated that the generation of oxidants by crystalline silica particles, and by silica activated cells, results in cell injury, activation of cell signalling pathways, and increased expression of inflammatory cytokines.

134. It is apparent from the work of Fubini and Hubbard that the particular vice of working with sandstone is that freshly ground or fractured silica is more inflammatory and fibrogenic than aged crystal, because of the greater presence of free radicals in freshly ground material. When silica is fractured, cleavage of the silicon oxygen bond takes place and reactions at these sites create surface radicals which decay over time.

135. In addition to the learning peculiar to his specialty, Professor Henderson relies upon a paper by Haustein and Ziegler entitled Environmentally Induced Systemic Sclerosis and like Disorders, published in the International Journal of Dermatology, April 1985 Volume 24: 147-151. The authors reported that:

From epidemiological data on the incidence of scleroderma and silicosis in the German Democratic Republic, it is clear that the likelihood of developing scleroderma is 25 times higher in workplaces where there is exposure to silica. Further, the probability of developing scleroderma is 110 times higher for patients with silicosis than for the normal male population.

136. Professor Henderson says that this data is consistent with the presence of silicosis having an adjuvant or additional effect upon that pathology which may have already resulted from the immunological response to the silica particles inhaled before the development of the silicosis.

137. The opinion of Professor Henderson is encapsulated in this evidence:

My understanding is that in silicosis one is dealing with inhalation of crystalline silica particles which interact with various cells in the lungs and promote the deposition of fibrous tissue in the lungs which, in its classic forms, takes the form of multiple small nodules scattered through the lungs. That at the same time the silica particles and/or the silicosis itself is associated with aberrations of immune responsiveness and the immune derangements as part of silicosis will contribute to the fibrosis and immune derangements are also thought to be responsible for the deposition of similar collagen containing fibrous tissue in the skin and other organs as part of scleroderma.

138. Dr Englert discounts the probability that the existence of silicosis plays any part in the development of scleroderma, but she does not go so far as denying the possibility.

139. Dr Englert concedes that it is logical that the mechanism by which silica induces scleroderma is via a respiratory route. She dismisses a percutaneous route as improbable and says that the respiratory route makes sense because silica delivered via that route causes silicosis.

140. The doctor postulates that the silica particles breach the alveolar membrane, go into the lymphatic circulation, and thence into the blood vessels and circulation to distant sites where, independently of damage already caused, their presence results in scleroderma.

141. Dr Englert's views on the suggested causal sequence that Professor Henderson believes probable are contained in her answer to a long question by Mr Bartley, in which he suggested that it was artificial to suggest that the cytokines and other chemical signals released in the lung are somehow confined to those cells in the lung which in response become fibrogenic. Dr Englert replied: "That’s your hypothesis, Mr Bartley. It may be very reasonable, okay, what I'm saying and I will continue to say is that it is not proven."

142. In cross-examination, discussing the pathogenesis of scleroderma, Dr Englert many times disclaimed expertise, saying variously: "Look I'm getting out of my territory", "This is not my area of huge specialty", "That’s a hypothesis, I am getting out of my territory", "I'm getting a bit out of my territory", "Look, I'm not a histopathologist" and, "I'm getting out of my territory, really". Histology is a study of the minute structures of the tissues. This is Professor Henderson's field of expertise. For this reason I prefer the evidence of Professor Henderson.

Discussion

143. Accepting Harrison's text, existing evidence indicates that cell mediated immunity plays a central role in the development of fibrosis in scleroderma, and that cytokines released from macrophages, endothelial cells, growth factors and other cells interact in a complex manner to stimulate fibrosis.

144. According to Professor Henderson, that is the same pathological process which causes silicosis, after which the silicosis itself continues to generate further antibodies and chemical signals that interact within the immune system to further stimulate fibrosis at distant sites. Professor Henderson describes the pathology as a derangement or aberration of immune response in the lung.

145. Mr Parker argues that the process by which macrophages engulf silica particles so that they may be removed from the lung is not a pathological process, but part of the natural process by which the body's auto immune system responds to pathogens.

146. I do not accept this argument. Because of the unique structure of silica particles, the immune system is unable to cope; the macrophages are unable to engulf the pathogen, and die. Their death releases chemical signals, which not only result in fibrosis surrounding the particle, but which mediate fibrosis at the site of the scleroderma. In Mr Hawchar's case the autoimmune process has caused the dual pathology of silicosis and scleroderma. These are not natural products of the body's auto immune system.

147. Mr Parker also submits that because the diagnosis of scleroderma predated the diagnosis of silicosis, the pathology described by Professor Henderson was not causally relevant. This does not follow.

148. The abnormal immune pathology postulated by Professor Henderson occurs in the lung as a precursor to both silicosis and scleroderma. Further, silicosis is known to exist well before it is radiologically apparent.

149. It is not necessary that Mr Hawchar persuade me to the point of certainty that his silicosis materially contributed to his scleroderma (Adelaide Stevedoring Co Ltd v Forst (1940) 64 CLR 538, Ramsay v Watson (1961) 108 CLR 642, E.M.I. (Aust) Ltd v Bes [1970] 2 NSWR 238).

150. In E.M.I. (Aust) Ltd v Bes Herron CJ said at 242:

I have concluded [that] the correct principle to apply… is that it is not incumbent upon the applicant, upon whom the onus rests, to produce evidence from medical witnesses which proves to demonstration that the applicant's contention is correct. Medical science may say in an individual case 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.

151. Professor Henderson is unable to prove to demonstration that the causative effects of silicosis upon the development of scleroderma are in accordance with the sequence of events as he believes them to occur. In this respect his opinion is similar to that of the medical witness in Ramsay v Watson (supra) whose opinion the High Court held the jury was entitled to accept in relation to the causation of Bright's disease by lead poisoning. The court, (Dixon CJ, McTiernan, Kitto, Taylor and Windeyer JJ) said:

Moreover, hypertension and Brights disease could, it seems, be together the complex and interacting consequences of lead intoxication. The jury were entitled in considering this aspect to give weight to the opinion of the experienced physician skilled in the relevant branch of medicine who had examined the patient. He gave his opinion as his inference of probability rather than as a logically established certainty. But to argue in the circumstances that it offended against the rules of logic is to mistake the nature of rational inference and of intellectual persuasion as to probability in the attribution of events to causes.

152. Dasreef's solicitors qualified a rheumatologist, Dr Carr, and a thoracic physician, Professor ABX Breslin. Both examined Mr Hawchar. Neither is called. I draw the inference that neither expert would advance the defendant's case.

153. I find that, as a general proposition, silica dust can cause a pathological condition of the lungs, being a derangement or aberration of the immune system that materially contributes to the development of scleroderma. I further find that this occurred in the case of Mr Hawchar.

Did Mr Hawchar's injuries result from a breach of duty by Dasreef?

154. Because Dasreef does not rely on allegations of contributory negligence it is unnecessary that I address statutory breaches of duty.

155. Mr Hawchar's injuries of silicosis and scleroderma were reasonably foreseeable by Dasreef as possible consequences of the work upon which he was engaged. Those injuries could have been prevented by Dasreef’s providing to Mr Hawchar a suitable respirator, then reasonably available, for use when he was cutting with an angle grinder. Further, Dasreef should have warned him of the risks associated with cutting sandstone with a hammer and chisel without a mask, and required that he use the P2 mask when he did this work, or when stone cutting was performed by others in his vicinity. I find that Mr Hawchar's injuries result from Dasreef's breach of duty.

Damages for silicosis

156. General damages are at large, because s3B(1)(b) of the Civil Liability Act 2002 excludes proceedings brought in the exclusive jurisdiction of the Dust Diseases Tribunal from the provisions of that Act, (with the exception of those provisions relating to gratuitous services).

157. The plaintiff claims only general damages and future medical expenses. Future medical expenses for silicosis will be met by the Dust Diseases Board pursuant to the Workers’ Compensation (Dust Diseases) Act 1942. In any event no evidence has been given as to the likely cost. I propose to allow only general damages.

158. Silicosis is a progressive disease. Mr Hawchar complains of increasing breathlessness. He now has difficulty in walking upstairs, and has an effort tolerance of only 200-300 metres. Dr Frankel, Mr Hawchar's treating respiratory physician, finds objective evidence of deterioration. Between May 2005 and May 2007, FEV1 declined from 3.7 L to 2.8 L, and FVC declined from 5.2 L to 3.49 L. The later figures are respectively 70 per cent and 69 per cent of predicted values.

159. The effect of silicosis in the particular circumstance of Mr Hawchar is aggravated by the effect of his scleroderma, which, by tightening the skin around his chest wall, further compromises his ability to inflate his lungs. In this respect he is in a worse position than persons whose only disease is silicosis.

160. Mr Hawchar is only 38 years of age. His life expectancy on the tables is 48 years, although Dr Patapanian thinks that the disease of scleroderma may reduce this span by 20 years. Dr Frankel said in his report of 13 June 2007 that:

He has not been too disabled from a respiratory perspective, until recently. I suspect he will become progressively more breathless, relating to scleroderma and/or silicosis. I believe that he will very likely develop progressive lung disease, with lung involvement, both indirectly and directly related to silica exposure.

161. The progressive lung disease directly related to silica is of course silicosis. As this disease progresses, Mr Hawchar will become increasingly disabled. His present disabilities and sufferings related to breathlessness will continue with increasing force for a period of approximately 18 years until his premature death. The contingency that this progression will not occur, while relevant to the assessment of damages, (Malec v J C Hutton Pty Ltd (1990) 169 CLR 638), is, in Dr Frankel's opinion, very unlikely.

162. Professor ABX Breslin examined Mr Hawchar for Dasreef. He is not called to contradict the evidence of Dr Frankel.

163. I recognise that notwithstanding the decision in Planet Fisheries Pty Ltd v La Rosa (1968) 119 CLR 118, it is appropriate that awards of damages in the Tribunal be fairly consistent. Mr Parker has drawn my attention to three decisions which he suggests provide some guidance to an appropriate amount of general damages in the present case: Shaw v Amaca Pty Ltd [2008] NSWDDT 3 (general damages $100,000); John Downes v AmacaPty Ltd [2008] NSWDDT 25 (general damages $150,000); and Vartuli v Alinta LGA Ltd [2007] NSWDDT 28 (general damages $65,000).

164. The plaintiffs in those cases, who all suffered from moderate silicosis, were respectively 67, 73 and 87 years of age, and their symptoms, although much more advanced than Mr Hawchar's present symptoms, developed relatively late in life. I take into account the good chance that by the time Mr Hawchar reaches the age of 50 he will have developed symptoms of moderate to severe silicosis, having previously endured over 12 years of significant, although less severe, suffering. It is because Mr Hawchar's damages are to be assessed as appropriate for his particular circumstances, and not in accordance with any scale, that the decision in Planet Fisheries is relevant.

165. I assess general damages in the sum of $150,000. I allow interest on $20,000 at 2 per cent for two years; $800. In accordance with my earlier findings, silicosis being a divisible disease, Dasreef is liable for 20 parts in 23 of the damage, that is $131,130.43.

What is the appropriate order to make in respect of the claim for damages for scleroderma?

166. In his statement of claim, Mr Hawchar claims provisional damages for silicosis and scleroderma and seeks an order that an award of further damages may be made with respect to "silica induced carcinoma of the lungs, massive progressive fibrosis, tuberculosis, silica tuberculosis, oesophageal dysfunction, renal disease and scleroderma lung”.

167. On the face of the pleadings a present claim for damages in respect of scleroderma is before me. Although I have found that this is not a dust disease, jurisdiction to determine the claim is conferred by s11(4) of the Dust Diseases Tribunal Act 1989, because it is ancillary or related to the claim brought in respect of silicosis.

168. A problem arises because, Mr Hawchar, in the event that I find that his entitlement to damages in respect of scleroderma is governed by the Workers’ Compensation Act 1987, wishes to waive this entitlement, so that he recovers no damages.

169. He is driven to this election, if it is available, because s151G of the Act restricts the damages payable to past and future economic loss, and s151A provides that upon recovery of damages, a worker ceases to be entitled to any further compensation under the Act in respect of the injury concerned.

170. Mr Hawchar's entitlements under the Workers Compensation Act 1987 in respect of his disease of scleroderma greatly exceed the value of his past and future economic loss. The Act requires that Dasreef make continuing weekly payments in respect of incapacity for work (s33), and that it pay the continuing cost of medical, hospital and rehabilitation treatment (s60), and the continuing cost of necessary domestic assistance (s60AA).

171. It is plain that at no time did Mr Hawchar seek to recover damages pursuant to s151G.

172. The Workplace Injury Management Act 1998 requires that a plaintiff comply with certain procedural steps before he/she can sue for damages. S262 provides that court proceedings cannot be commenced until a claim for damages has been made upon the employer. S280A requires that a claim for lump sum compensation in respect of the injury be made before or at the same time as the claim for damages. S315 requires that the claimant serve on his employer a "prefiling statement", and s318A requires the claimant refer the matter to mediation, before court proceedings may be commenced. Mr Hawchar complied with none of these requirements.

173. Further, s151H of the Workers Compensation Act 1987 provides that no damages may be awarded unless the injury results in a degree of permanent impairment of the injured worker that is at least 15 per cent, and that the degree of permanent impairment that results from injury is to be assessed in accordance with Part 7 (Medical assessment) of Chapter 7 of the Workplace Injury Management Act. Mr Hawchar led no evidence which would permit such a finding.

174. Dasreef, concerned to avoid future liability under the Workers Compensation Act, waived compliance with the procedural requirements of the Workplace Injury Management Act, (see Berowra Holdings Pty Ltd v Gordon (2006) 225 CLR 364), and, in the course of final address, formally admitted that Mr Hawchar's scleroderma has resulted in a degree of permanent impairment of at least 15 per cent.

175. Mr Parker submits that in this circumstance the Tribunal must award damages, whether or not Mr Hawchar desires to proceed with the claim. I do not accept this submission.

176. In Berowra Holdings Pty Ltd v Gordon the plurality judgment of the High Court stated at [15] that "In the adversarial system of justice, choice rests primarily with the parties and it is generally the case that the court's power of decision or order is exercised upon the application of a party."

177. The Uniform Civil Procedure Act 2005 expressly provides that:

90 Judgments generally

(1) The court is, at or after trial or otherwise as the nature of the case requires, to give such judgment or make such order as the nature of the case requires.

(2) ….

178. Pt 29 r 29.8 of the Uniform Civil Procedure Rules 2005 provides:

29.8 Dismissal of proceedings on plaintiff’s application

(1) On the application of the plaintiff in any proceedings, the court may make an order for the dismissal of the proceedings to the extent to which they concern:

(a) the whole or any part of the plaintiff’s claim for relief, and

(b) any cause of action relevant to that claim or part of the claim.

(2) Subject to subrule (3), such an order may be made at any time.

(3) In the case of a trial with a jury, such an order may be made only if the application for the order is made before the jury gives a verdict.

179. In The Ritz Hotel Ltd v Charles of the Ritz Ltd (No 8) (1987) 12 IPR 75 McLelland J considered the equivalent provision in the former Supreme Court Rules Pt 34 r 6A, and said:

The powers of the court under Pt 34 r 6A, to make an order for dismissal, or to impose terms upon the making of such an order, are general discretionary powers which are not to be confined by judge made rules or formula. Guidance may, of course, be found in what was decided or said in other cases but the function of the court is to act in the manner best calculated to achieve justice as between the parties in the circumstances of the particular case before it.

…

I agree with the proposition stated in several of the cases to which I have referred, that it is undesirable that a claimant should be compelled to pursue a claim if he no longer desires to do so.

180. In Wattyl Australia Pty Ltd v McArthur [2008] NSWCA 326 Beazley JA at [84] spoke of the complexity of the arrangements by which the Workplace Injury Management Act governed the access of injured workers to benefits, and the public purpose in the legislation achieving its intention of providing proper medical treatment to those workers.

181. In the circumstances it is appropriate that the Tribunal make an order for the dismissal of the proceedings to the extent to which they concern the claim for damages for scleroderma.

Orders

182. On the Plaintiff's application, his claim for damages for scleroderma is dismissed.

Judgment for the plaintiff in the sum of $131,130.43.

Liberty to apply.

Order pursuant to s11A of the Dust Diseases Tribunal Act 1989 that an award of further damages may be made with respect to silica induced carcinoma of the lungs, massive progressive fibrosis, tuberculosis, silica-tuberculosis, oesophageal dysfunction, renal disease, and scleroderma lung.

Mr A J Bartley SC with Mr F Tuscano instructed by Keddies Lawyers appeared for the plaintiff

Mr T G R Parker SC with Mr D T Miller instructed by Moray and Agnew appeared for the defendant