White v Pink Batts Insulation P/L

[2000] NTSC 27

White v Pink Batts Insulation P/L [2000] NTSC 27

PARTIES:RICHARD WHITE

v

PINK BATTS INSULATION PTY LTD formerly known as DIVIC PTY LTD formerly known as DIMET CORROSION PTY LTD formerly known as DIMET CORROSION PREVENTION PTY LTD

AND:

COMMERCIAL UNION ASSURANCE

TITLE OF COURT:  SUPREME COURT OF THE NORTHERN TERRITORY

JURISDICTION:  SUPREME COURT OF THE NORTHERN TERRITORY exercising Territory jurisdiction

FILE NO:138/93

DELIVERED:  5 May 2000

HEARING DATES:  8-19 February, 12-22 July, 29 September – 1 October 1999, 28 February – 1 March 2000

JUDGMENT OF:  THOMAS J

CATCHWORDS:

DAMAGES

Claim for damages for impaired respiratory function caused by employment – whether the system of work pursuant to which the plaintiff worked was negligent – whether the plaintiff thereby sustained damage, specifically through the development of small airways disease related to silica exposure –unreliable witness – accepted medical evidence did not support his claim – plaintiff failed to prove he has silica induced small airways disease, or any condition relating to his exposure to silica dust.

Bonnington Castings Ltd v Wardlaw [1956] AC 613, considered.
Commonwealth of Australia v McLean (1996) NSWLR 389, referred to.

REPRESENTATION:

Counsel:

Plaintiff:L King QC

First Defendant:  J Tippett

Second Defendant:  J Kourakis QC and J Rau

Solicitors:

Plaintiff:Bradley Allen

First Defendant:  De Silva Hebron

Second Defendant:  Hunt & Hunt

Judgment category classification:        C

Judgment ID Number:  tho20002

Number of pages:  100

IN SUPREME COURT
OF THE NORTHERN TERRITORY
OF AUSTRALIA
AT DARWIN

White v Pink Batts Insulation P/L [2000] NTSC 27
No. 138/93

BETWEEN:

RICHARD WHITE

Plaintiff

AND:

PINK BATTS INSULATION PTY LTD formerly known as DIVIC PTY LTD formerly known as DIMET CORROSION PTY LTD formerly known as DIMET CORROSION PREVENTION PTY LTD

First Defendant

AND:

COMMERCIAL UNION ASSURANCE

Second Defendant

CORAM:    THOMAS J

REASONS FOR JUDGMENT

(Delivered 5 May 2000)

1. This is a claim by the plaintiff for damages for impaired respiratory function caused by his employment as a sandblaster in Darwin between May 1971 and August 1974.

1. The first defendant is the successor to Dimet Corrosion Pty Ltd.  The second defendant is sued as the relevant insurer of Dimet Contracting Pty Ltd.

2. The essential issues in this claim are:

   1)Whether the plaintiff was employed by Dimet Corrosion Pty Ltd or Dimet Contracting Pty Ltd.

   2)If employed by Dimet Contracting Pty Ltd, whether Dimet Corrosion Pty Ltd so dominated the conduct of Dimet Contracting’s business that Dimet Corrosion Pty Ltd is responsible upon the basis of CSR Ltd v Wren (1997) 44 NSWLR 463.

   3)Whether the system of work pursuant to which the plaintiff worked was negligent.

   4)If so, whether the plaintiff thereby sustained damage, specifically through the development of small airways disease related to silica exposure.

   5)If he did, what measure of damage is by way of general damages, out of pocket expenses past and future and economic loss past and future.

   6)Whether the second defendant insured Dimet Contracting Pty Ltd against a liability to pay damages to, amongst other people, the plaintiff, pursuant to an agreement which may be inferred in the absence of all the documents.

   7)Whether the plaintiff is precluded by the Statute of Limitations from bringing this claim.

3. For the reasons which I will detail, I propose to deal only with the issues raised in (3) and (4) above.

   3)Whether the system of work pursuant to which the plaintiff worked was negligent.

4. Evidence as to the system of work was given by:

   Mr Medley (t/p 247 – 268) who is currently employed by the Department of Correctional Services in Darwin and has worked in this position for 17 years.  In 1972 Mr Medley gave evidence he was employed by Dimet Corrosion Pty Ltd in Whyalla, South Australia.  About 8 weeks before December 1972, his employers brought him to Darwin to do sandblasting work.  Apart from a short break Mr Medley worked at this job in Darwin until December 1973.  It is Mr Medley’s evidence that during this time Mr Richard White worked for the same company in Darwin.  Mr Medley does not give specific evidence about the actual hours worked by Mr White in this time.  The work involved sandblasting fuel tanks including fuel tanks at the RAAF base, barges, pylons and pieces such as plates off boats.  The material used for sandblasting was river sand.  In Whyalla Mr Medley had sandblasted with copper slag.  Mr Medley states he did a bit of everything; sandblasting inside tanks to remove the paint, operating the hopper which meant either shovelling sand into the hopper or turning the hopper on and off if there was a problem.  The sand would be dried, shovelled into heaps and then into wheelbarrows.  Mr Medley described the conditions in the barges and the problems with dampness and rust.  The equipment they used was brought up from Whyalla.  Mr Medley says the helmets were too heavy for the climate in Darwin.  The dust would clog up the airlines, carbon monoxide would sometimes come through.  The heat and humidity meant the helmet became unbearable to wear.  When working outside he would wear shorts and put a piece of rag round his mouth to keep out the dust.  Sometimes he would tie his t-shirt round his head but the sand would still come through and he had the sensation of sand in his mouth.  It is Mr Medley’s evidence that when working as an assistant in the open air the assistant “copped” all the sand with the various wind changes.  Whether working inside tanks or outside there was always a lot of sand dust.  Mr Medley gave evidence you can smell it and it was in your mouth.  Mr White also worked in these conditions.  Mr Medley observed him to be a good worker.  Mr Medley recalled there was a lot of work and he sometimes worked from 7.00 in the morning to 11.00 o’clock at night.  Mr Medley stated that on a couple of occasions he was given a dust mask which was just a paper mask.  Mr Medley described the difficulties of cleaning and maintaining the hood and the air hose lines.  A compressor was used to help ventilate the tanks at the RAAF base.  Before that happened conditions inside the tank were unbearable with a lot of dust and sand.  When Mr Medley first worked for Dimet Corrosion Pty Ltd in Darwin there were four or five employees and this increased to over 20 employees.  Mr Medley remembered a Mr Jones hurt his fingers in an overhead crane.  Under cross examination by Mr Kourakis QC, Mr Medley stated he had not seen Mr White between the end of 1973 until a few days before giving evidence at this hearing on 11 February 1999.  It is Mr Medley’s evidence that Mr White had contacted Mr Medley who with his wife had gone to dinner with Mr White and Mrs White at Kitty O’Sheas.  Mr White had paid for the dinner.  Mr Medley gave evidence that although he had not seen Mr White since the end of 1973, he regarded him as a good friend.  Mr Medley stated he used to wear overalls when he was sandblasting in a confined space because the sand could ricochet back and shatter clothing.  He described how it would become necessary to stop sandblasting and clean the helmet and the difficulties of working in a confined space.  Mr Medley gave evidence that Mr White was a young man at this time he also operated the hoppers and helped to clean up.  Mr Medley continued to work as a sandblaster for other companies.  It is Mr Medley’s evidence that in 1991 an x-ray showed he had marks on his lungs.  He had become a prison officer in 1981 but had continued in a second job as a sandblaster until a year before the date on which he gave evidence.  At the time of giving evidence, Mr Medley continues to work full time as a prison officer and in his time off spends a lot of time bushwalking.  He did not suffer coughing attacks nor had he ever coughed up sputum.  Mr Medley said he was not aware anyone who worked in Darwin with the companies by whom he was employed had died from a lung disease.  He was aware that a Mr Colin Ferguson in Whyalla had contracted asbestosis.

5. Mr Guiseppe Taccori gave evidence that he had obtained a job as a sandblaster in Darwin in 1974.  He thought the name of the firm he worked for was Dimet.  He worked in this job for six months.  During this time he suffered two injuries.  One when he tripped and fell and the second when a hopper being moved by a work mate fell on top of him.  Following this second accident, he was hospitalised.  He was paid compensation and his medical and hospital expenses were paid.  In 1981 – 1982, he had worked for three months in Sydney as a sandblaster.  Mr Taccori stated that in 1992 he noticed he couldn’t breath properly.  He said he now lives in Nimbin and has not had any health problems since living in Nimbin.  Mr Taccori described the sandblasting work in the tanks at the RAAF base as a horrible job.  He said it would not have been possible to do the job in shorts and a singlet because of the movement of the sand in a confined space.  He also wore a full face helmet which was attached to a leather suit with sleeves, gloves, protective boots and pants.  He said it was good money and at that time he was paid $18 an hour together with bonuses.  Mr Taccori said he was very particular about safety and always wore the protective clothing when he was sandblasting.

6. Mr Phillip Turner gave evidence that he is an occupational hygienist.  He prepared a curriculum vitae and a report which were Exhibit 10.  This report contains in paragraph 4 a work history concerning the plaintiff which was obtained by reading documents provided by Mr White’s solicitor.  The report states in paragraph 5 “Mr White has contracted a small airways disease”.  Mr Turner agreed in evidence that he is not a medical specialist and this was not a diagnosis he was qualified to make but rather was based on information he had received.  Mr Turner stated in his report and in evidence that silica exposure can be a very potent cause of disease.  He agreed that the likelihood of illness is related to both exposure and that the greater exposure over the greater period of time the more likelihood there will be of illness.  Mr Turner stated the most accepted disease with silica is silicosis and it was silicosis that he was referring to in paragraph 8 of his report headed “Foreseeability”.  Mr Turner agreed that in preparing his report he was not able to measure the air exposure in different environments and that he could have been more specific had he spoken to Mr White about the time Mr White had spent in a confined space as distinct from outside.  He gave evidence that protective clothing for a sandblaster was important, that a determined person could do it wearing football shorts and a t-shirt but it would be very uncomfortable and a risk to safety.  It could result in possible burns or other injuries.  I do not attach any weight to the report prepared by Mr Turner not because he is not eminently qualified in his field but because his conclusions are based on information he received indirectly from Mr White.  I will detail in the course of these reasons why I found the evidence of Mr White to be unreliable and to the extent that Mr Turner’s report relies on information obtained from Mr White I reject the conclusion that relies on such information.

7. Mr Wayne Nayda gave evidence at t/p 297 - 315.  Mr Nayda is a Sergeant of Police, in charge of the Prosecutions Section at Katherine Police Station.  Late in the year 1971, he commenced sandblasting work with Dimet Pty Ltd in Darwin.  He worked in this job until late 1973 or early 1974.  When he left, the Dimet Company was still operating in Darwin.  He did not recall meeting Mr White during this period of employment.  He did know Mr Medley who had moved to Darwin with him from Whyalla.  He also remembered a Ross Florence, a Wally Bonderenko and a person named Jones.  He described the work he did as a sandblaster which included the sandblasting of barges, fuel tanks and water tanks both interior and exterior.  He was required to dry out a load of sand and fill up the hoppers to allow the sandblasters to continue throughout the day.  The team took it in turns to fill the hoppers, dry the sand, do the sandblasting and clean up.  Sometimes the sand was recycled provided it did not contain paint or particles of material.  There was a lot of work and Mr Nayda often worked seven days a week, sometimes until late into the night.  Mr Nayda said that when drying the sand he wore shorts, a t-shirt and a pair of runners.  The drying of the sand involved shovelling and raking.  He often experienced sand in his mouth but said he was not provided with any face masks.  He was not given any warning about trying to avoid the sand nor was any ventilation provided.  When operating the hopper he would wear boots with shorts and a shirt and overalls on standby.  He stated that when working the hopper sand would blow all over him and it was necessary to make some adjustments because the hopper was blocked.  Mr Nayda said it was a regular occurrence for him to get sand in his mouth.  When working outside he wore a calico hood and goggles, when sandblasting in a confined space he wore a helmet.  Wearing the helmet made it very difficult to see and he would still have fine dust come up all over him.  The sand would blow up under the leather flap and fill his mask with dust.  Mr Nayda gave evidence about the discomfort of working in the heat and the difficulties of trying to use a compressor and a water catcher.  When shovelling sand or to get it out of the way, Mr Nayda would take off his overalls and wear shorts and a t-shirt.  There was always fine dust everywhere.  There was no sealed unit respirator provided for doing this work.  There was no system for inspection of the hoods.  Mr Nayda gave evidence about the technique for sandblasting that would be the most efficient and to avoid the sand blowing back because of the stinging effect of the sand.  A photograph of the sandblasting equipment was tendered and marked Exhibit 15.  Mr Nayda gave evidence in cross examination that the helmet was worn to enable the operator to breathe air free of dust but it did not always work that way because dust was always coming into the helmet.  The helmet was not sealed and did not fit snuggly.  Mr Nayda stated he was paid very well for the work he was doing.  He described the task of shovelling the sand after sandblasting or to reuse the sand, as taking anything from an hour to four or five hours.

8. Mr Richard Bonython gave evidence that he was a director of Dimet Corrosion Pty Ltd and subsidiary companies between 1968 and December 1974.  He stated Dimet Contracting Pty Ltd began operations in Darwin in 1970 or 1971 until a takeover by PGH in 1974.

9. From the evidence of Mr Medley I find that Mr White was employed at the same time as Mr Medley and worked with Mr Medley.  I make no findings at this time as to the name of his employers.  Mr Taccori and Mr Nayda were employed by a company which has been referred to as Dimet.  The reasonable inference on the evidence is that Mr Medley, Mr White, Mr Nayda and Mr Taccori were all employed by the same company.  From the evidence of Mr Medley, Mr Taccori and Mr Nayda which I have summarised above I am satisfied that the system of work pursuant to which the plaintiff worked was negligent.  In particular employees were not given adequate instructions.  They were not provided with adequate clothing, equipment or protective apparel.  Their general conditions of work were not to a satisfactory standard.

10. The next issue is whether, as a consequence of this negligent system, the plaintiff sustained damage, specifically through the development of small airways disease related to silica exposure.  The plaintiff bears the onus of proof on the balance of probabilities that the respiratory problems from which he claims he suffers are related to silica exposure at the time of his employment in the period between 1971 – 1974.

    4)Whether the plaintiff thereby sustained damage specifically through the development of small airways disease related to silica exposure.

11. In considering this issue I have thought it appropriate to deal firstly with the evidence of Mr White and his credibility as a witness.  For the reasons which I will detail, I did not find Mr White to be a credible or reliable witness.  His evidence is littered with exaggeration and obfuscation.  I do not accept him as a witness of truth for the following reasons.

12. Mr White consulted Professor Bryant in respect of his respiratory problems.  He was referred to Professor Bryant by Dr Armstrong in 1991.  Exhibit 43 is a letter Mr White wrote to Professor Bryant dated 2 February 1994.

13. In this letter Mr White advises Professor Bryant that he had visited Darwin from 20 –24 December and states his trip was productive.  Mr White then writes:

    “Unfortunately two of my past associates in sandblasting are in terminal stages of their progressive disease.  They worked 3½ + 5½ years longer in the business than I, but of course this strengthens my claim for damages at their expense I’m afraid.”

14. There is no factual basis for this statement and no evidence upon which Mr White could have formed a reasonable belief that it was true.  One man working for Dimet had asbestosis but he had worked in Whyalla and not Darwin.  I formed the opinion that this was written in an attempt to sway Professor Bryant’s opinion as to the probability that Mr White had suffered a serious disease as the result of exposure to silica.  That such a statement had been made by Mr White to Professor Bryant on a previous occasion appears from the context of a letter from Professor Bryant to Mr White’s treating doctor, Dr Armstrong, on 16 September 1993 included in Exhibit 61, when Professor Bryant wrote to Dr Armstrong that Mr White’s level of self reported smoking was not sufficient to have resulted in the degree of airways limitation that was present and then stated:

    “The only other significant exposure to irritant dusts that I can elicit is his exposure to silica between 1971 and 1975.  He does not have radiographic features of silicosis.  However it seems likely that his silica exposure there was intense as other workers employed at the same time have now developed features of silicosis.”

15. This is an exaggeration.  The only evidence to support such a statement is that Mr Medley who worked as a sandblaster for a much longer period than Mr White, had silicosis of the lung.  Mr Medley worked as a sandblaster between 1973 and 1991, a period of approximately 18 years.  However, on Mr Medley’s own evidence the silicosis of the lung has caused him no incapacity or discomfort.  He is now in full time employment as a prison officer and on his own evidence is physically very fit, going for long bush walks in his time off.

16. In his letter dated 18 February 1995 which is a reply to a series of questions posed by Clayton Utz, Mr White’s solicitor (Exhibit 61), Professor Bryant stated at paragraph 10:

    “In view of this man’s heavy silica dust exposure, and of the fact that a number of the other individuals with whom he worked have developed silicosis, it is possible that he will develop evidence of silicosis in the future.  However, as silica dust exposure ceased in 1975 with no evidence of silicosis having developed to this date this seems unlikely.”

17. In this statement Professor Bryant is relying on the truthfulness of the history given to him by Mr White both as to the extent of Mr White’s exposure to the silica dust and that of other persons with whom he worked developing silicosis.  Because I do not accept the truth of these two aspects of Mr White’s employment history, this must affect the Court’s view of Professor Bryant’s opinions.

18. On all the medical evidence Mr White does not have silicosis nor any sign of silicosis.

19. Under cross examination (t/p 428) Mr White agreed that he had told Dr Stevenson in November 1995 that of the team who were doing sandblasting work with him, men mostly in their 30’s at the time, five of the seven are now dead and one of the survivors is suffering silicosis.  Mr White stated under cross examination that he could not recall if he told Dr Stevenson that of the five, two had died from heart attacks and one in a car accident.  Mr White was then asked about another two of the men named Ferguson and McGrath and agreed they are not dead.  His answer when asked if they were dead was:

    “No, not yet.  And then there’s Barry Medley who’s got silicotic scarring, I believe.”

1. Mr White stated, again in answer to cross examination, that he could not recall if he had told Dr Stevenson that the two persons Ferguson and McGrath were not dead yet.

2. Mr White gave evidence relating to Exhibit 43 in which he agreed he had also spoken to Dr Stevenson about his workmates.  Mr White gave the following evidence in cross examination (t/p 428):

   “What you told  Doctor Stevenson in November 1995 was this, that you have found out that, of the team that were doing sandblasting work with you, who were mostly men in their 30s at the time, five of the seven are now dead and one of the survivors is suffering from silicosis; that’s what you told Doctor Stevenson?---Yes, that was my belief, yes.

   Well, who were the five of the seven who were dead?---Armour who’s died, and then two others apparently passed away of heart attacks, and then there’s Ferguson and Barry McGrath.

   Ferguson and McGrath aren’t dead?---No, not yet.  And then there’s Barry Medley who’s got silicotic scarring, I believe.

   Well, what did Armour die from?---I’m not sure.  I think it was a car crash.

   Mr White, did you tell Doctor Stevenson that of the five, two had died from heart attacks and one in a car accident?---I don’t recall.

   Did you tell him that the other two weren’t yet in their grave?---I don’t recall.”

3. I find that Mr White falsely exaggerated the condition of persons who had worked with him during this time in order to bolster his own claim and that in doing so he attempted to deceive the doctors, particularly Professor Bryant.

4. Mr White was questioned extensively about his hours of work during the period 1971 to 1974 and the actual work he carried out.  I am satisfied that the evidence he gave exaggerates and distorts both the time he spent at such work and the actual work he was required to do.

5. Mr White started part time work in his second last year in high school which was in 1971 and it was either 1971 or 1972 that he commenced in part time employment doing the work which is the subject of his present claim.  Mr White gave evidence he commenced work in the afternoons and evenings three to four days a week for two to three months to start with and then later spasmodically (t/p 33).  He was working part time after school hours.  When he started this work he was 17 years old.  He was working as the offsider to the man doing the blasting (t/p 36).  He gave evidence he was later asked to do work at the Darwin Wharf and in Francis Bay.  He describes himself as a “gofer” and that he was mainly operating the hopper.  Mr White described the sandblasting work inside the barges and the difference between working on the barges and on the pylons at the wharf.  Mr White said that when assisting the sandblasting he wore the same clothes as the clothes he had worn in the shed which he had described as football shorts, a t-shirt and a pair of old shoes.  He wore the same clothes when sandblasting in a confined space except with a hood.  From the evidence of Mr Taccori and Mr Medley it would appear unlikely that a person who was working as a sandblaster for any time in a confined space could work only in shorts and a t-shirt.  Mr White agreed in cross examination (t/p 130) that it required experienced people to do the sandblasting and when the experienced men were doing the sandblasting he was generally outside in the open air attending to the hopper and making sure the equipment was running smoothly.  This conflicts with his statement in paragraph 9 of his affidavit sworn 7 June 1995 (Exhibit 101) in particular 9(c) that 70 per cent of his work involved working in enclosed spaces.

6. Mr White gave evidence that he was asked if he wanted to have a go at the sandblasting which he did after that he went back to being a “gofer”.  He said after he had been there six months he was sharing the work equally.  He gave evidence that the experience of getting sand in your mouth was worse when working in a confined space than when in open surroundings.

7. In his affidavit sworn 7 June 1995 (Exhibit 101) Mr White stated at paragraph 17:

   “When working in the enclosed spaces there was generally a foul smell in the air.  I observed that some workers using the fibreglass shell occasionally ripped the air hose out and operated without the air inlet working.”

8. When cross examined on this it was suggested to Mr White that this could never have happened when working in a confined space.  Mr White replied (t/p 417) that “they’d rip it out and they’d reinsert it after they’d regained their composure.”  When paragraph 17 of Exhibit 101 was drawn to his attention, Mr White said “that’s correct, to the end of their run”.  I did not find this a credible answer.  It was an example of a number of occasions throughout his evidence that Mr White tailored his reply to suit his case when the absurdity of his statement was pointed out.  Mr Taccori’s evidence was to the effect that without the right equipment in the confined space you could blow yourself apart sandblasting.  In cross examination (t/p 261) Mr Medley was asked:

   “Yes.  But you couldn’t last long in a confined space, sandblasting, if that air supply through your helmet stopped?---No.  But even in confined spaces you didn’t last long in there anyhow because it was so – you come out of there, you were wringing wet anyhow.”

9. In his affidavit (Exhibit 101) Mr White referred in paragraph 12 to a calico skirt around the base of the helmet.  He stated: “The calico skirt was ineffectual in that it flapped and allowed sand particles to penetrate into the mask.”

10. Under cross examination Mr White gave evidence that a calico skirt was worn when sandblasting in an enclosed space.  When it was pointed out to him in cross examination that the calico would get torn to shreds Mr White replied that he thought the calico was covered with a leather coating.  I did not find this evidence credible but rather an attempt to bolster his own case when the absurdity of an earlier statement was put to him.

11. Another part of Mr White’s evidence which I consider reflects poorly on his credibility was given under cross examination (t/p 419):

    “And what did you wear – what did you wear when sand blasting in barges or other enclosed spaces?---Jeans like I said.  Old jeans.

    You see when you gave evidence in chief Mr King asked you this, at page 61: ‘When you went about the work did you always wear the clothing as you described yesterday but with the hood on when you were doing sand blasting inside the confined spaces?’  And you answered: ‘Yes, I used to wear desert boots from school.  I wear them just to school and then I just use the desert boots and then I’d have the football shorts and either a singlet or a T-shirt, mainly a T-shirt.’  Didn’t you answer in that way when Mr King asked you about sand blasting in enclosed spaces?---Well I may have answered incorrectly.

    Mr White you would never – you would never have even thought that you could sand blast in an enclosed space with shorts if you’d ever really done it; would you?---Well it says what I said.  I’ve misdescribed how I answered him that’s all.”

    I consider this to be another example of Mr White tailoring his evidence to suit his case.

12. In his affidavit of 7 June 1995 (Exhibit 101) Mr White states he worked part time from May/June 1971 five days a week from 4.00pm until 10.00pm.  He states in his affidavit that at the end of 1972 he commenced working full time with Dimet that he worked approximately 50 hours per week 5½ to 6 days a week between the hours of 7.00am and 10.00pm.  I am not prepared to find that his employment was as extensive as he maintains.  I have made allowance for the fact that it is now over 25 years ago and that he was then a young man in his teens.  However, even allowing for this factor I consider Mr White has deliberately exaggerated the period of time he spent working with this company in order to bolster his own claim.

13. Mr Medley, Mr Taccori and Mr Nayda all worked for the same company during the relevant period.  Neither Mr Taccori or Mr Nayda gave evidence to support Mr White’s statements about the extent of his working hours.  Neither Mr Nayda nor Mr Taccori remembered his working there at that time.  Mr Medley remembers Mr White working there during the period Mr Medley was employed in Darwin from the end of 1972 to end of 1973.  Mr Medley described him as a good worker.  However, Mr Medley’s evidence does not give any detail as to the hours of Mr White’s employment, the days of the week or even an approximation of the time Mr White spent each week or each month in such employment.  I accept Mr White was employed during this period to assist with the sandblasting operations of his employer.  I do not accept it was for the hours that he maintains, or that he received the intense exposure to the sandblasting operations as he would have the Court find.

14. The only documentary records of his employment are contained in Exhibit 42 which are copies of the 1972/73 and 1973/74 refund notices for Mr White.  The facsimile from the Australian Taxation Office states that they could find no other records for the other years requested and also states:

    “We do not have the amount of taxable income earned for these two years because this information was not recorded where the income was below the taxable threshold.  The threshold for these years was $1040.”

    This would indicate Mr White received an average of less than $20 per week during these two years.

15. These records are not in themselves sufficient to contradict Mr White’s claims as to the period he worked but they certainly do not support his assertions.

16. Mr Nayda has given evidence that he, Mr Nayda, was very well paid for the work he was doing.  Mr Taccori gave evidence to the same effect.  Mr White did not attempt to give evidence about his rate of pay.  On the basis of evidence given by Mr Nayda and Mr Taccori there is no reason to believe Mr White worked long hours and was so poorly paid that his income was below the taxable threshold.

17. The aspects of Mr White’s employment that I have addressed is to give some of the reasons why I consider Mr White has exaggerated his period of actual employment and the amount of exposure he had to silica.  Nevertheless, I do accept that he was exposed to silica in the course of his employment.

18. At the end of 1974, Mr White moved to Canberra and obtained employment including employment as a real estate agent with Barry O’Ryan Real Estate, Mawson ACT and Phillip Kouvellis Real Estate, Canberra.  In May 1985, Mr White opened his own real estate agency in Canberra known as Prime Real Estate.

19. In his Amended Statement of Particulars filed 16 December 1998, Mr White claimed that he was totally and permanently incapacitated from returning to the occupation of a real estate agent and salesman.  He also claimed amongst other matters, a total incapacity from returning to any employment.  He also claimed damages for reduced life expectancy and the necessity for a lung transplant within seven to 10 years.

20. The medical evidence adduced in these proceedings does not support any of these claims.  I am satisfied Mr White exaggerated his condition and his limitations.  In his affidavit sworn 7 June 1995, Mr White stated the following at paragraph 54 and paragraph 55:

    “54.I continue to suffer symptoms related to chronic airways limitation.  I have shortness of breath and wheezing upon physical activity.  Even walking up stairs causes breathing difficulties.  Romping with my children, vigorous sexual intercourse, snorkeling, and any vigorous exercise must be avoided.  Even walking 200m causes shortness of breath and wheezing.  Exercise also brings on dry irritating coughing.  I have resting posture which reflects my breathing pattern and shoulder girdle muscle shortening and wasting.  I have worked hard at exercises given to me by my physiotherapist, and at generally maintaining a healthy diet and as much exercise as I can cope with.  Unfortunately improvements that I make are often hindered by respiratory tract infections which affect my general condition and make exercise progress difficult.  I have had to learn secretion clearance techniques.  These are not always effective.  My capacity for normal activity is severely reduced.

    55.My ability to participate in normal family and work activities is significantly affected by my condition.  I cannot carry out many of the tasks which I would otherwise have done about the home, and cannot play with my children normally.  My sons are now aged 13 and 10 and I am unable to participate in regular family activities such as kicking a football or playing cricket with them.”

    Having now heard all of the evidence I find that these paragraphs grossly exaggerate Mr White’s limitations.

21. Mr White gave evidence that from 1989 onwards he had problems sleeping.  During 1991/92 he found it increasingly difficult to work and was becoming very fatigued.  He said he wanted to keep the real estate agent business but was finding he was too fatigued to work.  He had episodes of coughing and breathlessness.  He found it difficult to walk upstairs or up steep blocks of land when he was showing properties to clients.  He would become breathless and cough uncontrollably which he found embarrassing when trying to present properties for sale.  It was Mr White’s evidence in chief that he was forced to delegate the work and that he took steps to engage an office manager.  In July 1994, Mr John Moore was engaged to supervise the sales staff and to run the office as a business manager.  Mr White stated that he had been told by his doctors that it was silly for him to go on trying to administer the business.  This statement is not supported by the evidence of Professor Bryant or other treating doctors who do not make reference to this advice.  In September 1990, Mr White purchased John Cassell Real Estate Agency.  His evidence is that when he purchased this agency, he thought he would be able to run both Prime Real Estate and John Cassell Real Estate Agency (t/p 338).  He stated that he told Mr Denoukis and Mr Gamble that he was not going to be well enough to help with both real estate agencies.  This was after Mr White had consulted Professor Bryant.  Mr White gave evidence in cross examination that Anking Holdings Pty Ltd was the company that purchased Cassell Real Estate Agency.  Prior to 1992 Anking Holdings Pty Ltd ran Prime Real Estate.  Eventually a Mr Denoukis and a Mr Gamble joined him as share holders of “Anking”.  Mr White agreed under cross examination that part of the reason he no longer had an interest in Anking was because he had a business difference with Mr John Gamble who had purchased shares in Anking.  He gave evidence under cross examination that these differences related to whether Mr and Mrs Cassell should be allowed to remain in the business, whether the properties should be auctioned and Mr Gamble’s concerns about the valuation and the purchase price for John Cassell Real Estate Agency.  Mr White gave evidence in cross examination (t/p 341) as follows:

    “So Mr White, what I suggest to you is that the reason that your involvement with Anking ended was not because you said to Mr Gamble, ‘Look, I’m too sick to be involved’, but because Mr Gamble and Mr Denoukas said to you, ‘We don’t want you in this any more’?  That’s what happened, isn’t it?---No, I suggested to him that I was sick and that I wanted to go out and then they – they were arguing about how much things were worth and how much the building was worth and how much we’d paid for John Cassell Real Estate and how the building valuation was arrived at.  That’s why there was a difference of opinion.”

22. From further evidence given by Mr White it would appear that Mr Gamble and Mr White each retained lawyers in respect of the dispute which was subsequently settled between them.

23. I do not consider Mr White was being truthful in his assertion that the reason he sought to withdraw from the business was because of his illness.  In fact a large part of his reason for withdrawing was the quite involved and protracted argument he had with the other shareholders, Mr Gamble and Mr Denoukis.

24. Following Mr White’s withdrawal from “Anking”, Mr and Mrs White bought a shelf company Lodbury Pty Ltd of which they were both directors.  Lodbury Pty Ltd ran Prime Real Estate and various loans were made to the directors.  Mr White was asked a number of questions in cross examination as to his financial affairs.  His answers were vague and evasive.  I do not propose to detail every instance where his evidence on his financial dealings between 1991 and 1996 was unsatisfactory but will give some examples.  He was being asked certain questions in cross examination relating to Exhibit 19 which is the Lodbury profit and loss statement.  The following was his evidence in cross examination (t/p 383):

    “Again Mr Adriaanse is the only person who can explain why that is so, is that right?---Well, I can’t see why he wouldn’t be putting everything in there.

    Mr White, what’s more, that large indebtedness to you in the 1996 year was in fact funded by the Lodbury overdraft increasing by something in excess of $100,000 over the same financial year, that’s how it was funded, wasn’t it?---I’m unsure of that.

    Mr White, don’t you remember having to go to the bank to explain and ask them to allow an increased overdraft to Lodbury, increased to the extent of over $100,000?---No, we went to Terry Snow’s office in Capital Property Group; Erik Adriaanse, Terry Snow, myself and the bankers, and they sat down and went through.

    In the end, information as to how your company was meant to pay for this increased overdraft had to come from you.  What did you tell them?---It came from Erik Adriaanse.

    What came from Erik Adriaanse?---How things were going to work and what was going to be done.

    Mr White, at this stage you were an invalid pensioner; how did your professional advisers convince the bank to allow another $100,000 and more in overdraft for your company?---Because Mr Snow guaranteed it.

    How did you explain to Mr Snow how you might be able to repay the amount so that his guarantee would be safe?  What did you say that he was quite happy to risk his own money for you?---I didn’t say anything.  I don’t know what he thought.”

    I formed the impression Mr White was being deliberately vague and evasive as to his true financial position.

25. In addition to the company Lodbury Pty Ltd, Mr White was a director of a company named Kofeld Holdings Pty Ltd which was not trading, it was a family trust.

26. In 1997, Mr and Mrs White purchased and became directors of a company named Janidol Pty Ltd.  Mr White gave evidence this company was purchased so that Janidol Pty Ltd could apply for a licence if his wife ever intended to go back into real estate (t/p 411).

27. Mr White was also during this time a director of a company named Helkpin Pty Ltd.  The purpose of this company was to purchase properties.  Mr White was not able to explain why money was distributed from Kofeld Pty Ltd to Helkpin Pty Ltd or when the company was purchased indicating as he did in response to a number of questions in cross examination that his accountant Mr Adriaanse would know what had occurred and why certain transactions were made.  Mr Adriaanse was never called by the plaintiff to give evidence.  No explanation was given as to why Mr Adriaanse was not called.  I am entitled to assume that Mr Adriaanse’s evidence would not have assisted the plaintiff.  I do not accept that Mr White was being frank in his answers concerning his financial dealings since 1991.  I formed the impression he was being vague and evasive so as to avoid releasing information about his true income and expenditure.

28. Mr White was asked a number of questions in cross examination about his expenditure on monies for gifts and other expenses.  He gave the following evidence (t/p 370):

    “What actually happened, Mr White, was that over the year June 1995 through to July 1996, the overdraft for Prime Real Estate increased by well over $100,00; that’s so, isn’t it?---That’s correct, yeah.

    And effectively, you used extended overdraft facilities to stay at the Hilton and dine like this?---I’m unsure of that.”

1. At this time Mr White had been on the invalid pension since 1994 and claimed he had no capacity for work.

2. Mr White was asked a number of questions in cross examination as to reasons why he did not participate more in the business of Prime Real Estate.  Mr White gave the following answers in cross examination (t/p 397):

   “Why couldn’t you do that job between 10 and 2?---Because it wasn’t my function to do that job.

   Why didn’t you make it your function.  You’re the boss – you can’t go out on the road, why didn’t you do that?---I think because of the – because of the reason I stated previously.  I wasn’t able to always be there and to be able to liaise you needed someone who was there full-time and able to liaise with the staff.

   Mr White, would you agree with this general proposition, that if there had been a vendor or purchaser phoning up for the first time to see about doing business through your agency, it would be better and more effective if someone as experienced as you took the call, than Daphne or Dallas?---It could be, yes.

   It’s not could be, Mr White; it’s obvious, isn’t it?---Yes.”

3. I do not accept that Mr White gave evidence frankly as to the work he had a capacity to perform.

4. In 1993 Mr White acquired Rose Wilson Real Estate.  Mr and Mrs White became the directors and Mr White was the licensed agent.  Mr White agreed that as the licensed agent he was accountable for the conduct of the business (t/p 405).

5. In 1992 Mr White had purchased the rent roll for Rex Realty.  Mr White gave the following answers in cross examination (t/p 406):

   “Why were you buying an extra rent roll in 1992 given the precarious nature of your health?---Because I wanted to keep the business as I stated to you before.  It was my intention to keep the business.

   Didn’t that involve more work – obviously it involved more work; didn’t it?---But I was asked previously if I sold the rent roll for a profit and I said I didn’t think it was sold for a profit and one of the reasons that it needed to be profitable was to expand it and that’s one of the reasons we were purchasing any small rent rolls we could was to make it more profitable.

   So it comes down to this Mr White.  In the time that you had described a deteriorating respiratory condition you were moving to expand the rent roll of Prime Real Estate?---Well I knew it was available and so I think I made inquiries through the accountant and the solicitor and we bought it.

6. Mr White evaded answering the question “Didn’t that involve more work – obviously it involved more work; didn’t it?”  As occurred on a number of occasions Mr White’s answer was not responsive to the question.

7. I am satisfied that the acquiring of the additional rent rolls from Rex Realty in 1993, which was about 18 or 20 properties, and becoming the licensed agent for Rose Wilson Realty in 1993, did involve Mr White in more work.  He as the licensed agent took on a greater responsibility during a period when he claimed his health was deteriorating.  The nature of his work may have changed to being entrepreneurial in nature but it required his active involvement.

8. Mr White denied that he had told Mr Stevenson that during the early part of 1995 he was walking 4 kilometres a day.  Mr White stated that was just another inaccuracy the doctor had taken down (t/p 408).

9. Under cross examination, Mr White gave evidence that he and his wife purchased a company named Janidol Pty Ltd for $250.  When asked if this occurred in March 1997 Mr White replied that he was unsure as to the exact timing.  At that time Mr White was on the invalid pension.  Mr White gave evidence that this company has not traded and was purchased only with the expectation that his wife may be able to do some work in real estate.

10. In 1996 Prime Real Estate, which is the trading name for Lodbury Pty Ltd, sold the rent roll, computer and office furniture to L.J. Hooker.

11. I do not accept Mr White’s assertions that ill health has caused or reduced his ability to earn an income or continue to work as a real estate agent.

12. Mr White was shown certain documents which were extracted from his file with his accountant Mr Adriaanse.  Exhibit 45 is a three page handwritten note which makes reference to purchase price of the rent roll for Rose Wilson Real Estate.  Mr White denied that he had any financial interest in Rose Wilson Real Estate and stated it was a Mr Allan Bailey who purchased it, he was the licensed agent under which Rose Wilson Real Estate operated.

13. Exhibit 46 was also extracted from Mr White’s file with Mr Adriaanse.  It is a document titled “Income/Outgoing Details”.  This document refers to Mr White having shares in Rose Wilson Real Estate valued at $90,000.  Mr White gave evidence that he hadn’t paid for his share yet (t/p 438).  Mr White was asked why he would tell the bank he had the shares and he stated that possibly he was applying to the bank to buy the shares he could not be sure what happened but he did not pay any money to Alan Bailey who maintained ownership of the company.

14. Similarly Exhibit 47 document titled “Lodbury Pty Ltd Statement of Financial Position as at 31 July 1993” shows the asset of Lodbury Pty Ltd as share in Rose Wilson $80,000.  This document also came from Mr White’s file with his accountant Mr Adriaanse.

15. Mr White’s explanations in respect of these documents was not credible.  I believe he was being evasive and less than frank in his evidence about his financial dealing in respect of Rose Wilson Real Estate.

16. Exhibit 48 from the same file are two profit and loss statements from Lodbury Pty Limited for the year ended 30 June 1993.  Mr White was asked to compare these with the tax return for Lodbury Pty Ltd for the financial year ended 30 June 1993 (Exhibit 18).  Mr White agreed the profit and loss statement for Lodbury Pty Ltd in his taxation return for the year ending 30 June 1993 showed a gross income of $389,838.  He agreed that in the first profit and loss statement (Exhibit 48) it shows professional fees as being $419,379.26 some $30,000 more than the income shown in the taxation return.  Mr White also agreed the profit shown for Lodbury Pty Ltd in the year ending 1993 as per the first profit and loss statement (Exhibit 48) was $80,440.10, whereas the taxation return showed a nil profit.  Mr White could not explain this and said that the question would have to be put to Mr Adriaanse.  Mr White gave the same answer when shown the second profit and loss statement for financial year 1993 for Lodbury Pty Ltd also included in Exhibit 48 which does match the 1993 tax return.  Mr White maintained Mr Adriaanse was the only person who could explain this.

17. Again I do not accept Mr White was being candid with the Court but rather evaded giving a truthful account of his financial position at that time.

18. Exhibit 49 is a facsimile from Mr White to Erik Adriaanse and Associates dated 20 February 1992.  It also includes letter dated 25 February 1992 from Mr Adriaanse and Associates to Mr Peter Horsfield.  The information on the facsimile is essentially similar to the information set out in Mr Adriaanse letter.  Mr White did not deny this when shown the two documents.  Mr White’s taxable income for the year ending June 1992 was $23,905(Exhibit 50).  This is a great deal less than the income as set out in the letter (Exhibit 49).  Mr White agreed that they were trying to make a good impression about how the money was going to come in.  Mr White then denied under cross examination that he engaged in the process of “beefing up” his earnings for the purposes of a loan but reducing what was on a tax return so that he paid less tax.  He denied that he was attempting to show a minimal income for the purpose of this case.

19. I do not accept Mr White’s evidence in this regard.  I am satisfied he inflated his income for the purpose of obtaining a loan and reduced it on other documentation to incur less tax and for the purpose of this case.  I do not consider he was being frank about his real income.

20. Mr White agreed that his taxable income in accordance with his tax returns for 1992 was $23,905 for 1993 $26,915 and for 1994 $36,003 (see also letter dated 6 June 1995, Exhibit 50).  Mr White gave evidence that in December 1994, he applied for a Gold Visa Card from Citibank.  He was shown copy of letter from his accountant to Citibank dated 9 December 1994 in which it was stated that his gross annual salary is $52,500 also included in Exhibit 50.  Mr White was not able to answer the question as to whether he had provided this information to his accountants.  Again I am satisfied he was evading the question and not being truthful with the Court as to his financial activities at that time.

21. Mr White was cross examined in respect of the documents which now form Exhibit 52.  The first document is copy of a Notice of Assessment from the Australian Taxation Office for the year ending 30 June 1989, showing a taxable income for that financial year of $10,946.  The second document is a Notice of Amended Assessment from the Taxation Office for the year ending 30 June 1990, showing a taxable income of $4,751.  Mr White was not able to explain why in the third document a letter dated 24 February 1992 to the St George Building Society, his accountants Mr Adriaanse and Associates Pty Ltd had stated his gross income earned for the year ending 30 June 1989 was stated as being $61,946 a difference of approximately $50,000 from the amount stated on the taxation assessment.  Similarly, Mr White could offer no explanation as to why in the same letter his accountant’s stated his gross income for the year ending 30 June 1990 was $44,825 some $40,000 greater than the amount stated for that year on his taxation assessment.

22. Again I do not consider Mr White was being frank in his answers or telling the truth to this Court about the real state of his finances at that time.  He appears to be again providing one set of figures to obtain a loan and another set of figures to the Taxation Office.

23. In his evidence to this Court, I am satisfied Mr White has grossly exaggerated his incapacity due to his respiratory problem.  This also affects his credibility.  In his amended statement of particulars, Mr White claims inter alia:

    1.A total incapacity to return to any employment including that of real estate agent.

    2.Inability to undertake light or moderate exercise.

    3.Tendency to develop recurrent and lower respiratory tract infections.

    4.      Reduced life expectancy.

    5.      Possible need of lung transplant within 7 – 10 years.

    6.      Oxygen dependency.

    I do not accept Mr White’s evidence that he has a total and permanent incapacity to return to any employment.

24. The overwhelming preponderance of the credible medical evidence is that Mr White is not so incapacitated.  Dr Geoffrey Field gave evidence he could see no reason why Mr White could not work as a real estate agent.  Dr McKenzie states Mr White should be able to play tennis, walk up hills and be able to do just about anything other than run a marathon.  Dr Lee gave evidence he would encourage Mr White to continue in his job as a real estate agent and that this would not worsen the condition.  Dr Lee also considered Mr White was capable of reasonable activity in terms of employment and should be able to play tennis and go for a brisk walk.  Professor Alpers gave evidence Mr White may not be able to do a 100m sprint or play rugby, he could certainly walk briskly and should be able to function at least in clerical duties of a real estate agent.  Professor Bryant ultimately concludes that Mr White could still play a game of tennis and keep up a desk job.  One of his own treating doctors, Dr Armstrong, is of the opinion Mr White would be capable of carrying out his duties as a real estate agent.  Professor Alpers made observations of a similar nature.

25. There is no evidence Mr White has reduced life expectancy.  Professor Bryant, who has been his treating doctor ultimately concluded that there has been no significant change in Mr White’s underlying small airways obstruction FEV1/FVC ratio since 1991.  His vital capacity has not changed since 1993.  Earlier in his diagnosis Professor Bryant had indicated Mr White had a reduced life expectancy.  However, at the conclusion of his evidence Professor Bryant stated that he no longer considered Mr White had a life threatening disease.  There is no other credible medical evidence to suggest there is any reduction in Mr White’s life expectancy.

26. With respect to the issue of the need for a lung transplant, Dr McKenzie gave evidence that he could not imagine any situation arising where Mr White would need a lung transplant.  Professor Bryant concluded that it is unlikely Mr White will need a transplant.  There is no credible evidence to support a finding that Mr White will require a lung transplant.

27. Mr White has a canister of oxygen at his home.  Professor Bryant gave evidence that he has continued to tell Mr White that this is not necessary.  Professor Alpers gave evidence Mr White does not need a container of oxygen with him as there is no evidence that he has hypoxia during the day time.

28. Another issue relating to Mr White’s credibility concerns his admission to St Vincents Hospital on 17 May 1999 for four days.  A test taken on 21 May 1999 showed his carbon monoxide haemoglobin (carboxy haemoglobin) level was 2.1 per cent.  I accept the evidence of Professor Alpers that this would indicate Mr White is still a current cigarette smoker.  Professor Alpers gave evidence a non-smoker would have a reading in the range of 0.2 per cent to 0.3 per cent.  Professor Alpers then gave evidence to the effect that the way you can get carbon monoxide in the blood without being a smoker is if you are heavily exposed to exhaust fumes.

29. Subsequent to this evidence from Professor Alpers, Mr White was recalled on 21 July 1999.  Mr White denied that he was a current smoker as at May 1999.  Mr White gave evidence that he had to leave the premises of St Vincents Hospital while he was an inpatient each day to go to cardiotherapy services for physiotherapy.  Mr White said this meant him walking three street blocks a distance of six to eight hundred metres and would then return.  Mr White stated he walked along Victoria Street which has very heavy vehicular traffic.  Traffic was congested.  Presumably the Court was to infer from this evidence that Mr White could have reached a reading of 2.1 per cent on his carbon monoxide haemoglobin from the traffic fumes to which he was exposed.  Under cross examination Mr White said he breathed through a hanky that he carried.  He spoke of having to continually stop and rest as he walked this distance.  Mr White could not remember when cross examined whether he mentioned to anyone at St Vincents Hospital that he was having trouble walking 600 metres along a congested Victoria Street.

30. I did not find any of this to be credible evidence and formed the impression it was evidence given in an attempt to counter evidence that had been given by Professor Alpers which evidence I accept as to his carbon monoxide haemoglobin reading on 21 May.  Letter from Clayton Utz dated 27 September 1999 to De Silva Hebron (Exhibit 95) makes it clear Mr White was aware of the evidence given by Professor Alpers when Mr White was recalled to give evidence on this aspect on 21 July 1999.  It was another example of Mr White giving evidence that he thought would assist his case rather than paying regard to its truth.  I am aware in making this finding that on 16 July 1999, Mr White underwent a urinary test to determine whether there was evidence he was still smoking and the subsequent report disclosed “urinary cotinine not detected” (Exhibit 95).  I have been unable to ascertain what the word “cotinine” means from either a standard dictionary or a medical dictionary.  However, I have assumed this report favours Mr White and demonstrates no evidence of smoking as at the date of this report.

31. Throughout the course of this case there is considerable evidence that exercise and weight reduction would greatly assist Mr White improve his condition.  He was specifically counselled by Dr Armstrong and physiotherapist Ms Catherine Bray to take up a program of exercise and reduce weight.  There is no credible evidence from Mr White as to why he has not pursued this advice more fully.

32. There is evidence that when undertaking lung function tests, Mr White did not take a full breath (Dr Field).  I have some doubts about whether when undertaking the lung function tests Mr White was making an honest effort.  Mr White did not present as a credible or reliable witness and I will detail other examples of this under the heading of medical evidence.

    Medical Evidence

33. The plaintiff claims that his condition is small airways disease or primarily small airways disease related to exposure to silica during the period of his employment in Darwin between 1971 – 1974.

34. I accept that Mr White was exposed to silica during the period of his employment between 1971 – 1974.  Whilst I have found that he exaggerated the period of time he was actually employed and that he was not employed for the number of hours each week that he states or the intense exposure to sandblasting that he maintains, I nevertheless accept that in this employment he was exposed to silica.  To establish causation the plaintiff must establish a material contributing cause.  Any cause which is more than minimal is to be regarded as material.

35. I apply the principle expressed by Lord Reid in Bonnington Castings Ltd v Wardlaw [1956] AC 613 at 621:

    “…..  What is a material contribution must be a question of degree.  A contribution which comes within the exception de minimus non curat lex is not material, but I think that any contribution which does not fall within that exception must be material.  I do not see how there can be something too large to come within the de minimis principle but yet too small to be material.”

    See also Commonwealth of Australia v McLean (1997) 41 NSWLR 389.

36. The alternative explanation that has emerged on the evidence is that the plaintiff has asthma, probably related to cigarette smoking and that there is no evidence of silica induced airways disease.

37. On the plaintiff’s own evidence his health was good until 1985 when he entered his own real estate business trading as Prime Real Estate (t/p 69).  He consulted Dr Lowe and was diagnosed with an upper respiratory tract infection.  This did not cause any incapacity for employment.  In July 1989 he consulted Dr Armstrong for persistent bronchitis.  This condition improved with antibiotic therapy.

38. Mr White consulted Dr Armstrong again in February 1991 relating to another bout of bronchitis.  Dr Armstrong referred Mr White to Professor Bryant who arranged for Mr White to be admitted to the smoking clinic at St Vincents Hospital for a week of intensive therapy between 17 and 25 June 1991.  In October 1991, Mr White was admitted to the Freemasons Hospital to assist him to cease smoking.  Mr White agreed in cross examination that he continued to smoke after 1991.  In March 1992, Dr Stewart May counselled Mr White to stop smoking.  Mr White gave evidence in cross examination that in1991 he attended hospital to give up smoking.  He gave Dr Swinburn a history of his smoking and stated that he had smoked 20 cigarettes a day at the peak since he was 16.  In 1991 Mr White was approximately 37 years of age.  Mr White stated he did have a relapse and gave evidence to the effect that four or five years ago he went to a restaurant in Canberra one night and smoked cigarettes, the number of which he could not recall (t/p 1102).  I did not find the evidence given by Mr White as to his past smoking habits to be reliable.  Mr White informed personnel at the Prince of Wales Hospital Department of Respiratory Medicine on 22 January 1992, that he smoked for 17 pack years.  This does not accord with the history he gave Professor Bryant.  In a report from Professor Bryant to Dr Armstrong dated 16 September 1993, Professor Bryant states in paragraph 3:

    “One could not be dogmatic about the cause for his chronic air flow limitation.  He does give a history of smoking cigarettes (5/day from the age of eighteen to twenty six and three/day from the age of twenty six to thirty three) but this level of self reported smoking is not sufficient to have resulted in the degree of air flow limitation that is now present.  …..”

1. I consider Mr White was not frank in his own history of his smoking habits relayed to Professor Bryant.

2. In a report dated 23 July 1991 from Professor Bryant to Dr Armstrong, Professor Bryant states in the first paragraph:

   “Your patient was unable to stop smoking despite extensive Outpatient treatment and he was therefore admitted to St. Vincent’s Private Hospital for a week of intensive therapy between the 17^th and the 25^th June 1991.”

3. This would indicate considerable efforts had to be made to address the smoking addiction.  Professor Alpers, whose evidence I detail later in these reasons, gave evidence that Mr White’s admissions to hospital for this purpose indicated an addiction to nicotine which would be difficult to overcome and he would not be surprised if Mr White did revert to smoking again.  I accept the evidence of Professor Alpers.  I do not rely on Mr White’s evidence that there was only one relapse after July 1991.

4. Mrs White gave evidence that her husband will wake during the night and appears to be short of breath.  Mrs White stated that Mr White uses the oxygen bottle beside his bed and then he is 100 per cent.  Mrs White also gave evidence that her husband uses bronchia dilators.  He uses them during the day if he becomes breathless and after using the bronchodilators his breathing improves within half an hour (t/p 484 – 485).  This positive reaction to bronchodilators is indicative of a condition of asthma on the evidence given by Dr Field.

5. I accept Mr White was referred by Dr Armstrong to Professor Bryant in 1991.  Professor Bryant is a Specialist Respiratory Physician.  Professor Bryant is a Thoracic Physician at St Vincent’s Hospital and Medical Director of the Lung Function Laboratory at that hospital.  Professor Bryant holds a number of appointments including Associate Professor of Medicine at the University of New South Wales.  The curriculum vitae of Professor Bryant was tendered and marked Exhibit 60.  A number of medical reports prepared by Professor Bryant were tendered and marked Exhibit 61.

6. I propose now to summarise the evidence given by each of the doctors called in these proceedings.

7. Professor Bryant gave evidence commencing on 17 February 1999 that Mr White had irreversible narrowing of his airway passages which is not steroid responsive and hence is not asthma.  When giving evidence in examination in chief Professor Bryant stated that Mr White’s condition was caused by his exposure to silica during the period of his employment in 1971 to 1974.  Professor Bryant detailed a list of authoritative articles dealing with the relationship between exposure to silica and small airways disease.  A memorandum prepared by Professor Bryant detailing the research and the literature with Professor Bryant’s conclusion based on this literature was tendered Exhibit 103.  These include articles on the substantial and tissue damaging reactions to silica which can occur without the classical radiographic changes of silicosis (t/p 532).  It is relevant to interpose with the comment that all doctors called to give evidence in these proceedings are agreed that there is no evidence Mr White has silicosis.  Professor Bryant gave evidence that when he first saw Mr White in 1991 his diagnosis was that Mr White had asthma, however he added subsequent tests have disproved this.  The only apparent cause for his lung condition that Professor Bryant could determine was silica exposure.  A lung biopsy was performed.  They did not obtain a satisfactory lung biopsy.  Professor Bryant said that his fear at that time was that a further lung biopsy could limit future treatment by making lung transplantation more difficult.

8. Included in Exhibit 61 is a letter from Mr White’s solicitors to Professor Bryant dated 1 February 1995 which asks amongst other questions:

   “6.What is your view as to the likely rate of decline in his lung function?”

9. In his reply dated 18 February 1995, Professor Bryant answers this question in the following way:

   “6.  It is always difficult to give a[n] accurate prognosis in patients with chronic airflow limitation because the disease does not run a very predictable course.  Given that Mr. White is not currently being exposed to any known factors which are likely to aggravate his condition and that he will continue to seek prompt treatment for any chest infections it is probable that his condition will continue to deteriorate at a rate similar to the rate of deterioration over the last few years.

   Prognosis in chronic airflow limitation is best based on readings of FEV1 (measured after bronchodilator).  Chronic airflow limitation is usually of life threatening severity at a stage when the FEV1 falls to 0.5L.  At this stage the patient is likely to be housebound, is unable to live independently, requires constant nursing care, and is often oxygen dependent.

   I have taken four FEV1 readings on Mr. White in the last 12 months (2.44L, 2.49L, 2.85L, 2.21L).  This gives an average FEV1 reading for 1994 of 2.50L.  His average reading for 1992, when I took 2 readings (2.98L & 2.74L), was 2.86.  This gives an annual rate of decline in FEV1 of 180mls.  If the present rate of decline in this man’s FEV1 continues at its present rate it can therefore be calculated that his chronic airflow limitation is likely to be of life threatening severity in approximately 11 years.”

10. Under cross examination (t/p 549) Professor Bryant gave evidence it was his opinion that Mr White has got moderately severe small airways obstruction related to silica dust exposure.  He arrived at the diagnosis in 1992/1993.  He said this diagnosis took account of Mr White’s history together with the symptoms described and Professor Bryant’s own clinical observations.  Professor Bryant agreed that in arriving at his diagnosis he carried out lung function tests and also exercises tests.  These tests were, Professor Bryant agreed, an important component in arriving at his diagnosis.  As at September 1993 Mr White had undergone nine lung function tests.  A lung biopsy was carried out in July 1992.  Professor Bryant agreed that he had never been able to isolate the actual presence of silica dust in Mr White’s lungs.  Mr White has had a CT scan every one or two years, totalling 16 since 1991, and these have shown no evidence of silicosis.  Neither did the CT scan show bronchial wall thickening.  Professor Bryant gave evidence that he believed Mr White had airways narrowing as demonstrated by every single lung function test which he has had.  Professor Bryant stated that the deterioration in Mr White’s lung function has resulted in limitation of Mr White’s ability to exercise, his capacity to breathe and inhibits his everyday activities.  Professor Bryant stated in his belief this made Mr White totally and permanently incapacitated.  This evidence in chief and in cross examination was given on 17 February 1999.

11. Professor Bryant resumed his evidence on 19 February 1999 (t/p 608).  In examination in chief Professor Bryant was taken to his report dated 28 August 1998 and stated there was no significant change in Mr White’s FEV1 reading which had not changed significantly between the years 1994 and 1998.  FEV1, being the maximum amount of air that a person can blow out in one second and is the most useful way of expressing airway limitation.  Under cross examination Professor Bryant said he did not believe Mr White should have a lung biopsy purely for medico legal purposes and that a lung biopsy was not necessary for the management of his condition.  Professor Bryant said he would only have reconsidered a lung biopsy if after discussions with Mr White he was satisfied that Mr White was prepared to accept the potential risks with the procedure involved.  Professor Bryant agreed that Dr Maxwell had recommended a lung biopsy because without this morphological evidence Mr White’s case may be regarded as unproven.  Professor Bryant stated he took offence at the suggestion by counsel for the defence that he was becoming too closely involved in Mr White’s legal case and stated he was solely concerned with Mr White’s treatment.

12. Professor Bryant was referred to a letter to him from Mr White dated 1 May 1998.  In this letter, Mr White told him that he had withdrawn his previous permission for his solicitors to access him directly and that he would expand on this when Mr White came to see him.  Professor Bryant agreed this was an unusual request.  Professor Bryant stated he was aware Mr White was considering changing solicitors but denied he was acting in the role of a confidante.  Professor Bryant was referred to an exercise test that was performed on 26 August 1993.  The purpose of the exercise tests is to demonstrate whether a person has reduced exercise capacity and if so, a possible explanation for that.  An important measurement is the heart rate and ventilation being the amount a person is actually breathing in and out.  The exercise test is reduced to a graph that shows ventilation over oxygen transference.  Professor Bryant gave evidence that he could not say from the result of the test whether or not Mr White ceased exercising because he had an intense sensation of breathlessness or whether he ceased exercising because he didn’t feel like doing it, or was anxious.  Professor Bryant was referred to the exercise test in 1998 and agreed that again poor effort was a factor in the exercise test.  He stated whether this is from foxing or anxiety is impossible to tell.  The fact that the oxygen saturation was falling made Professor Bryant worried that there was impairment of lung function.  Professor Bryant gave evidence that there was a substantial deterioration in lung function between 1991 and approximately 1994.  The FEV1 and all of the other things based on the course of therapy used have been relatively stable since 1994.  His present rate of loss would be 50 millilitres per year which is the normal rate of loss for a normal male person of Mr White’s age.  However, since 1991 Mr White’s loss in lung function has exceeded the loss which would be expected by virtue of age related changes alone.

13. Professor Bryant gave evidence that Mr White had stopped smoking in 1991.  This conclusion was based on Mr White’s own report and on tests when Mr White came in of his expired carbon monoxide level, which is a common indicator of whether or not a patient has been smoking recently.  Professor Bryant said he rejected the smoking history as being the cause of small airways disease because it was insufficient to cause such a disease.

14. Professor Bryant had obtained a history in 1996 that Mr White’s total smoking history was three pack years which is 20 cigarettes a day for one year.  In the history taken on 16 September 1993, he had recorded five cigarettes a day between the age of 18 and 26.  Professor Bryant agreed that if Mr White had been exposed to far less silica than Professor Bryant had assumed that would make a difference to his conclusions.

15. Professor Bryant agreed that the result of the FEV1 testing can be the product of significant error if the patient does not breathe as much as that person can.  He also agreed that a person who does these tests as often as Mr White would become familiar with how the tests are carried out and the expected results.

16. It is Professor Bryant’s evidence that Mr White never responded to steroids, but on several occasions he did respond to asthma bronchodilator sprays.  He gave evidence Mr White responded to a point on a number of occasions where one can conclude on those results that he had asthma.  Professor Bryant said he was concerned in arriving at a diagnosis to exclude the diagnosis of asthma.  For this purpose he obtained FEV1 readings, gave Mr White oral steroid tablets, sealed ventilation to determine whether his airflow narrowing could be favourably influenced by those medications and could never find any evidence of improvement.  Professor Bryant was aware Dr May had already done a methacholine challenge and obtained a negative result.  Professor Bryant gave evidence that Dr May had concluded the diagnosis lay between adult onset asthma and non allergic asthma and some other organic problem rather than anything related to silica.  Professor Bryant agreed Dr May had concluded Mr White was responding in a way more like asthma than anything else and that the condition was most likely asthma.  Professor Bryant said he felt Dr May’s other test results did not support this diagnosis.  Professor Bryant agreed Mr White responded very significantly to post bronchodilator elimination of obstruction or restriction.  Professor Bryant agreed these are the sort of changes you get when you are an asthmatic particularly adult onset asthma.  Asthma can arise in a person spontaneously or as a result of some allergic reaction.  An asthmatic is usually described as having central airways disease.  Professor Bryant agreed at least four of the tests conducted on Mr White show there is some central airways disease.  These were results Professor Bryant was prepared to adopt.  It is Professor Bryant’s evidence that central airways disease is asthma.  The central airways become inflamed from time to time causing a restriction that is removed using inhalers or bronchodilators.

17. Professor Bryant resumed giving evidence on 20 July 1999.  Since giving evidence on 19 February 1999, Professor Bryant had seen Mr White between 17 and 21 May 1999.  Professor Bryant had prepared a further report dated 8 June 1999 (Exhibit 87).  In this report Professor Bryant commences by advising Dr Armstrong that Mr White was admitted to St Vincent’s Private Hospital under his care on 17 May and discharged on 21 May.  “He was admitted because of recent symptoms of cough with purulent sputum and increased breathlessness.”  Professor Bryant then states commencing the final paragraph on the first page of his report:

    “While Mr White was in hospital I took the opportunity of repeating his spirometry as well as a methacholine provocation test.  His spirometry is difficult to interpret because of reduced patient effort.  The reduction in the FEV1/FVC ratio and the reduced FEF 25-75% indicate the presence of airflow limitation but this is mild in severity and review of his test results since I first saw him show that there has been no significant deterioration in his FEV/FVC ratio since 1991 and no significant change in his vital capacity since 1993.

    His methacholine provocation test shows a 20% reduction in FEV1 at a cumulative dose of 3.5 micromoles.  This indicates a very mild increase in bronchial responsiveness.  It is not consistent with a diagnosis of asthma but is in keeping with chronic bronchitis.

    The reduction in this man’s vital capacity is out of proportion to the level of his airflow limitation.  The cause of this is uncertain.  There is no CT scan evidence of any pleural disease, there is no CT scan evidence of any interstitial lung disease and his carbon monoxide gas transfer has always been normal, suggesting that interstitial lung function is normal.  He does not have significant obesity (BMI 27) and screening of his diaphragm has previously not shown any evidence of any paradoxical diaphragmatic movement.  It is therefore most likely that the cause for his reduced vital capacity is due to a combination of respiratory muscle weakness, physical deconditioning, and the chronic effects of mechanical back pain.

    In previous reports I have expressed the opinion that Mr White’s airflow limitation is deteriorating and is likely to have a significant effect on his life expectancy within the foreseeable future.  However, with the benefit of these recent test results, which show that there has been no significant change over a period of many years, I am now of the view that his pulmonary function has been stable since 1993.”

18. When asked in examination in chief on 20 July 1999, Professor Bryant said he had not changed his diagnosis, he is using the words “chronic bronchitis” interchangeably with his previous diagnosis of small airways disease related to exposure to silica.  Under cross examination Professor Bryant said he believed Mr White had chronic bronchitis and small airways disease, both problems together.  Professor Bryant agreed that it commonly occurs that a smoker will develop chronic bronchitis whilst they smoke and then continue to suffer from the condition even after they have given up smoking.

19. Professor Bryant gave the following evidence in cross examination by Mr Kourakis QC (t/p 1039):

    “If you don’t argue against the proposition that smoking could have caused the chronic bronchitis from which he suffered in the mid-1980’s, on what basis do you need to postulate as a cause to that chronic bronchitis exposure to silica in the mid-70s?---The basis for my views were that this man’s lung function had appeared to deteriorate after he had quit smoking and this is unusual in my experience and it occurred over a short – a relatively short period of time, namely over several months to several years and that made me concerned that I was overlooking an alternative cause for his problems.”

20. Professor Bryant agreed that what is unusual about Mr White’s respiratory function tests over the years is their extreme variation.  He agreed this variation cannot be explained by a diagnosis of silica induced chronic airways obstruction.  Professor Bryant stated it could be due to Mr White having variable airflow limitation, in other words he could have asthma. It was Professor Bryant’s evidence that he did not believe this was the case because Mr White did not usually respond to a bronchodilator.  He had not improved when treated with steroids and the results of the methacholine provocation test was not consistent with asthma.  Professor Bryant agreed there is a form of asthma that is steroid resistant.  Professor Bryant also agreed that Mr White’s lung function tests showed airflow obstruction which was not severe and was not declining.  It is Professor Bryant’s evidence that other reasons which could explain the variations in the lung function tests results is a variation in patient effort because of pain or muscle weakness or a lack of desire to do the test.  Professor Bryant agreed that prior to 1998 when a respiratory muscle test was carried out he had not thought to conduct such a test which may explain the variability in the lung function test.  Professor Bryant stated that he could find no evidence of significant change in Mr White’s airways disease since 1993.  Professor Bryant was referred to the document titled Analysis – Lung Function For FEV1 (Exhibit 100).  He was asked a series of questions in cross examination about why he gave the average FEV1 reading for 1994 of 2.50L in his report to Mr White’s solicitors on 18 February 1995 and in his report to Mr R. Slattery, an insurance officer responsible for benefit payment, dated 19 August 1996 (Exhibit 61) stated in the final paragraph on p 1-2:

    “His best post-bronchodilator FEV1 reading in 1991 was 3.52L (75% of predicted).  In 1994 the mean value of his readings was 2.76L (58% of predicted) and his most recent reading (25 July 1996) was 2.56L (56% of predicted).  Given this rate of deterioration I am concerned about his prognosis.  I have warned him that his condition will need to remain under constant treatment and close supervision as it seems likely that he will be subject to repeated chest infections needing recurrent episodes of treatment and that his exercise capacity will become increasingly restricted.  Because of the variability of the test results, a recognised feature of this type of medical condition, I am unable to be dogmatic about the precise rate at which his condition is declining.  However it is my belief that his present level of impairment is likely to increase with time and that substantial impairment is probable within the next ten years.  I believe that it is more probable than not that he will require additional home treatment such as a nebuliser and home oxygen and it is possible that there will be a need for more dramatic forms of treatment such as lung transplantation.”

1. Dr Field said he had been involved with all the lung function tests for the Dust Diseases Board in NSW for over 20 years.  Dr Field said referring to the literature studies that there was a consistency which suggested that maybe the inhalation of silica aggravated the effect of smoking.

2. Dr Field made further reference to the problem of research which had been done on the basis of cross sectional studies and stated there are problems with comparing matters from cross sectional studies.  Under cross examination, Dr Field agreed that the fact Mr White was hyperventilating at the time of the tests to which he had referred, could be explained on the basis that he was in some physical distress.  He found such a high respiratory rate difficult to explain on the basis of anxiety alone.

3. In re-examination Dr Field was referred to the lung function test conducted at St Vincents Hospital on 8 May 1991.  It is Dr Field’s evidence that the results of this test do not differ in any significant way from the tests taken in January 1992 and the results are similar to the results Dr Field obtained in 1992.  The tests in the report dated 8 May 1991 are in Dr Field’s opinion consistent with mild asthma.

4. Dr McKenzie commenced his evidence on 16 July 1999.  Dr McKenzie was called as a witness for the defence.  Dr McKenzie is a respiratory physician.  A cirriculum vitae and report dated 20 January 1999 prepared by Dr McKenzie were tendered and marked Exhibit 78.  Dr McKenzie’s conclusions are set out on pp 6 and 7 of his report and include the following:

   ·     Mr White has moderately severe asthma probably aggravated by reflux oesophagitis, which seems to be at least moderately severe.

   ·     He had significant exposure to silica but the duration was relatively short at 3½ years.

   ·     There is no evidence of silicosis.  Silicosis never presents as an asthmatic condition.

   ·     With appropriate treatment and attention to certain conditions there is no expectation of significant deterioration of his asthma in the foreseeable future.

   ·     His level of incapacity which had been described by Mr White to Dr McKenzie is out of all proportion with the documented mild to moderate impairment of pulmonary function.

5. In his evidence, Dr McKenzie stated Mr White had told him he smoked about 10 cigarettes a day for a period of 20 years ceasing in 1992.  Dr McKenzie gave detailed evidence as to the lung function test.  Dr McKenzie was referred to the lung function test (Exhibit 94).  Dr McKenzie stated that in looking at the results of these tests, if this was the best at which the patient could perform, the only diagnosis would be asthma.  Dr McKenzie was referred to the tests taken by Dr Field in January 1992.  Dr McKenzie stated he considered these the most reliable of the tests.  He gave evidence that if there was any significant small airways disease that was affecting lung function, you would be able to see indications of that on the CT scans.  Dr McKenzie was asked if dust deposition had affected Mr White’s lung function.  Dr McKenzie gave the following answer (t/p 898 - 9):

   “---Dust deposition can’t account for the large airway narrowing that was demonstrable in 1991 at a time when there was minimal, if any, evidence of small airway narrowing per se.  Therefore, I think that whatever’s happened subsequent to that cannot be explained by dust deposition either because there hasn’t been any, nor has there been any dust deposition within 20 years of time since then.  What has happened since that time has been a diminution in the total lung capacity and in the vital capacity which is a restrictive, if you like, problem, but in the absence of any obvious cause for a restriction of lung volume.  So the changes in his lung function in the last 8 years cannot be accounted for by any kind of dust disease that I’m aware of.  Dust disease is not associated with dramatic variations in lung function such as we’ve seen and talked about.”

6. Dr McKenzie gave his analysis of the literature by the authors referred to in the course of these proceedings.  Research authors such as Churg, Hendrick and Becklake.  Dr McKenzie is of the opinion that the probability is dust exposure alone will not cause small airways disease sufficient to cause significant disability.  The probability of that is very low and that is in people exposed to high levels of dust for 30 years.  Dr McKenzie stated that in Mr White’s case (t/p 900):

   “…(a) the lung function tests don’t support small airways disease, they support central airways disease, if anything.  The pattern of development of this is not typical of what occurs in occupational – in dust induced lung disease where there is an insidious decline in function in a relatively predictable fashion.”

7. Dr McKenzie was asked about Dr Churg who is a highly regarded expert in this area and has written articles being articles on which Professor Bryant placed considerable reliance.  Dr McKenzie acknowledged the work of Dr Churg but discounted the relevance of Dr Churg’s theories in respect of Mr White.

8. It is Dr McKenzie’s evidence that on the history of Mr White and having regard to the results of exercise tests, lung function tests, CT scans, radiological results and other physiological tests, it is his diagnosis that Mr White has moderately severe asthma.  Dr McKenzie gave evidence that Mr White’s gas exchange part of his lungs is fine and that he just has some airway narrowing.  In Dr McKenzie’s opinion Mr White’s capacity is not seriously limited.  It is Dr McKenzie’s evidence that even a person with one lung removed is not usually disabled and Mr White is in a far better position than that.  He should be able to do just about anything, other than running a marathon.  Dr McKenzie asserts Mr White could play tennis and walk up hills.  He is not seriously limited.

9. Dr McKenzie was asked questions and gave very detailed answers in respect of the exercise tests undertaken by Mr White.  Dr McKenzie gave his conclusion that there was a very abnormal physiological response to exercise.  There were two obvious conclusions for this.  Mr White was extremely anxious which can cause a patient to hyperventilate or he was simply panting because he wanted to.

10. Dr McKenzie stated Mr White certainly does not need a lung transplant now.  He could not imagine any situation in the future where Mr White would need a lung transplant.  Lung transplants are never done on people with asthma.  Dr McKenzie stated he had looked at all 16 CT scans.  They all showed the lungs to be normal.  The latest CT scan was technically the best and reported by the radiologist unequivocally as normal.  Dr McKenzie resumed giving evidence on 30 September 1999. Dr McKenzie was asked how he determined the diagnosis of asthma in Mr White.  Dr McKenzie gave this answer (t/p 1275):

    “---Well, Mr White’s history is absolutely typical for asthma.  I think some of the best accounts of this are found in Doctor Armstrong’s notes, in which he describes a couple of severe attacks in – I don’t – I can’t be sure of the dates but in or around 1990 or 1991, on a couple of those occasions he had an infection and he had a lot of wheezes in the chest, which is a typical sign of asthma.  He had shortness of breath, cough and sputum production.  That is a typical history of asthma.  When I think Doctor Field saw him in 1991 he made a further confident diagnosis of asthma.  I think other specialists also arrived at the same conclusion.  I think virtually every expert who’s seen him has agreed that he must have at least some asthma.”

11. Seeing the results of the lung function tests and other results confirmed the diagnosis of asthma.  It is Dr McKenzie’s evidence that Mr White has airway narrowing but this is not small airways disease.

12. Dr McKenzie was taken to the methacholine challenge test that was conducted at St Vincents Hospital on 21 May 1999 (Exhibit 86).  He gave evidence that the methacholine challenge test is an aid to the diagnosis of asthma you would rely on it if none of the other criteria had been met.

13. Dr McKenzie was asked to comment on Professor Walters’ finding of restrictive lung defect i.e. stiff lungs consistent with the alveolar septal disease noted on at least some of his airway biopsies.  Dr McKenzie states he could not find any evidence that Mr White does have restrictive lung defect in any of the lung function tests which are considered to be acceptable.  He assumed Professor Walters did not have access to the 1991 and 1992 lung function tests when he came to his conclusion. It is Dr McKenzie’s evidence that the more recent lung function tests are marred because Mr White tends not to breathe in at all or to blow out at all so that by poor effort or poor coordination, he lacks the ability to do the test to best standard. Dr McKenzie stated that the CT scans have shown no change to Mr White’s lungs.

14. Dr McKenzie further stated that the biopsy test shows no evidence that the alveolar wall thickening is due to dust because no dust was seen.  Dr McKenzie gave evidence he has examined hundreds of patients with silicosis.  It is completely outside his experience or knowledge of the literature to see a case of disability or abnormality of lung function attributable to silica in someone who has one perfectly clear chest x-ray, let alone 16 clear CT scans.  Dr McKenzie could find no evidence of silica in the lungs or any evidence that silica has caused damage to the lungs.

15. Under cross examination Dr McKenzie agreed that he had seen Mr White on only one occasion and in addition had looked at a great number of documents including tests results.  He agreed that a preliminary diagnosis can change over time however his diagnosis of asthma has been strengthened by reading the documents of the treating physicians and the local medical officer.  Dr McKenzie acknowledged he is at a disadvantage compared to those who have seen Mr White more frequently.  His evidence is that the diagnosis of asthma is based on the medical history of Mr White and the demonstration of reversible airflow obstruction.

16. It is Dr McKenzie’s evidence that even allowing for the fact that Mr White may not have had sufficient protective apparatus when exposed to the sandblasting and that there was intense exposure to fine particles of silicone dust over three years there could be no damage to the lungs in the absence of frank silicosis.  Mr White had told him he was exposed to a lot of dust.  However, there was not a skerrick of evidence in the radiographic series of any retained dust in the lungs.  The only logical conclusion to come to is that whatever dust was inhaled was subsequently able to be removed.  It was put to Dr McKenzie in cross examination that a number of articles by persons such as Churg, Becklake, Hendrick and Burge showed that there can be silica related damage to the small airways without accompanying evidence of frank silicosis.  Dr McKenzie gave the following reply (t/p 1296):

    “---You’ve mentioned five articles there but they’re – they’re all actually referring to the one study.  I think at least three of the other articles you mentioned were reviews of the literature so the study that we’re talking about that shows damage to small airways by silica is based on the microscopic study of lungs by a pathologist and the – and the main study that’s been quoted widely is the one by Andrew Churg.  Now, the demonstration of a microscopic abnormality in a small airway does not translate into a disease or any – or indeed any impairment of function, much less disease.”

17. Dr McKenzie did not agree that the literature showed that workers exposed to silica may develop obstruction in the small airways in the absence of frank silicosis.  Dr McKenzie did not agree that Mr White with his history of exposure to fine silica in Darwin in the 1970’s and his history of cigarette smoking could have small airways limitation related to silica exposure notwithstanding the fact that there’s no evidence that he’s got silicosis.

18. Dr McKenzie repeated his assertion that the lung function test at St Vincents Hospital of 1991 and the tests by Dr Field in January 1992 are technically acceptable because there is sufficient data.  Dr McKenzie considers that the Registrar who interpreted the tests at St Vincents Hospital misinterpreted these tests.

19. Dr McKenzie stated that he earlier gave evidence that the tests carried out by Professor Bryant in August 1997 were technically acceptable but now believes he may have been wrong about that.  He was adamant there was no evidence of a physical limitation in Mr White on the basis of a lung problem, other than the possibility of exercise induced asthma which Dr McKenzie considered has not been excluded as it should have been.

20. Dr Lee gave evidence (t/p 780) on 15 July 1999.  Dr Lee is a thoracic physician.  Dr Lee reviewed Mr White on behalf of Professor Bryant in July 1993 and because of the uncertainty about Mr White’s condition and because Dr Lee has a long experience of people with dust disease.  A report dated 21 July 1993 together with a cirriculum vitae of Dr Lee were tendered (Exhibit 75).  Dr Lee stated in his report (par 2):

    “Quite obviously, he does not have silicosis nor does there appear to be a basis for lodging a compensation claim for his respiratory problem.  Whether this is regarded as primarily asthmatic in character or associated with a component of irreversibility involving the small airways, is of considerable nosological interest but almost certainly irrelevant in terms of an occupational disorder if for no other reason than the interval of almost twenty years between his sandblasting activity and the development of exertional dyspnoea.”

21. He gave evidence there was a component of small airways disease but in order for there to be any significant impact upon lung function there must be extensive small airways disease present.  There was no such extensive small airways disease present in Mr White.  The CT scan did not show any evidence of silicosis.  Dr Lee stated in respect of Mr White, the absence of paroxysmal component makes Mr White a relatively unusual asthmatic.  Asthma is most commonly associated with the large airways.  Mr White’s condition was located in the large airways.  Dr Lee noted that Mr White inhaled with some reluctance because he felt the medication was not doing him any good.  It is Dr Lee’s evidence that this could be as a consequence of failing to follow advice as to the application of the treatment.  Dr Lee gave evidence that he would encourage Mr White to continue to work as a real estate agent.  By doing so he will not worsen his condition.  Dr Lee considered Mr White was capable of reasonable activity in terms of employment and should be able to play tennis and go for a brisk walk.  A regular exercise program to maintain optimal fitness was to be encouraged.  It is Dr Lee’s opinion that Mr White had lung function which was clearly asthmatic and with significant response to bronchodilator.

22. Under cross examination Dr Lee stated that (t/p 790): “disability is objectified into a person’s life and there are a number of other factors that influence disability, it is not really specifically a medical issue.”  Dr Lee stated he had obtained a history of smoking from Mr White which was that Mr White had smoked for about 20 years from the age of 17 to the age of 37 smoking an average of 10 cigarettes a day.  He agreed this level of smoking would be unlikely to cause any significant small airways disease.  Dr Lee accepted that there may be involvement of the small airways in this case.  Mr King QC, for the plaintiff, put a series of assumptions to Dr Lee relating to Mr White’s exposure to silica during the period 1971 – 1974.  Dr Lee stated if sandblasting had been carried out on a day to day basis for 12 months there would have been a risk to the plaintiff of serious consequences.  Sandblasting is a notoriously dangerous activity.  However, if sandblasting had been so intense as described by the plaintiff, one would expect there to be evidence of the disease long before.  The interval of time between exposure and onset of complaints Dr Lee found very difficult to explain.  Exposure in teenage years or early adulthood has more effect than exposure in later years.  Dr Lee was aware of the hypothesis in the papers written by Dr Churg that there is a synergistic effect between exposure to silica and cigarette smoking.  Dr Lee gave evidence that considering the history of Mr White’s exposure to silica particles during sandblasting, it was possible that that could have produced in Mr White small airways disease short of producing frank silicosis.  As Dr Lee stated “possible is where I’d put it.”  Dr Lee said that the model with asbestosis was the lung was damaged not long after the dust material settled there but there can be a significant period of time before symptoms are produced.  It is Dr Lee’s evidence that Mr White’s major disease process is in the large airways, he has some abnormality in his small airways.

23. In re-examination by Mr Kourakis QC, Dr Lee agreed that Mr White’s ratio of FEV1 to FVC (maximum air that can be blown out after a maximum breath in) has always been in the range 60 per cent to 70 per cent.  This means the measured function is stable and the disease is not deteriorating.  Dr Lee gave evidence that the tests undertaken by Mr White indicated to him that Mr White’s condition was asthma.  Dr Lee was referred to the lung function studies performed for Professor Bryant in the early 1990’s.  On the readouts there is a history of smoking for 17 pack years which means an average of 20 cigarettes a day for 17 years.  This is a lot of cigarettes and would increase the possibility of smoking being the cause of any obstruction in Mr White’s airways.  Dr Lee gave evidence as to the importance of a regular exercise program and keeping fit.  Dr Lee’s evidence is that where patients have silicosis which is progressive, this is readily visible on a plain chest radiograph and more sensitively detected on a CT scan.

24. Professor John Alpers who is with the Flinders Medical Centre at Flinders University, was called by the defence on 15 July 1999.  Two reports of Professor Alpers dated 25 March 1998 and 28 October 1998 together with his curriculum vitae were tendered and marked Exhibit 76.  Professor Alpers described Mr White as a 10 pack smoker on the basis of a history that he smoked 10 cigarettes a day for 20 years.  He agreed that in his report dated 28 October 1998 he described Mr White’s exposure to smoking as six pack years.  Cigarette smoking is dose related injury over time.  There was a discrepancy between the lung function results and Mr White’s claim that after 100 metres of walking he became short of breath.  His lung function tests show he should be able to play golf and lead a normal exercise life.  In March 1998 at Flinders Medical Centre, an impedance oscillometry was performed on Mr White which is a sophisticated form of lung function manoeuvre.  In this test no effort is involved.  The investigation showed three things:

    1.Mr White has increased central upper airways or throat airways resistance with some closure of the large airways.

    2.Peripheral or small airway closure or resistance.

    3.Significant bronchodilator response.  When he was given bronchodilator the resistance fell.

25. Professor Alpers’ diagnosis is that Mr White has mild asthma.  Professor Alpers gave evidence relating to key hole surgery which is the name given to a method of taking a lung biopsy which Professor Alpers described as not carrying any preclusion risk for transplantation.  Professor Alpers gave evidence (t/p 845):

    “….. this man does not have silicosis, based on the CAT scan and the lung biopsy, in the conventional sense of nodular silicosis.  There are various forms of silicosis, but the common form is that one.  It’s – to have an abnormality of the airways which is described in the literature, but mostly in association with coal workers and others who have nodular disease, but to have just airway disease from silica is, I think, extremely rare.  I’ve never seen a case.  And while it is – has been reported, I think in some of the studies, it is an unusual phenomenon, and it would be unusual to get the condition occurring some 10 or 12 years after the exposure.  That would be – most airways injury occurs at the time of the insult.  And a delayed effect like this on any airway problem which is most unusual.”

1. In his report dated 28 October 1998, Professor Alpers states at p 2 par 6:

   “At this stage I do not believe that Mr White will require a lung transplant in the future as it is difficult to assess his true deterioration.  Effort and variable performance contributes to the variations in spirometric values that have been recorded over 1991 - 1998.  I also note in this regard he has gained at least 10 kg in weight from 1988 through to 1998.  This will also have an effect on lung function and upper airflow.”

2. Professor Alpers was asked to comment on the lung function tests performed by Mr White over a period of years.  Professor Alpers commented on their variability, they did show his airflow obstruction had not changed dramatically over the years.  He stated it is a pattern you get in asthma or recurrent respiratory infections another contributing factor to the abnormal airflow maybe the effort he is putting in at the time.  Professor Alpers’ evidence is that the various lung function tests show Mr White has significant reversibility of his lung function and that suggest the airway abnormalities are those associated with asthma.  It is Professor Alpers’ evidence that with Mr White’s level of lung function he should be able to function reasonably well and increase his capacity by exercising.  He could work performing clerical duties, as a real estate agent and conduct house inspections.  There is no reason why he would need to take oxygen during the day.  Professor Alpers was referred to tests taken on 21 May 1999 and stated these showed a level of 2.1 per cent carboxyhaemoglobin in Mr White’s blood.  Professor Alpers gave evidence this indicates Mr White has carbon monoxide in his blood, the assumption is he is a current cigarette smoker.  Professor Alpers went on to state that the way you can get carbon monoxide in the blood without being a smoker is if you are heavily exposed to exhaust fumes.  He gave the example of a New York foot policeman walking the beat in the streets of New York who can develop levels of carbon monoxide up to 4 per cent.  He stated this was an unusual circumstance for non-smoking individuals and the test is also used in his laboratory to check the veracity of the person who says they are either smoking or not smoking (t/p 850).

3. Under cross examination Professor Alpers agreed it was not appropriate to take a further lung biopsy from Mr White.  Professor Alpers said he could not feel sure about the effect of smoking on Mr White’s lungs.  This was because he was uncertain as to the veracity of Mr White’s past history as to smoking.  The fact that he was admitted to St Vincents Hospital in 1990 to get him off cigarette smoking shows he was clearly nicotine addicted.  His evidence is that nicotine is an addiction that persists and Professor Alpers is not surprised that Mr White has continued to smoke.  Professor Alpers agreed that usually smokers do not present with problems until later in life.  Exposure to dust combined with smoking will add to the potential pathology.  Under cross examination Professor Alpers agreed that Mr White has small airways disease present and this is a contributing factor to his lung problem of some significance.  One part of his lung problem is an asthma component.  It is Professor Alpers’ evidence that if Mr White had asthma alone it would be expected that he would have more airway reaction.  He is on regular inhaled corticosteroids which does reduce the bronchial reactivity.  If it were not for this treatment he may be much more asthmatic than is currently evidenced.  Professor Alpers agreed Mr White had significant exposure to silica.  Professor Alpers said the exposure to silica may be a contributing factor but he thought if Mr White continued to smoke that would be more injurious in the long term.  Professor Alpers then gave evidence in cross examination as follows (t/p 862 – 863):

   “It was a very long time frame following his exposure to the then production of respiratory symptoms.  It was at least 10 to 12 years.  Most of those symptoms were upper airway diagnoses from Doctor Armstrong in the form of sinusitis and upper respiratory infections, and it wasn’t really till the late 1980s that, if at all, that he actually had any bronchial disease first manifest.  And I think that’s asking a lot for the silica injury caused in early 70s to then be presenting at that period of time, if it was the major factor.  Silica, when it gets into the lung, it does cause immediate effects: it involves the macrophages of the alveolar tissue; it causes fibroblastic formation and direct injury.  If he had an exposure at the time he would’ve had significant disease soon after he was working in that environment and probably it may well have been progressive from there on.  But there was this huge time gap, and I think that’s – that does not fit at all with your proposition.”

4. Professor Alpers went on to say he thought it likely that there could be a contribution to the lung condition from silica exposure the percentage of the contribution is unknown.  A lung biopsy would be the only way to prove it and that has not been deemed appropriate.  An airways disease does not normally occur after a gap of 10 – 15 years after exposure.  Professor Alpers recommended exercising and returning to full time capacity as the way toward rehabilitation.

5. Miss Catherine Bray (t/p 228) gave evidence that she is a physiotherapist with a practice in Sydney specialising in cardiopulmonary physiotherapy.  Mr White has been a patient of hers since September 1993, having been referred by Professor Bryant.  Ms Bray prepared a number of reports with respect to Mr White which are all included in Exhibit 11.  In her report dated 18 December 1998, Ms Bray stated at p2 par 4:

   “I reviewed and treated Mr White one to two monthly in the four years following his original referral, less frequently in the last eighteen months.  Treatments have involved breathing control training, thoracic joint mobilisation techniques and graded exercise.  The initial improvements observed have not been maintained and over the last 24 months Mr White’s general fitness has deteriorated.  This in turn has made it increasingly difficult to manage respiratory tract infections and the airways secretion characteristic of Mr White’s infective episodes.  Mr White’s irritative coughing has become increasingly difficult to manage and has resulted in notable musculoskeletal dysfunction and pain, the extreme of which has been his ongoing cervical spine problem.”

6. Under cross examination Ms Bray stated she had provided a regular exercise program for Mr White.  Ms Bray detailed the exercise program that she had devised for Mr White together with a weight program which was terminated and has not yet resumed because of neck pains and other problems not related to his respiratory condition.  Ms Bray gave evidence in cross examination that she had suggested to Mr White he invest in an exercise bike to use at home in particular a recumbent bicycle.  Ms Bray said she first raised this with Mr White toward the end of 1996 when Mr White told her he was having difficulty in walking.  Ms Bray had discussed a walking program with him in particular to keep down his weight.  The exercise bike Ms Bray had in mind would cost from $1500 to between four or five thousand dollars.  Ms Bray gave further evidence an exercise bike can be hired for between $2 and $5 a day.

7. Ms Bray gave evidence Mr White was admitted to St Vincents Hospital between 11 and 17 August 1997.  She agreed that in the course of this admission Mr White had physiotherapy treatment which can be exhausting.  Ms Bray said she was not surprised that he had been able to go out and have a dinner which included alcohol at the Hilton Hotel.  Her evidence is Mr White would have been on antibiotics which would have relieved his condition.

8. Ms Bray stated she had recommended to Mr White a period of walking in ten minute blocks.  On one occasion he had told her he was so disabled he could not walk round his own backyard.

9. This concludes my summary of the medical evidence given in these proceedings.

10. Having heard and considered all the medical evidence I prefer the evidence of Dr Field and Dr McKenzie which is supported on a number of important aspects by the evidence of Dr Lee and Professor Alpers.  I do not accept the evidence given by Professor Bryant, Dr Maxwell and Professor Walters as to their diagnosis of Mr White’s condition.

11. I concluded the evidence given by Dr Field and Dr McKenzie demonstrated a very rigorous and independent analysis of all the data and information concerning Mr White.  This combined with the depth of experience of both specialists in this field provided a more credible and reliable diagnosis of Mr White’s condition.

12. I did have a number of concerns about the evidence of Professor Bryant which are as follows:

    ·     Professor Bryant’s opinion must to some extent rely on a history given him by Mr White which history I have found to be unreliable.

    ·     Professor Bryant’s conclusions about Mr White’s condition as reflected in his report dated 8 June 1999 (Exhibit 87) and his evidence on 20 July and 29 September 1999 differ in a number of important aspects from his report dated 18 February 1995 (Exhibit 61) and his evidence given on 17 and 19 February 1999.  This difference is not all explainable on the basis of new information.  Much of the evidence on which Professor Bryant drew his final conclusions had been available for many years it was just a different way of interpreting the data.

    ·     The final conclusions of Professor Bryant given in evidence after vigorous and thorough cross examination as to Mr White’s present condition and future health prospects ultimately accord more closely with the findings of Dr Field and Dr McKenzie.

    ·     In his evidence on 17 February 1999 Professor Bryant expressed the view that Mr White was totally and permanently incapacitated.  This differs markedly to the evidence given by Professor Bryant on 20 July 1999 that Mr White is capable of playing tennis of working in an office, driving to properties and showing people around.  When re-examined on 29 September 1999 Professor Bryant did say he thought Mr White would have difficulty doing a full range of work as a real estate agent.

    ·     Professor Bryant ultimately resiles from his earlier findings as to Mr White’s reduced life expectancy and need for a lung transplant.

    ·     I am not able to reconcile the differing view expressed by Professor Bryant in his letter to Mr White’s solicitor dated 18 February 1995 and his letter to Mr Slattery, the insurance officer, on 19 August 1996.

13. Dr Maxwell gave evidence on 12 July 1999 which was after evidence given by Professor Bryant on 17 and 20 February 1999 and before Professor Bryant gave evidence on 20 July 1999.  Accordingly, Dr Maxwell was not privy at the time he gave evidence to the considerable change of opinion expressed by Professor Bryant in his evidence of 20 July 1999 and 29 September 1999.

14. In his evidence Dr Maxwell stated Mr White was totally and permanently incapacitated in returning to his position as a full time real estate agent and salesman.  He also stated Mr White had a reduced life expectancy as a consequence of the development of silica induced small airways disease.  Dr Maxwell gave further evidence that in forming these opinions he had relied on the conclusions Professor Bryant had drawn from certain tests carried out on Mr White.

15. As Professor Bryant subsequently resiled from the conclusions to which Dr Maxwell was referring that must necessarily diminish the weight I could attach to Dr Maxwell’s opinion.

16. Professor Walters referred to Mr White having “stiff lungs” and referred to the “alveolar septal disease noted on at least some of his airway biopsies”.  None of the other medical evidence supports such a finding.  This may be explained on the basis of Professor Walter’s evidence that he had not reviewed the lung biopsies himself.  Professor Walters did agree under cross examination that the lung function test did cast some doubt on the conclusion of restrictive lung deficit arising from exposure to silica.  Professor Walters is the only specialist who places any significance on a finding there was some thickening of the alveoli wall.

17. I formed the impression that Professor Walters had either not had access to all of the data and information relevant to Mr White or alternately had not had an opportunity to review it all and this must affect the weight I attach to the evidence of Professor Walters.

18. In preferring the evidence of Dr Field and Dr McKenzie, I am aware that they each saw Mr White on only one occasion and did not have the benefit of continuous observation as did his treating specialist, Professor Bryant.

19. I have already detailed my reasons for my concerns in respect of the evidence given by Professor Bryant.  I have no such concern in respect of the evidence of Dr Field and Dr McKenzie.  Both doctors had made a very thorough analysis of the medical information relating to Mr White.  Both doctors rejected the theory that Mr White’s respiratory problems were in any way related to his exposure to silica during his employment in 1971 – 1974.  I found both Dr Field and Dr McKenzie to be credible and reliable witnesses with a thorough grasp and understanding of Mr White’s medical history, the significance of the various tests and diagnostic tools, such as CT scans and lung biopsies which Mr White had undergone, his reaction to various tests and his reaction to various forms of treatment.  I am satisfied that the findings of Dr Field and Dr McKenzie should be accepted by this Court.  Both doctors were well aware of the research and the literature on which Professor Bryant was relying and both gave reasons for rejecting these theories in the case of Mr White.

20. Dr Field was adamant that in the absence of silicosis there could be no evidence sufficient to convince him that silica exposure causes airway disease in people without silicosis.

21. On all the evidence in this case particularly the results of the 16 CT scans and the lung biopsy, Mr White does not have silicosis and this seems to be a point on which all doctors are agreed.

22. Dr Field gave evidence to the effect that in all his experience he had never encountered a case where dust induced bronchitis settled then came back 10 years later.  This was not clinically acceptable to Dr Field.  I accept the opinion of Dr Field that it is not clinically acceptable to find Mr White could have left the job where he was exposed to silica in 1974 and that 10 years or later the effects of such exposure could come back.  This view is supported by the evidence of Dr McKenzie and Professor Alpers.

23. In view of this evidence from Dr Field, which I accept, even if Mr White was exposed to silica over the duration and with the intensity that he maintains the effluxion of time between this exposure and his complaints of respiratory problems would, on the medical opinion that I accept, be a reason for rejecting a claim that his respiratory problems are in any way related to his exposure to silica between 1971 – 1974.

24. Dr McKenzie is also of the opinion that Mr White does not have small airways disease.  I accept this opinion and Dr McKenzie’s opinion that in all probability dust exposure will not cause small airways disease sufficient to cause significant disability even in persons exposed to high levels of dust for 30 years.  Dr McKenzie has examined hundreds of patients with silicosis.  It is completely outside his experience for a person to have a disability or abnormality of lung function attributable to silica when there is a perfectly clear chest x-ray and as Dr McKenzie says “let alone 16 clear CT scans”.  Dr McKenzie concluded there was no evidence of silica in Mr White’s lungs or any evidence that silica has caused damage to the lungs.  I accept this opinion.

25. Dr Lee and Professor Alpers have both given evidence which supports the evidence of Dr Field and Dr McKenzie on some important aspects.  To the extent that the evidence of Dr Lee and Professor Alpers does support the findings and conclusions of Dr Field and Dr McKenzie, I accept the evidence of Dr Lee and Professor Alpers.  Dr Lee gave evidence  there was no extensive small airways disease present in Mr White and for there to be a significant impact on lung function there must be small airways disease present.  Dr Lee supported evidence given by Dr Field and Dr McKenzie that even if sandblasting had been intense as described by Mr White it was difficult to explain the interval of time between exposure and onset of complaints.  Professor Alpers supports the evidence given by Dr Field and Dr McKenzie as to the discrepancy between the lung function results and Mr White’s claims about shortness of breath and limited capacity to exercise.  Professor Alpers supports the diagnosis of Dr Field and Dr McKenzie that Mr White has asthma.  Professor Alpers recommended exercising and returning to full time capacity as the way toward rehabilitation.

26. Dr Field and Dr Lee both observed that Mr White may not be using inhalers in the correct manner and this could be affecting the benefit of such treatment.

27. My most significant finding on all the medical evidence is that I accept the findings and conclusions of Dr Field and Dr McKenzie and where their opinions conflict with the opinion of Professor Bryant and other doctors called on behalf of the plaintiff, I reject the opinions of the plaintiff’s medical experts and accept the opinion of Dr Field and Dr McKenzie.

28. Applying the principle expressed in Bonnington Castings Ltd v Wardlaw (supra) by Lord Reid at 621 as set out earlier in these reasons, the plaintiff has failed to prove that he has silica induced small airways disease, or any condition which is related to his exposure to silica dust between 1971 and 1974.

29. For these reasons, Mr White cannot succeed in this claim.  Accordingly, I enter judgment in this matter in favour of the defendants.

30. I grant leave to the parties to make an application, if that is necessary, on the question of costs.

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