McFarlane v Boral Limited

[2007] NSWDDT 9

Dust Diseases Tribunal

of New South Wales

CITATION:	McFarlane v Boral Limited [2007] NSWDDT 9
PARTIES:	Paul Anthony McFarlane Boral Limited
MATTER NUMBER(S):	218 of 2000
JUDGMENT OF:	Curtis J at 1
CATCHWORDS:	Dust Diseases Tribunal :- Asthma Causation
DATES OF HEARING:	08/08/05, 28/11/05, 29/11/05, 30/11/05, 01/12/05, 21-22/08/06, 27/04/07, 20/06/07 & 27/06/07
DATE OF JUDGMENT:	29 June 2007
LEGAL REPRESENTATIVES:	Mr D R Campbell SC with Mr F Tuscano instructed by Bussoletti Lawyers Mr A C Scotting instructed by Moray and Agnew

JUDGMENT:

Dust Diseases Tribunal of New South Wales

Matter Number 218 of 2000

Paul Anthony McFarlane

v

Boral Limited

29 June 2007

JUDGMENT

CURTIS J

Introduction

1. The plaintiff, Paul Anthony McFarlane, suffers from asthma. He claims that this disease was caused by his exposure to calcium oxide and calcium hydroxide dusts in the course of his employment with Boral Ltd, trading as Blue Circle Southern (Boral) at Marulan between 1980 and 1988.

2. The evidence of Dr K S Basden, a mining engineer, establishes that the risk of Mr McFarlane contracting asthma from the dust was foreseeable, and could have been obviated by Boral taking reasonably practicable measures to protect him from that risk.

3. Boral asserts that Mr McFarlane suffers from idiopathic late onset adult asthma, entirely unrelated to the dusts to which he was undoubtedly exposed at work.

Narrative

1. Mr McFarlane was born on 11 March 1961. He is now aged 46. He left school at about the age of 15, and was at the age of 19 employed by Boral to work at its Marulan complex, commencing on 20 May 1980.

2. These works at Marulan are quite extensive. Limestone, calcium carbonate, is mined at a quarry on the site and crushed in a mill. The crushed limestone is heated in a kiln to drive off the carbon and produce calcium oxide. Some of this is sold in bulk. The remainder is slaked with water to produce calcium hydroxide, which is transported from the plant for use in the manufacture of cement. At the time Mr McFarlane worked at the plant, open conveyor belts transported the crushed limestone, the calcium oxide, and the calcium hydroxide between the various operations. There were frequent spillages, and dust pervaded the atmosphere throughout the whole of the works.

3. Mr McFarlane's first job was filling 25 kg bags with calcium hydroxide delivered through a nozzle. The process was extremely dusty and he worked with an air hose attached to a hood covering his head. There was no washroom provided and his clothes remained covered in dust throughout and after his shift. He was also called on to do general cleaning throughout the plant, using a shovel and wheelbarrow to clean up spillages.

4. After seven months Mr McFarlane decided to resign because of the dust. He was persuaded by management to stay on the basis that he was given different work. He became a lime plant assistant, inspecting, greasing, and cleaning the kiln. This work was outside, and, although he was still called upon to attend to spillages from time to time, it was generally less dusty.

4. In 1983 Mr McFarlane was transferred to the bulk loading section in the hydration plant, which loaded both calcium oxide and calcium hydroxide onto road trucks or rail trucks. This was much dustier work. The trucks were brought to a position underneath large hoppers containing the material, which was directed through adjustable chutes into the trucks. Mr McFarlane was positioned upon a steel grid platform over the trucks and operated the controls, which directed the chutes and opened and closed the air rams controlling the flow of material from the hoppers into the chutes. He was in this work exposed to considerable amounts of both calcium oxide and calcium hydroxide dust.

5. On 12 March 1986 as Mr McFarlane opened an air ram to start filling a road tanker, a huge gust of calcium hydroxide, possibly caused by the spontaneous clearing of some blockage in the hopper, poured into the tanker, and a plume of dust rose into the atmosphere where he was standing. Mr McFarlane said:

It was just a complete whiteout, I could not see. And I tried to breathe with the mask and all that come in was dust… I don't know whether I panicked or what happened, but I had to feel my way to the doorway and climbed down the ladder 6 m to get out of it because it was just there, it wouldn't clear… I couldn't breathe, the dust had gone already in and I just felt like vomiting and just almost passed out…. I was totally overwhelmed, totally overwhelmed thinking I was going to die because immediately I couldn't get any air in… it was very very frightening.

6. Mr McFarlane says that this incident happened towards the end of his shift. He stopped work and waited for the company bus to take him from Marulan to Goulburn where he lived. He says that as he waited for the bus he struggled to breathe, had pain in his chest and his throat was very wheezy. When he got home he had a shower and collapsed on the bed, where he lay until his wife came home and took him to the Goulburn Base Hospital. He was there treated with oxygen, Ventolin and a nebuliser.

7. For reasons which I will later address, I regard Mr McFarlane as an unreliable witness. However records of the hospital establish that he presented at 6:35 pm with breathlessness. Records of a local medical clinic confirm that Mr McFarlane attended on the 14th of March 1986, telling a general practitioner, Dr Anderson, that he had inhaled lime dust two days previously, causing his "throat to close". Dr Anderson recorded that Mr McFarlane had been given Ventolin and oxygen therapy at Goulburn Hospital and that an x-ray had been performed. On examination he noted widespread bronchospasm. He prescribed Amoxil, Ventolin and Becotide and supplied a work certificate. Mr McFarlane says he was off work for a period of time and paid by his employer.

8. Despite some doubts suggested by counsel for Boral, arising from discrepancies as to the person identified by Mr McFarlane as that person to whom he reported the incident, the contemporaneous material persuades me that the incident occurred as described by Mr McFarlane.

10. Mr McFarlane says that after the event he suffered from chronic asthma. He says that he was constantly taking Ventolin at work, and at times had to leave the plant and go home to use a nebuliser. He named three supervisors as persons who knew of his condition and his absences. None of these men are called by Boral to rebut this evidence.

11. On 1 December 1988 Mr McFarlane was promoted to supervisor of calcium oxide and calcium hydroxide production. In 1995 he was appointed supervisor of the quarry.

12. On 4 September 1997 Mr McFarlane's wife, who had been accused of some criminal offence, committed suicide. Mr McFarlane was given bereavement leave until November 1997. He took annual leave in December 1997 and January 1998, and returned to his work as quarry supervisor on 3 February 1998. Although most of this work was conducted from his office, Mr McFarlane also worked in the field in a dusty environment. He said that his symptoms of asthma were aggravated by the dust and he was unable to continue working.

13. On 17 February 1998, Mr McFarlane attended upon his general practitioner, Dr Ragg, complaining of an increase in his symptoms. Dr Ragg formed the opinion that Mr McFarlane's asthma was poorly controlled, referred him to a respiratory physician, Dr Tony Whelan, and certified him unfit for three months. Dr Ragg had treated Mr McFarlane’s asthma since April 1992, when he joined Dr Anderson's practice, admitting him to hospital on at least three occasions with severe symptoms.

14. Dr Whelan examined Mr McFarlane on 28 May 1998 and was told that his asthmatic symptoms had increased in the last 12 months. He found widespread expiratory wheezes audible in the chest, and spirometry confirmed moderately severe, partially reversible, airflow obstruction with an FEV1 of 56% of expected, and a vital capacity of 68% of expected.

15. Dr Whelan formed the opinion that Mr McFarlane was likely to remain symptomatic indefinitely, and that he was unable to do any work where he was exposed to irritant dust. Dr Whelan's findings were similar to those he recorded at an earlier examination of Mr McFarlane in December 1990. At that time he noted that Mr McFarlane had moderately severe airways obstruction, an FEV1 60% of predicted, and FVC 72% of predicted.

16. In July 1998 Mr McFarlane was given clerical work in an air-conditioned office. Boral commissioned dust counts by a Dr Alan Rogers, which suggested that the dust in the location of the office was not excessive. Nevertheless after four weeks Mr McFarlane stopped work because his condition had deteriorated. He alleged that the asthma was exacerbated by dust in the office.

20. Although that allegation at first glance seems implausible, spirometry performed by Dr Whelan confirms an objective worsening of Mr McFarlane’s symptoms. On 24 June 1998 Dr Whelan recorded that Mr McFarlane had spent five weeks in Thailand where his symptoms improved, and he was able to walk long distances, swim and play golf. Spirometry performed on that day demonstrated FEV1 to have risen to 2.9 L, more than half a litre greater than previously. On 12 August, after Mr McFarlane ceased work, FEV1 had fallen to 2.3 L, 54% of expected. In evidence Dr Whelan said that this demonstrated "a definite reduction in his airway function coinciding with his worsening symptoms".

21. I accept that Mr McFarlane ceased work because of a deterioration in his symptoms. That deterioration is unlikely to have been caused by dust in the office, and was probably either spontaneous or related to his being extremely hypersensitive to the dust at the site.

17. At a further examination in October 1998, Dr Whelan noted that FEV1 was reduced to 54% of expected and vital capacity 64% of expected. He then formed the opinion that Mr McFarlane should leave work altogether, pending review by an occupational physician.

22. In April 1999 Boral offered Mr McFarlane clerical work at its Berrima premises. Mr McFarlane discussed this offer with Dr Whelan. He says that he was told by Dr Whelan that he should not accept the offer because it was at a cement works.

18. With the exception of three days casual work as a hotel barman, and one as a courier, Mr McFarlane has not worked since that time. He maintains that he has remained totally unfit for any form of employment. That was a view at one time supported by Dr Whelan. On 3 May 2000 Dr Whelan wrote that Mr McFarlane suffered from severe asthma and endogenous depression. He stated that:

Unfortunately little if any progress has been made regarding his asthma. He requires a lot of medication but is still very restricted by dyspnoea and wheeze and has severe airflow obstruction on spirometry. I feel the prospects for a full or partial return to work are very poor. I think he will remain disabled.

I do not think he can return to his occupation, and I believe he will be most unlikely to return to this work at any time.

It is conceivable that his condition could improve in the future but he cannot return to a dusty environment. Retraining for a sedentary job away from a dusty environment would be necessary. His other disabilities make retraining a dubious proposition.

In my view Mr McFarlane is permanently unable to do his work, and permanently unable to do other duties at present.

19. On 14 September 2000 Dr Whelan measured Mr McFarlane's FEV1 at 48% of expected and vital capacity at 57% of expected. In a report of 6 December 2002 he wrote that:

Mr McFarlane has not been able to work at all over the last two years. This is purely because of his respiratory disease.

… he is unable to work in an environment where he's exposed to irritant dust, as his previous occupation with a quarrying and mining firm is out of the question. He has tried to return to work and exposure to even small concentrations of dust lead to exacerbation of his symptoms. I believe he would be able to work in a sedentary occupation away from this sort of respiratory irritation.

… he is on fairly maximum treatment and really it has not reversed his airflow obstruction and subsequent symptoms.

20. Mr McFarlane continued under the care of Dr Whelan. On 8 March 2004 Dr Whelan wrote to Mr McFarlane's solicitors stating that his situation had not significantly changed, that he continued to experience debilitating asthma with shortness of breath, cough and wheeze, and that he remained unfit for work although "part time sedentary work may be possible in the future".

21. Notwithstanding Dr Whelan's concerns, objective measures of Mr McFarlane's asthma demonstrated a gradual improvement after 2002. On 20 November 2002 spirometry commissioned by Dr Burns at St Vincent's Hospital Sydney demonstrated FEV1 at 75% of predicted and forced vital capacity at 85% of predicted. On 26th August 2003 Professor Breslin's spirometry demonstrated FEV1 at 92% of predicted and forced vital capacity at 95% of predicted. On 14 July 2005 Professor Breslin found both FEV1 and forced vital capacity to be 85% of predicted and reported that this was a significant improvement since he first tested Mr McFarlane in August of 2000.

22. It may be accepted that these results were achieved while Mr McFarlane continued his regime of medication, and do not reflect his underlying condition. Nevertheless both Dr Burns and Professor Breslin, physicians qualified by the plaintiff and defendant respectively, believe Mr McFarlane is capable of non strenuous work in a dust free environment.

28. Because Dr Whelan was the treating doctor most intimately concerned with Mr McFarlane's health I accept his opinion that Mr McFarlane was totally incapacitated for work from 12 August 1998 until 20 November 2002, the date upon which Dr Burns performed his spirometry. On 6 December 2002 Dr Whelan had written that Mr McFarlane "would be able to work in a sedentary occupation away from this sort of respiratory irritation".

29. Since 1998 Mr McFarlane has spent much of his time in Thailand, where he says the climate is beneficial and he is less troubled by his symptoms. He does not work nor does he look for work.

The psychiatric evidence

19. In or about August 1999 Mr McFarlane became severely depressed. On 6 January 2000 he was referred by Dr Whelan to Dr Bhandari, a consultant psychiatrist. Dr Bhandari diagnosed a major depressive illness with possible psychotic features which "had developed in the context of significant financial difficulties, chronic medical illness, and a loss of role functioning as a result of being unable to work".

20. By August 2000 Mr McFarlane's depressive illness had worsened to such an extent that Dr Bhandari arranged for his admission to a psychiatric hospital where he was treated between 17 August 2000 and 23 August 2000. His depressive symptoms improved during this initial period of hospitalisation but did not completely resolve. Mr McFarlane was further admitted to the hospital between 24 February 2001 and 5 March 2001, and between 13 September 2001 and 21 September 2001.

25. Boral qualified Dr Doral Samuell, a clinical and forensic psychiatrist, to express an opinion. Dr Samuell, in a report of 18 July 2005, stated that "It was Mr McFarlane's sense of loss of his capacity to work that was a significant cause of the psychological difficulty".

26. Both Dr Bhandari and Dr Samuell are of the opinion that, while the death of Mr McFarlane's wife may have contributed to his psychological state, his physical impairment constituted a material contributing factor. Dr Bhandari said that Mr McFarlane's mental state reflected the sum of all of his stressors.

34. Although Mr McFarlane did not seek treatment from Dr Bhandari after September 2001, he was, on 28 March 2002, examined and tested at the request of Boral by Ms S M Chadwick, a clinical psychologist. In her report Ms Chadwick wrote:

Mr McFarlane's score on the Beck Depression Inventory-11 does suggest a significant level of depression, consistent with the history he gave. He describes sadness and pessimism about the future. He claimed to derive little pleasure from things he used to enjoy and to feel as a total failure as a person and to dislike himself. He described tending to blame himself for anything that happens and indicated that he would like to kill himself. He reportedly cries more than he used to, feels restless, is less interested in people and has trouble making decisions. He indicated that he feels worthless, has little energy, sleeps poorly, is more irritable, has some trouble concentrating and is too tired to do most of the things he used to do. He also indicated that his appetite is not as good as it was.

She also wrote:

He was diagnosed by his treating psychiatrist as suffering from major depression with psychotic features. He was hospitalised on two occasions. He claimed to be still depressed. The symptoms have been described elsewhere. He is trying to cope with these problems without the use of medication but remains very pessimistic about his future, and in my opinion, his depression is still of clinical proportion. He no longer has any regular contact with the community health centre or with Dr Bhandari, but in my opinion, needs to have some ongoing review as he has reportedly seriously considered suicide, allegedly due to feeling useless and being very pessimistic about his future.

27. In his evidence in chief Mr McFarlane was asked: "Did you have any experience of any respiratory symptoms that you can recollect prior to about [February] 1986? He answered "No". He was further asked: "Before [February 1986] had you ever taken Ventolin before?". He answered "No". He did say that he had the occasional bout of bronchitis, with a sore throat and flu type symptoms.

28. On 25 July 1985 Mr McFarlane had attended the Medicheck Referral Centre in Bathurst Street Sydney at the request of Dr Anderson. The attendant medical officer recorded that "In past 18/12 he has experienced episode of "tightness" in the throat, wheezing and dyspnoea. These are provoked by exercise, dust and relieved by Ventolin. Findings in check: lung function tests . (Rhonchi all areas of chest. He has a respiratory infection.)"

29. Lung function tests conducted at this examination disclosed an FEV1 62.4% of predicted, and a Vital Capacity 72.3% of predicted. (It is common ground that Mr McFarlane did have a bronchial infection at the time of this examination however Professor Breslin, who gave evidence for Boral, is of the opinion that the diminution in FEV1 is far greater than might be expected from this infection, and is consistent with asthma.)

30. In cross examination Mr McFarlane gave inconsistent answers to questions bearing upon his medical history.

31. The following questions and answers which appear at pages 60, 61, 63, 64, and 71 of the transcript are illustrative:

Was it the case that for 18 months before [the Medicheck examination] you had been suffering from episodes of tightness in the throat?

No.

Did you tell the person at Medicheck that in the last 18 months you had been suffering from episodes of wheezing?

No.

Had you in fact suffered episodes of wheezing in the last 18 months prior to the Medicheck examination?

I did suffer from breathing difficulties with the bronchitis, wheezing, if you want to call it.

During the 18 month period prior to the medicheck examination had you suffered episodes of shortness of breath?

Yes.

Do I understand your evidence to be this, sir, that at least in the 18 months prior to the Medicheck examination, so from the start of 1984 onwards, you suffered episodes of bronchitis that gave rise to tightness in the chest, wheezing and shortness of breath, is that right?

Similar effects but I only knew it as bronchitis.

You suffered it on more than one occasion?

Yes.

Did it have the effect of taking you off work?

Sometimes I think it did, yes.

What was it stopped (you) working, what physical symptom?

The condition of the lung, pain, the pain and exhaustion, ongoing effects of infection.

But not breathlessness?

I don't recall breathlessness.

Listen carefully to my question. Your case has been that you had no significant respiratory complaints or chest problems prior to 1986, is it not?

Well, that's not the case.

What is not the case?

Because I clearly did. I did have infections in the chest before 1986.

So you had symptoms of breathlessness before 1986?

No.

The breathing difficulties you have experienced started on 12 March 1986, and on your evidence, have continued to date?

Yes

That is a history [you have repeated to] all the doctors in this case is it not?

I imagine so, yes, I've only [answered] the questions what they've asked.

All the doctors have asked you whether you had any breathing problems or chest problems prior to 1986, have they not?

They have asked me and I had wheezing.

I think breathing problems was the word put to you?

Breathing well, yes in cases , breathing problems, yes.

You have not told any of those doctors in response to that question that you suffered episodes of bronchitis prior to 1980s, have you?

I don't think so no.

You may have misunderstood the question. I had understood you to say a moment ago that you did not have breathing problems before 1986 but before that you said you had no symptoms of breathlessness before 1986, which is correct?

I had bronchitis before 1986, but I did not have breathlessness before.

No breathlessness before 1986, no breathing problems before 1986, is that the case just so I am clear?

Yes. Breathing problems with the lungs, sure.

You suffered breathing problems, on your understanding prior to 1986 as a result of infections, is that right?

That's correct yes.

You have not told any of the doctors in this case that you suffered from regular infections prior to 1986 that gave rise to any breathing difficulty, have you?

No.

Post-March 1986 were you suffering from wheezing?

Yes.

Post 1986 were you are suffering from shortness of breath?

Yes.

Post-1986 [were] you suffering from tightness in the throat?

Yes.

You reported those same symptoms to the Medicheck officer in July 1985 did you not?

No.

32. When examined in chief about the death of his wife, Mr McFarlane said that his ability to cope and mental processes were significantly affected "for a short time". He said that he had six weeks off work because of her death.

33. In fact Mr McFarlane was off work for five months between 4 September 1997 and 3 February 1998. Three weeks after his wife died, Mr McFarlane was referred to the Southern Tablelands Mental Health Service, being then suicidal. He received counselling for approximately 2 months. He sought treatment from Dr Ragg in October 1997, returning in November 1997 to tell the doctor that he was feeling worse. He was depressed, anxious, and not sleeping.

34. Mr McFarlane's reactions to the death of his wife are quite understandable. His dismissal of those reactions as disabling him "for a short time" is not credible.

38. Mr McFarlane was not an impressive witness. I discount his account of his prior medical history, and his claim to be presently totally disabled. I accept the history recorded by the Medicheck document to be wholly accurate. I do accept Mr McFarlane's evidence of his asthmatic symptoms because the nature and extent of the pathology has been confirmed by clinical signs and objective spirometric testing. I accept his evidence of depression because of Dr Bhandari's clinical opinion, the fact that Mr McFarlane did require repeated hospitalisation, and because of the psychometric testing and opinion of the psychologist, Ms Chadwick, qualified by Boral.

35. I find that Mr McFarlane suffered from mild but chronic bronchitis or asthma causing wheezing, shortness of breath, tightness in the throat and occasional incapacity for 18 months prior to the dramatic episode of 12 March 1986. Because of my view of the medical evidence I find it unnecessary to differentiate between the available diagnoses of bronchitis or asthma.

Causation
A review of the scientific literature in evidence

1. A Hazardous Substance Fact Sheet, first published by the New Jersey Department of Health and Senior Services in January 1986 identifies calcium oxide and calcium hydroxide as hazardous substances. Of calcium oxide the fact sheet states that: “Breathing calcium oxide can irritate the lungs causing coughing and/or shortness of breath". and that "In the long-term… Calcium Oxide can irritate the lungs. Repeated exposures may cause bronchitis to develop with cough, phlegm, and/or shortness of breath". Of Calcium hydroxide, the publication states that: "Breathing Calcium Hydroxide can irritate the nose, throat and lungs causing coughing, wheezing and or shortness of breath".

2. In a paper published in the medical journal Chest in September 1985, Brooks et al first described "Reactive Airways Dysfunction Syndrome” (RADS). The abstract of the study states that: "This investigation suggests acute high level, uncontrolled irritant exposures may cause an asthma like syndrome in some individuals which is different from typical occupational asthma. It can lead to long-term sequelae and chronic airways disease. Non immunological mechanisms seem operative in the pathogenesis of this syndrome."

3. A study by Tarlo and Broder, published in Chest in August 1989 suggested that irritant induced asthma is not uncommon. Unlike Brooks et al, Tarlo and Broder, "In the recognition that irritant levels in the workplace can fluctuate significantly, and in many industries, accidental spills are relatively common", did not limit their studies to instances of a single exposure to an irritant substance. Their paper concludes: "Therefore, our findings indicate that irritant induced occupational asthma has features similar to occupational asthma caused by sensitisers … We consider irritant induced occupational asthma to be a form of occupational asthma caused by a single or multiple exposure to irritants". One of the subjects included in the study suffered from irritant induced asthma after exposure to Calcium Oxide.

4. In a review of Reactive Airways Dysfunction Syndrome published in Chest in 1996, Alberts and do Pico considered the mechanism of RADS and wrote:

Four major hypotheses have been proposed to explain the persistent bronchial hyperresponsiveness in patients with RADS. There may be others. The first is that following the extensive inflammation associated with the short-term exposure, subsequent reepithelialization and neural reinnervation may result in a significantly altered receptor threshold in the airways resulting in non-specific bronchial hyperresponsiveness. The second hypothesis is that damage to the bronchial mucosa may lead to increased airway permeability. This would then allow inhaled materials easier access to irritant receptors and, in turn, hyperresponsiveness. The third, as suggested by Boulet, is that the high-level toxic exposure and subsequent inflammatory reaction in the airway may result in a massive release of mediators that, in turn, alter smooth muscle responsiveness for a prolonged period of time. The fourth, not uniformly supported by pathologic findings, is that airways inflammation persists.

Alberts and do Pico went on to say:

Recently, persistent asthmatic conditions have been reported to develop as a result of repeated moderate or high-level inhalation exposures as opposed to the single massive exposure associated with cases of RADS. These repeated lower-level, though not trivial, exposures do not fit the strict criteria for RADS but may result in asthma via very similar mechanisms.

5. The possible mechanisms canvassed by Alberts and do Pico are consistent with RADS being caused by repeated significant exposure to the irritant substances calcium oxide and calcium hydroxide, which substances are known to cause irritation in the lungs, bronchitis, cough, phlegm, wheezing and/or shortness of breath.

A review of the medical evidence

6. Dr A J Whelan has treated Mr McFarlane since 1990. In a report of 6 December 2000 to the general practitioner, Dr Whelan recorded Mr McFarlane's history as follows: "He told me that he had no asthma symptoms of any type before 1986. He told me that in that year he was very heavily exposed to hydrated lime dust and he dates his asthma from that time… it is highly likely that his asthma was precipitated by heavy exposure to hydrated lime as I mentioned above. He had no asthma symptoms or any other respiratory complaint before this episode".

7. In February 1991 Dr Whelan asked Dr Peter Giannoutsis to express an opinion as to whether Mr McFarlane's asthma had an occupational basis. In a report to Dr Whelan of the 11 June 1991, Dr Giannoutsis set out the work history given to him by Mr McFarlane:

He had been working for the Blue Circle Cement Company since 1980 where he stands on a mesh grate whilst hydrated lime comes down a chute from a hopper onto the back of a truck and when the truck tray is full he causes the operation to cease. On one particular day when he had been performing a task which he had done similarly for a period of three years to 1980 and 1983 and then, on his return in 1986, a particularly vicious gust of wind blew into his face the dust from the loading procedure which caused him to feel quite suddenly out of breath and as a consequence of which he climbed down the ladder and by the time he reached the bottom had developed a sense of tightness and wheeze never experienced previously and which persisted for a period of some three weeks. Since that time over the last five years, he is aware of almost a chronic background wheeze, accentuated on occasions when the hydrated lime is particularly heavy in his work environment. The symptoms came on quickly, causing him to become quite frightened and on one occasion he has taken himself off to hospital."

Upon this history he expressed the opinion:

"I had advised him that it is highly likely that he has been sensitised by the hydrated lime dust in his environment as a direct cause of his asthma and have suggested that he seek alternative employment within the organisation but away from such dust".

8. It is common ground among the other doctors whose opinions are in evidence that the relevant mechanism in cases of RADS is irritation, not sensitisation and immunological response. Mr McFarlane is not atopic. That is, he does not have a genetically determined disposition to contract asthma as an allergic disease. Dr Whelan said in evidence that the consensus of medical opinion is that people who are atopic are more likely to develop asthma. I believe that Dr Giannoutsis, a very experienced physician, did not intend by the word "sensitised" to indicate that the aetiology of Mr McFarlane's asthma was by sensitisation to the inorganic substance calcium hydroxide. Rather I believe him to be expressing the opinion that the aetiology of the asthma was to be found in irritation by calcium hydroxide.

9. Dr Michael Burns, a specialist physician, was qualified by the plaintiff's solicitors. He examined Mr McFarlane on 8 January 2001 and provided a report dated 9 January 2001. Dr Burns was given a history that Mr McFarlane was loading bulk tankers with calcium oxide and calcium hydroxide for about three years, and that in March 1986 he was engulfed in a cloud of calcium hydroxide which he inhaled. He expressed the following opinion: "Mr McFarlane appears to be a typical case of the Reactive Airways Dysfunction Syndrome (RADS) which was first described by Brooks et al in 1985 and subsequently generally accepted as an entity. In this syndrome, an injury to the airways occurs from a sudden mass inhalation of irritant material such as acid, alkaline or noxious gas. It leads to a permanent asthma like disorder in many if not most of its victims. In Mr McFarlane's case this is likely to be what has happened and as he still has severe symptoms after five years, is unlikely that any improvement will occur".

10. In a supplementary report of 24 August 2005 Dr Burns expressed the opinion that RADS may develop in persons who had some pre-existing asthma, and that it may also occur in persons who have suffered from chronic or persistent bronchitis caused by chronic low level irritant exposure.

56. In that report Dr Burns said that, while it was unlikely that pure calcium hydroxide caused Mr McFarlane's condition, he believed an element of unconverted calcium oxide was present in the calcium hydroxide cloud which enveloped Mr McFarlane. Later, in evidence, Dr Burns stated that, because of his further research into the literature, he now thought it likely that calcium hydroxide caused Mr McFarlane's asthma.

12. In evidence Dr Burns said that Mr McFarlane may have become asthmatic because of exposure to calcium oxide over the four or five years prior to the events of March 1986. This opinion is consistent with the study of Tarlo and Broder, although Dr Burns does not refer to that study in his evidence.

14. Professor A B X Breslin, another eminent physician, is of the contrary opinion. On 25 August 2000 Professor Breslin examined Mr McFarlane for Boral. Mr McFarlane told Professor Breslin that he had "no chronic respiratory symptoms whatever until the episode of this spill on 12 March 1986" and that he had never been free of chest symptoms since that date. Upon this history Professor Breslin thought that Mr McFarlane suffered from Reactive Airways Dysfunction Syndrome.

15. Subsequently Professor Breslin was given a copy of the Medicheck document of 25 July 1985, in which Mr McFarlane gave a history that, for the proceeding 18 months, he has suffered episodes of tightness in the throat, wheezing and dyspnoea, the episodes being provoked by exercise and dusts and relieved by Ventolin; spirometry demonstrating objective evidence of airflow limitation.

16. In a supplementary report of 13 May 2005, Professor Breslin noted that cement manufacture was not, in a number of publications, mentioned in the list of reported causes of occupational asthma. Although his own Medline search of 14 May 2005 indicated that cement workers reported a number of symptoms, including asthma, Professor Breslin said that "These publications do not support the concept that working with cement and its manufacture is a risk factor for the development of asthma, but rather that asthma is seen amongst workers in the cement industry; asthma is a common disease however, and the mere existence of asthma in a particular industry does not mean that industry is causing the asthma".

17. Professor Breslin concluded that because of Mr McFarlane's prior symptoms, the demonstrated airflow limitation, and the fact that there were no recorded instances in the literature of RADS resulting from high-level exposure to calcium hydroxide, that "On the balance of probabilities it seems to be unlikely that his asthma commenced because of his work at Blue Circle Cement. There may have been transient periods of deterioration in his asthma due to the dust exposure at work but I can find no evidence that his asthma was permanently worsened by his work at Blue Circle Cement".

54. This issue has been clouded by the failure of Mr McFarlane to honestly recount his medical history to the doctors who have examined him. The earlier opinions of Dr Whelan, and that of Dr Giannoutsis are unreliable because they are based upon a false assumption that the asthmatic symptoms began suddenly in March 1986.

55. The opinion of Professor Breslin is based upon what I regard as the correct history, however I cannot accept his conclusion that Mr McFarlane's asthma was unrelated to his exposure to calcium oxide and calcium hydroxide dust in the years preceding the incident of March 1996.

56. Mr McFarlane's Statement of Claim pleaded that "…from on or about 20 May 1980 to about 1999, the plaintiff was regularly exposed to and inhaled large quantities of calcium hydroxide dust, calcium oxide dust and hydrated lime dust in respirable form" and that "As a consequence of exposure to an inhalation of calcium hydroxide dust, calcium oxide dust and hydrated lime dust in respirable form the plaintiff suffered injury". Unfortunately Professor Breslin expressed no direct opinion, in his reports or in his evidence, upon this question.

57. In a very general answer to a question asked in chief, Professor Breslin discounted the diagnosis of Reactive Airways Dysfunction Syndrome on the grounds that Mr McFarlane suffered from pre-existing asthma. In the course of this answer he said that occupational asthma can occur in a number of ways including sensitisation to allergens [which was not the case here]. He also said:

"Another type of occupational asthma is where there is an irritant substance and there may or may not be a sensitisation period, but there usually is, and the irritation builds up over a period of time, but it's probably not an immunological reaction. So that's a sensitisation period but not to things that produce antibodies, but just to things that sensitise and inflame the airways."

58. Professor Breslin was asked by counsel for Boral whether calcium hydroxide or calcium oxide had been identified as sensitisers in respect of occupational asthma. He replied "Definitely not" because "In order to sensitise your airway the substance really needs to be a very complex substance, mostly organic such as house dust mites, such as flour, such as wood dust, very complex substances that turn on the immune system. A relatively simple substance like calcium hydroxide or calcium oxide are not going to be sensitisers, but you see that's why-you could say the same about ammonia or chlorine, that's not a complex substance either and that can cause reactive airways dysfunction and it has, and it's been reported to, but through non sensitisation methods, through a sudden injury".

It seems to me that the doctor is here turning his mind to the development of occupational asthma through sensitisation to allergens, and dismissing that possibility because calcium hydroxide and calcium oxide are not "very complex substances that turn on the immune system".

61. The more relevant question is whether calcium hydroxide or calcium oxide had been identified, not as sensitisers, but as irritants, causing persistent bronchial hyperresponsiveness through the mechanisms postulated by Alberts and do Pico.

59. The cross examination of Professor Breslin proceeded, without success, in an attempt to convince the doctor that the Medicheck records were not diagnostic of pre-existing asthma. The possibility that, if the asthma was pre-existing, it was nevertheless caused by irritation from harmful dusts, was not raised.

60. The examination of Dr Burns by counsel for Mr McFarlane proceeded for the most part to examine Dr Burn’s reasons for rejecting the possibility of pre-existing asthma. He was ultimately asked this question: "Do you in short adhere to your opinion that this man developed asthma as a result of the exposure that he reported that he suffered in March 1986?" The doctor answered "Yes".

61. At the conclusion of Dr Burns’ examination in chief, and before cross-examination commenced, I asked, without objection, this question: "Could he have become asthmatic because of the gradual accretion [sic] of Calcium oxide over four or five years? The doctor answered "Yes".

71. Dr Whelan in evidence said that if Mr McFarlane had asthma before 1986, that asthma could have been caused by calcium hydroxide and calcium oxide acting as irritants.

Conclusion

62. I find that the bronchitis or asthma suffered by Mr McFarlane prior to March 1986 was caused by his exposure to calcium oxide and calcium hydroxide dust in the course of his employment in the bulk loading section at Marulan. I further find that whichever pulmonary condition afflicted him before March 1986, that condition was aggravated by the event of 12 March 1986 causing the development of a patently asthmatic disease, and that disease was further permanently aggravated by the conditions of his work in the bulk loading section from 1986 to 1995.

66. In reaching this conclusion I have taken into consideration the following facts and circumstances:

(a) Mr McFarlane is not atopic and has no congenital disposition to develop asthma. There is no family history of asthma;

(b) He had no symptoms before he was exposed to copious quantities of calcium oxide and calcium hydroxide dust.

(c) Those substances have been identified as hazardous and capable of causing long-term irritation to the lungs;

(d) The content of the scientific papers in evidence;

(e) The evidence of Professor Breslin that occupational asthma may be caused by irritant substances;

(f) The evidence of Dr Whelan that Mr McFarlane's symptoms before 1986 may have been due to asthma contracted as a result of calcium oxide and calcium hydroxide acting as irritants.

(g) The opinions of Dr Burns, first, that RADS may develop in persons who have some pre-existing asthma and may also occur in persons who have suffered from chronic or persistent bronchitis caused by chronic low level irritant exposure, and second, that Mr McFarlane may have become asthmatic because of exposure to calcium oxide over four or five years prior to the events of March 1986.

74. Mr McFarlane is entitled to damages.

General damages

75. Mr McFarlane first contracted asthma at about the age of 23. In 1986 the disease became severe, requiring constant medication and intermittent treatment in hospital. From 1998 his asthma has been permanently disabling, resulting in a severe depressive illness. He is now 47 years of age and has suffered from breathlessness for 24 years. He has a life expectancy of a further 38 years during which his asthmatic symptoms will continue. I think it probable that he will remain depressed. I assess General damages in the sum of $150,000. I allow interest on $75,000 at 2 per cent for 24 years:$36,000.

Past loss of earnings

76. It is plain to my mind that Mr McFarlane's cessation of work in February and again in August 1998 was in some degree related to his psychiatric condition following the suicide of his wife. Nevertheless the defendant must take the plaintiff as it finds him. Medical examination and objective testing conducted on each occasion found that his asthma was acute. Dr Ragg and Dr Whelan thought him unfit because of the asthma. It may be that if he did not have his psychological problems he could have soldiered on, but that is not to the point. His asthma materially contributed to his incapacity.

77. In about August 1999 Mr McFarlane became severely depressed and that depression was caused, or materially contributed to, by his asthma, notwithstanding some possibly continuing effects of his wife's death.

78. I find Mr McFarlane was totally incapacitated by the combination of his physical symptoms and depression from 12 February 1998 until 30 November 2002.

79. On 30 November 2000 the plaintiff suffered injuries in a motor vehicle accident. The parties have agreed that he was incapacitated by those injuries from that date until 30 August 2000, a total of 35 weeks. During that period the compensible injuries in this action would not have been productive of economic loss, and he is not entitled to loss of earnings.

80. The parties have agreed that, but for his injury, Mr McFarlane would have earned $850 per week nett from 12 February 1998 to 30 November 2002 (203 weeks) with the exception of the period 30 November 2000 to 30 August 2000 (35 weeks). He is entitled to $850 per week for the balance of 168 weeks in respect of this period of incapacity ($142,800).

81. I find that from 1 December 2002 McFarlane has been able to work in such jobs as taxi driver, courier driver, or shop assistant earning approximately $600 gross per week. The parties have agreed that such a wage reflects $500 per week nett. They have further agreed that were it not for his injuries Mr McFarlane would have earned $1050 per week from 1 December 2002 to date. He is entitled to $550 per week for 238 weeks from 1 December 2002 to date ($130,900). Past loss of earnings totals $273,700. Interest upon this sum is agreed at $78,000.

Future loss of earnings

82. Future loss of earnings are agreed at $386,886.

Out-of-pocket expenses

83. These are agreed at $12,500 for the past, and $48,320 for the future. Interest on past out of pocket expenses is agreed at $3,250.

Summary of damages

84. General damages $150,000

Interest on general damages $36,000

Past loss of earnings to $273,700

Interest on past loss of earnings $78,000.

Future loss of earnings $386,886

Past and future out-of-pocket expenses $60,820

Interest on past out-of-pocket expenses $3,250

Total $988,656.00

85. Judgment for the plaintiff in the sum of $988,656.00.

86. Defendant to pay the plaintiff’s costs.

Mr D R Campbell SC with Mr F Tuscano instructed by Bussoletti Lawyers appeared for the plaintiff

Mr A C Scotting instructed by Moray and Agnew appeared for the defendant