Ruth Louise Lindbeck v Home Care Service of NSW & Abrotrait Pty Limited t/as O'Sullivan Interiors
[2002] ACTSC 29
Ruth Louise Lindbeck v Home Care Service of NSW & Abrotrait Pty Limited t/as O’Sullivan Interiors [2002] ACTSC 29 (12 April 2002)
CATCHWORDS
NEGLIGENCE – alleged exposure to chemicals – duty of care
DAMAGES – action against employer and contractor – attribution – assessment.
Workers Compensation Act 1987 (NSW)
Australian Capital Territory Schools Authority v El Sheik [2000] FCA 931
Fox v Wood (1981) 148 CLR 438
Griffiths v Kerkemeyer (1977) 193 CLR 161
Grljak v Trivan Pty Ltd (unreported, 19 April 1996)
Leonard v Smith (1992) 27 NSWLR 5
Morgan v Tame [2000] NSWCA 121, (2000) 49 NSWLR 21
No. SC 579 of 1998
Coram: Master T. Connolly
Supreme Court of the ACT
Date: 12 April 2002
IN THE SUPREME COURT OF THE )
) No. SC 579 of 1998
AUSTRALIAN CAPITAL TERRITORY )
BETWEEN:RUTH LOUISE LINDBECK
Plaintiff
AND:HOMECARE SERVICE OF NSW
First Defendant
AND: ABROTRAIT PTY LIMITED T/AS O’SULLIVAN INTERIORS
Second Defendant
ORDER
Coram: Master T. Connolly
Date: 12 April 2002
Place: Canberra
THE COURT ORDERS THAT:
There be judgment for each defendant against the plaintiff
The parties be heard as to costs
This is a claim for damages for personal injuries arising from what is alleged to be workplace exposure to chemical agents. The plaintiff was employed by the first defendant as a service coordinator at office premises in Morrisett House, Queanbeyan. The office is situated on the ground floor of that building, with external doors to a car parking area. In September 1995 the first defendant engaged the second defendant to undertake alterations to the interior of the office. The plaintiff alleges that in the course of these renovations a large container of glue used to bond laminate to wood was left exposed, and that as the solvent in the glue evaporated she became exposed to dangerous levels of chemicals. She alleges that as a result of this exposure she has developed a reactive airways dysfunction syndrome and a chronic fatigue syndrome. The plaintiff brings this action against both defendants. A third party claim was resolved during the hearing.
The hearing extended over six days in September and December of 2001, and involved a considerable amount of evidence from various expert witnesses on the question of the extent to which an open can of glue would lead to levels of chemical presence in the room. Before coming to this material, however, it is necessary to make a finding of fact on the question of whether an open container of glue was left in the premises.
The plaintiff was born in 1960 and educated to Higher School Certificate level in the Australian Capital Territory. She trained and qualified as a registered nurse in the early 1980’s and then left the workforce for some time as her children were born. She did some work as a relief worker at a childcare centre in the late 1980’s, and then again cared for her own family which has grown to five children. In 1994 she commenced work with the first defendant as a casual field worker. Home Care Service of New South Wales is a government agency responsible for the provision of home help to persons in the community with particular needs. In April 1995 the plaintiff commenced work in the office as a service coordinator on a permanent part time position.
She says that during 1995 the Service was preparing to transfer its records from manual files to a computerised system, and that as a consequence renovations were being planned for the office. She says that she asked her supervisor, Ms Thompson, whether it would be necessary to work in the office while the renovations were being done, and was told that it would be.
Mrs Lindbeck said that on Wednesday 27 September she noticed a very strong foul smell coming from the tea room area after she had been at work for a while. She says that she went to the kitchen tearoom area and saw a worker. She says that the smell was very strong in this room, and that she observed that the smell was coming from a metal container about 700 millimetres tall which she said was half-full of a yellow liquid. It is her evidence that the smell continued all that day, and she noticed a headache that evening. She says the headache was really bad, and she took some Panadol.
She says that she worked again the next day, being the Thursday, and noticed the strong smell as still being present, but not as strong. She still had a headache. She says on Friday she did not attend for work, but rather went on a holiday with her family to the South Sydney Juniors holiday resort on the Hawkesbury river, where the family had been regularly holidaying during the September/October school break. She says that she was really tired when she arrived, and still had a headache. She says that late on Friday she started coughing. She says it was a dry irritating cough which persisted through Saturday and Saturday night. On Sunday morning the coughing was continuing, and her husband took her to the Hawkesbury Hospital.
The report from the Hawksbury District Health Service states that she was examined and a peak flow test was performed. Ventolin was given, which improved her peak flow. A provisional diagnosis of asthma was made. The report states that the plaintiff gave a strong family history of asthma, and states that she “did not give a history of any precipitating events preceding this episode of illness.”
The coughing continued and she again presented at the Hawkesbury Hospital on the Monday. The report says that again Ventolin improved the peak flow reading, and she was given Venotlin and steroids. She says that she continued to feel unwell with a cough during the week of the holiday, and saw her general practitioner, Dr Davis, upon her return to Queanbeyan on Friday 6 October 1995. He records her as having marked coughing and distress with shortness of breath and exhaustion. He took a history in October that she had been exposed to a strong adhesive days before the onset of the symptoms.
She was referred by Dr Davis to Dr Chapman, an ear nose and throat surgeon. He took a history of the onset of an incapacitating paroxysmal cough while on holidays at the Hawkesbury River. He noted that she was being treated by her general practitioner in an appropriate manner, and reviewed her in November, where he found that she had improved symptomatically. He referred her on to Dr Hurwitz, a thoracic physician. In his report of April 1996 Dr Chapman said that the cause of the condition was unclear, but he felt that either an infection, probably viral, or an allergic response to some unidentified exposure would be the most likely diagnoses. His report did not refer to any chemical exposure.
Dr Hurwitz examined the plaintiff in February 1996, and took a history of a persistent cough, which was starting to improve. His history is that she had been exposed to fumes from laminating on the day before the cough started. He reported that “My clinical impression at that time was that Mrs Lindbeck had had a reactive airways dysfunction syndrome possibly as a consequence of exposure to fumes at work.” He reviewed her again in March 1996 when he reported that the histamine challenge was normal, indicating that she had had an acute insult to the airways causing an initial cough which had subsequently resolved. He reported in July 1996 to the workers compensation insurer that “when I last saw Mrs Lindbeck she was well and had totally recovered from her exposure.”
The plaintiff’s case is that, while the initial coughing symptoms have resolved, she has developed a complex of symptoms involving lethargy and depression, which has been variously described as chronic fatigue syndrome, post traumatic stress syndrome, and chronic post traumatic fatigue syndrome. It is the plaintiff’s case that she is unfit to work as a consequence of these symptoms, which are attributable to the exposure to the laminating glue on or about 27 September 1995 at the workplace.
It is necessary to make a finding of fact in relation to the circumstances of the exposure. It is common ground that a glue was used to perform laminating at the workplace, and that the glue was a product known commercially as AnchorWeld 101. Product information sheets were in evidence going to the chemical composition of this product, and the various experts who prepared reports and gave evidence as to the properties of this product. The plaintiff’s case is based on exposure by reason of a 20-litre tin of Anchorweld about half full and left open in the office. The defendant’s case is that there was only one application of the product to a small area, and that the glue was never in an open 20 litre tin, but rather was contained in a small bottle.
Mrs Lindbeck says that the office was chaotic during the renovations, and that she asked her husband to come in to the office to take some photographs, with a view to them being later used for a staff newsletter. She says that these photographs, which were tendered in evidence as exhibit B, were taken on Thursday 28 September. Mr Lindbeck can not recall when the photos were taken in that week, but said he thought it may have been on the Wednesday. He did say, however, that the photos were taken after his wife had complained of a headache. On both of their evidence, the photos were taken after the exposure to the laminating glue. The photographs show the area where the laminating was to be done, and clearly show that there is an area which is unlaminated. Mr Harris submitted that it must follow that the photographs were taken at some point in the week before the laminating, and so before the smell. It does seem to me that this is correct.
Mrs Lindbeck’s evidence as to seeing a drum with a yellow substance which was the source of the smell has been the basis from which various experts have worked out levels of chemical exposure. It is common ground that the substance used by the worker to laminate the kitchen was a product known as “AnchorWeld 101”, an industrial adhesive that is supplied commercially in 20 litre drums. Her description of a metal container would match a 20 litre drum. In the photographs a 20 litre drum is visible, but it is marked “Boral Top Cote” and it is, I am satisfied, not a container of laminating glue. That drum is a plastering product.
The recollection of Mrs Lindbeck is the only evidence to support the proposition that the glue was in an open 20 litre drum. Mrs Pocock was a coworker, and she gave evidence that there was a degree of chaos during the renovations. She remembered Mr Lindbeck coming in to take photographs, which she agreed showed the work before it was completed, and before the cupboards had been installed and the laminating done. She agreed that the cupboards were supplied in a fully laminated condition, and that the only laminating that was done was a small area in the kitchen.
Ms Pocock said that on one day she noticed the usual workers present and a younger boy. She says that just before lunch “we could smell a strong smell”. She said that she looked into the kitchen area she noticed that the smell was very strong and unpleasant. She asked the person what he had just used, and he said “laminating glue”. She says that she then went out to lunch with the plaintiff, sitting outside the office, and then after lunch she propped open the front door.
Ms Pocock did not give evidence about seeing any drum of glue, and when asked whether she saw what product was being used in cross-examination said that she did not notice.
Mr Lyall Keane gave evidence that he was the worker employed by the second defendant to do the fitout on this job. He said that all of the kitchen cupboards were supplied in a pre-manufactured state with the laminate in place from a company called Stirling Interiors in Sydney. Mr Keane himself picked the products up in Sydney and drove them to Canberra.
He says that there was one piece of laminating work to be done on site, involving making good the side of one cupboard. He said that he picked up the laminate that he needed for this job at the Stirling Interiors factory in Sydney, and also obtained the necessary glue. He said “it came in a liquid form and it was placed out of a 20 litre drum into a one litre container”. He says that this was an ordinary drink bottle type of container of the sort that would originally have held soft drink. He says that this bottle would not have been full.
He said that the laminating job involved replacing a piece of laminate about 900 millimetres to 1 metre by 450 to 500 millimetres on to the side of a cupboard. I am satisfied that this area is shown in its unlaminated state in the second of the photographs in exhibit B. He says that his 13 year old son was helping him on this job, it being the school holidays, and that his son applied the glue from the drink bottle by using a roller. He says that his son did this job in the hallway rather than in the kitchen area itself. He said that he worked with his son on this job for about half an hour. He says that he probably used 200 to 250 millimetres of the glue, and he then resealed the bottle. He says that he had the bottle with the extra glue with him for some time, but has since thrown it away.
Mr Keane says that there was never a 20 litre drum of AnchorWeld present on the premises, but there were 20 litre drums of paint and gyprock plaster materials.
Mr David Stirling, the proprietor of Stirling Interiors, also gave evidence. He said that he recalled providing Mr Keane with a small container of AnchorWeld glue, which he said was in a small Coca Cola bottle or something like that. He said that his firm usually supplied pre-laminated cupboards and the like, and that if laminating had to be done on site he would usually arrange for one of his workers to perform the work. He says that he recalls that, because this job was in Queanbeyan and that there was only one small area to be laminated he supplied the laminate and glue to Mr Keane. He says that he never on sold 20 litre drums of AnchorWeld.
Mr Keane’s son was also called to give evidence. He could recall coming to Canberra while a schoolboy to do some work with his father during school holidays, but had no other recollection of the job. There was evidence that Mr Keane’s son was asthmatic, and his father said that he had not been affected by the laminating operation. This is only relevant in that the experts agreed that a person with asthma would usually be more susceptible to chemical irritants.
The evidence of Mr Keane and Mr Stirling is that there was never a 20 litre tin of Anchorweld at this office. Their evidence is consistent, and makes sense, as there would seem to be no need for a large container for what was only a small laminating job. Ms Pocock did not say that she saw a tin of adhesive. The plaintiff says that she saw the tin, but there was medical evidence from her general practitioner that part of her symptomatology is that her memory can be poor. She agreed in cross-examination that she did not know whether Mr Keane had a small container of laminating glue or a large tub, or what precise work he did in laminating the cupboard (at transcript page 123). There is a photograph in exhibit B of a 20 litre tin of building product in the office, which was not Anchorweld, but which the plaintiff may have a recollection of seeing at the time.
Taking all of the evidence into account I prefer the versions of Mr Keane and Mr Stirling. I am not satisfied that there was an open 20 litre container of glue present in this workplace. I am satisfied, on the balance of probabilities, that Mr Keane laminated one area on the side of a cupboard using Anchorweld 101 glue which he had obtained from Mr Stirling and which was contained in a plastic drink bottle of about 1 litre in size, and which was not full of glue. I am satisfied that this process took about half an hour, and that it did create a noticeable smell. I am satisfied that this involved the use of no more than 250ml of glue.
I am satisfied that the laminating operation occurred at about the time Mrs Pocock says she observed the workman and smelt the glue, that is around lunchtime, and that there was a strong smell noticeable through that afternoon. I am satisfied that the plaintiff and Mrs Pocock left the office for lunch due to the smell, and that the door was kept open through the afternoon, as Mrs Pocock says.
Expert evidence as to the effect of exposure to the chemicals contained in AnchorWeld101 was lead by both the plaintiff and the defendant. I am satisfied that both Dr Crank, of the School of Chemistry at the University of New South Wales, who reported for the plaintiff and Dr Patney, of the Department of Chemistry, Materials and Forensic Sciences at the University of Technology, Sydney, who reported for the defendant, are relevantly qualified experts able to give evidence of both the chemical composition of the substance and the impact of chemicals on the human body.
Both experts agreed that the presence of a strong smell, while indicating the presence of chemicals, is a most inexact indicator, and that you cannot determine the level of toxicity by relying on reports of smell. Dr Patney said that, for these chemicals, they are detectable by smell at concentrations of about 2 parts per million, which is well below any levels considered to be unsafe. Both experts gave evidence as to their understanding of the likely levels of chemical exposure, based on their understanding of the facts. Both experts, it seemed to me, very properly identified where they were making calculations or giving opinions based on their expertise, and where they were relying on assumptions based on their instructions. Both experts adopted common standards.
Dr Crank in his report based his calculations on the assumption that a 20 litre drum of the adhesive was left open all day on 27 September. I am not satisfied that this is the case. He goes on
“There is no information about the quantity of the adhesive used, but the product leaflet states that 1 litre is required for each 5 Square metres of surface being glued. When two surfaces are to be glued together, both surfaces must be coated with the adhesive. The instructions require both surfaces to be allowed to dry (10-15 minutes) before joining them. It seems probable that several litres of Anchor Weld was used in the gluing of cupboards etc on 27 September.”
This seems to assume that all the laminating was done on site, which is contrary to the evidence.
Dr Patney’s report is based on the assumption that only about 250ml of glue was used on the day to laminate the one panel.
The report of Dr Patney is based on assumptions that I have found to be made out on the balance of probabilities. His report refers to an area of gluing of about 900ml by 600ml. He seems to have been mistaken in looking at the photographs as to where this area was, but it seems to me that nothing turns on this, as his calculations are clearly based on the appropriate area, indeed, if anything, they are based on a slightly larger area, as Mr Keane said it was about 500ml wide rather than 600ml.
The assumption of Dr Cranks that a 20 litre tin of glue was left open all day is inconsistent with my findings. The assumption that several litres of Anchorweld was used on the day I find to be incorrect. It seems to be based on an assumption that all of the laminated surfaces in the new kitchen area were glued on site. The evidence satisfies me that the only gluing that was done on site was to one panel that was about 1 metre by 500 millimetres, that is a half a square metre. On Dr Cranks calculations based on the instructions, this would amount to a square metre of surface, each half square requiring gluing, and this would amount to some 200 ml of glue being used, which is consistent with the evidence of Mr Keane and the assumption in Dr Patney’s report.
Dr Crank and Dr Patney were broadly in agreement as to the nature of the adhesive, and that the solvents hexane, toluene and acetone were present in proportions of about 50%, 20% and 15% by volume respectively. The solvent acetone is variously described thus and as methyl ethyl ketone.
The experts were in general agreement as to the relevant standards. Worksafe Australia publishes standards for exposure to hazardous chemicals, which were referred to by both experts. It is apparent that there are two sets of standards, being Threshold Limit Values, being atmospheric levels set for workers exposed for an average 8 hour day, and Short term Exposure Limits, being levels set for workers exposed for single instances.
I am satisfied that the Threshold Limit Value (TLV) and Short Term Exposure Limits(STEL) in parts per million (ppm) for the relevant solvents are:
Solvent TLV STEL
Hexane 50ppm 1000ppm
Toluene 100ppm 150ppm
Acetone 200ppm 300ppm.
The experts used a common methodology to determine the airborne solvent concentration, but these were of course based on their assumptions as to the volume of material. Dr Crank said that for each litre of glue, the levels of solvent would be:
Hexane about 1490 ppm
Toluene about 560ppm
Acetone about 660ppm.
He said that this would exceed safety standards, and this is indeed the case. I have found, however, that only a maximum of 250ml was exposed, and for only one short procedure that took about half an hour. Dr Patney did his calculations based on 250ml of glue, and said that this would produce levels of solvent at the following rates:
Hexane 343ppm
Toluene 154ppm
Acetone 173 ppm.
He said that as the levels of Hexane and Acetone were well below the Short Term Exposure Limit, the concentration should not have posed a health risk. He acknowledged that the levels of Toluene at 154 ppm was marginally above that limit of 150 ppm, but said that this is an academic calculation based upon a lump mass introduced all at once of 250ml of Anchor Weld, whereas in fact the material was applied over the half hour. He noted also that doors were opened, and an air conditioning system running, which would have resulted in lower concentrations than those theoretically calculated. He concluded that the level of exposure was safe.
Dr Crank made his calculations on a further assumption that there was no ventilation or air movement within the office. I do not find this assumption to be made out. I find that the door was opened and kept open during the afternoon, and that there was a central air conditioning/heating system that involved a degree of air movement. The plaintiff acknowledged in cross-examination the presence of vents in the ceiling in the office. Mrs Pocock gave evidence that both the front door and the door to the internal corridor were propped open and kept open for the whole of the day. Where Mrs Pocock’s evidence differs from Mrs Lindbeck’s on this point I prefer the evidence of Mrs Pocock. Mrs Pocock agreed there were four of five air conditioning outlet vents in the ceiling of the office.
It is apparent that on these figures the levels of Hexane and Toluene are above the Threshold Limit Values set by Worksafe Australia, but Dr Patney said that these were levels for constant exposure over an 8 hour day, and are inapplicable to a single exposure.
In cross-examination Dr Crank conceded that if the only area that was glued was the one panel, lower amounts of solvent would have been released. He agreed that, on the assumptions made by Dr Patney, which I have found to be in accordance with the evidence as I have found it to be, Dr Patney’s calculations as to exposure levels were accurate. He also agreed that if the laminating was a one off operation over about 30 minutes the appropriate exposure levels would be the Sort Term Exposure Limit (at transcript page 239).
Based on my findings of fact, that the only exposure occurred by way of a single instance of laminating which involved the use of no more than 250ml of glue for about half an hour, I prefer Dr Patney’s calculations. I draw comfort in relying on the science here from the fact that Dr Crank conceded that, if the facts were as assumed by Dr Patney, he would be in agreement with Dr Patney.
I find that the levels of chemical exposure on the day on which the gluing occurred, which was probably 27 September 1995, was within the appropriate standard, being the Short Term Exposure Limit set by Worksafe Australia for the use of these types of chemical agents. I make this finding in respect of each of the solvent agents Hexane, Toluene and Acetone, noting that the Toluene level was on calculations based on 250ml of product exposed in a single lump and absent air flows marginally above the Worksafe Australia level.
The fact that the levels were consistent with Worksafe Australia Standards does not itself dispose of the issue of liability, although it does seem to me that a defendant who shows that a level of chemical exposure was within approved safety standards does do much to demonstrate that a due standard of care has been taken.
Dr Patney was of the opinion that for a single use of about 250ml of this product, adequate ventilation was provided in this office worksite by way of open doors and the airflow through the air conditioning and heating vents. He agreed with Dr Crank that the product information for Anchorweld indicates that it should only be used in a well-ventilated area. Dr Crank, on his assumption that there was no air flow at all and that the product used was a number of litres taken from an open 20 litre tin reported that there was inadequate ventilation, and that the use of the product in these circumstances was unsafe.
In cross-examination Dr Crank agreed that his opinion would differ if there was adequate ventilation by way of a propped open door, and working air conditioning and heating vents. He maintained, however, that if there was a smell there was inadequate ventilation, but agreed that the presence of a smell is a very inexact measure. I am not satisfied that the presence of any chemical smell from a single use of a chemical glue indicates a breach of a duty of care. This would, it seems to me, impose an unrealistic and unreasonable standard of liability, with implications that all minor maintenance tasks in workplaces could require the total evacuation of the workplace. This would apply, it seems to me, as much to painting as gluing, as the relevant agents in this case, being solvents, can be present also in paints. I was pointed to no authority that indicated that it is a breach of an employers duty of care to undertake such maintenance in a workplace.
I am not satisfied that the use of a small quantity of laminating glue to laminate one panel while office workers continued in the outer office amounted to a breach of duty of care on behalf of the defendants to the plaintiff. Accordingly, I would on this finding direct a judgment for both defendants against the plaintiff. If I be wrong in this, however, I should also continue to examine the questions of causation and assessment of damages.
Causation
In order to establish a claim for damages a plaintiff must not only establish a breach of a duty of care, but also establish that that breach lead to the loss complained of. In this case, the defendants deny that, even if there was negligence established in exposing the plaintiff to the adhesive, the loss claimed to be suffered by her was caused by such exposure.
It is the plaintiff’s case that she is particularly susceptible to chemical exposure, and that the exposure in this case has lead to a reactive airwaves disorder, and to an ongoing sensitivity to environmental chemicals, and psychological difficulties, and a condition of chronic fatigue syndrome.
It is a well known principle that a defendant must take the plaintiff as they find them. This rule, however, operates when it is established that negligence has occurred and caused damage. The Full Court of the Federal Court recently restated the position in Australian Capital Territory Schools Authority v El Sheik [2000] FCA 931 where Wilcox J (with whom Higgins J agreed) said at [26]:
“If negligence be shown, a defendant must take a plaintiff as he or she is, it is no answer to say that the plaintiff has suffered a degree of injury exceeding what would be suffered by a normal person without the special vulnerability. However, in assessing the question whether a defendant has been guilty of negligence, the fact that the defendant was unaware of the special condition is of considerable importance. A defendant must exercise reasonable care, having regard to the information actually or constructively known to the defendant. It follows that, in the present case, the question of breach of duty must be evaluated on the same basis as if Mr El Sheik did not suffer a special vulnerability.”
The position was concisely stated by Spigelman CJ in Morgan v Tame [2000] NSWCA 121, (2000) 49 NSWLR 21 where he said at p27 that
“the ‘eggshell skull’ or ‘psyche’ rule is a rule of compensation not of liability……The ‘eggshell skull’ principle makes a defendant liable for damage of an unforseen extent, but not for unforseeable damage of a different kind.”
The defendants had no knowledge of any particular sensitivity that the plaintiff may have had to chemicals.
The plaintiff claims that the chronic chough that she developed while on holidays was the onset of Reactive Airways Dysfunction Syndrome. The evidence of the plaintiff is that the exposure to the chemicals occurred on the Wednesday, and I accept this evidence. The plaintiff says that she again noticed the smell on the Thursday, but it was less severe. I have found that the exposure occurred as a result of one episode of applying a veneer on the Wednesday. The plaintiff says that she developed a really bad headache on the Wednesday evening, for which she took Panadol. On the Thursday she continued to have a headache. She left for her holiday at the Hawkesbury river on the Friday, and continued to have a headache, and tiredness. She says that late on Friday she began to develop a cough. The Hawksebury District Hospital notes recorded a visit at 10 am on Sunday with a history of a 24 hour cough.
Evidence was given by a number of doctors that Reactive Airways Dysfunction Syndrome is, by definition, a syndrome that manifests itself within 24 hours of exposure to the chemical irritant.
Dr Sutherland, a clinical immunologist and consultant physician who reported for the defendant said in September 2001:
“Mrs Lindbeck may have suffered from a transient form or reactive airways dysfunction syndrome, following an occupational exposure to chemicals on the 27th and 28th of September 1995. This diagnosis was made on clinical grounds by Dr Hurwitz, a thoracic physician who assessed her early the following year. There are two reasons to have reservations about accepting this diagnosis. The first is that a literature search has not revealed any reports of reactive airways dysfunction syndrome caused by exposure to the chemicals under question in this case. The second…is the question as to whether or not the onset of symptoms did occur within 24 hours of the inciting exposure, as is required by currently accepted definitions for reactive airways dysfunction syndrome.”
It seems to me significant that in a case such as this, which seeks to link a condition to an industrial chemical, there has been no evidence presented of any cases where the claimed condition has been linked to the chemical agent, and Dr Sutherland’s evidence that a literature search failed to find such a link is important.
Dr Hurwitz, in a report of 23 July 1996 gave a history of the cough starting the day after the exposure. In his evidence he said that, where a person had been exposed over a long period they may develop a sensitivity which could then be provoked. It was put to Dr Hurwitz that, if it was a single exposure, it is one of the cardinal diagnostic features of Reactive Airways Dysfunction Syndrome that symptoms appear within 24 hours, and he agreed, saying
“One would expect it to appear within that period of time.”
He was then asked whether it would make a difference to his diagnosis if the symptoms were first reported more than 24 hours after a single exposure, and he said:
“I guess it would depend on how many hours more than 24, if you- you know if one says sort of 3 or 4 days then I think that would have been stretching the time limit a bit. If it was within the days- you know, plus or minus a couple of hours, then one would have to presume that it was still possible.”
Dr Hurwitz agreed in re-examination that, if the plaintiff had been exposed to the chemical on Wednesday and Thursday, and developed a cough some time of Friday, that would still be within the acceptable time frame.
Dr Hurwitz described the condition as being, as its name would suggest, a reaction in the membranes of the airwaves to a chemical insult. Thus the most obvious symptom of the condition is the cough. The development of a cough on Friday night, on the plaintiffs case, or 24 hours before Sunday morning, on the hospital notes, does it seems to me put it at the outer margin for it to be considered a reactive condition from a single exposure to the laminating glue which occurred before lunchtime on Wednesday.
Dr Hurwitz subjected the plaintiff to clinical tests in early 1996 which satisfied him that her lung condition was abnormal at the time of his first consultation, which he attributed to the Reactive Airways Dysfunction, but that her lung condition had resolved by March 1996.
Dr Haber is a consultant physician and Fellow of the Royal Australian College of Physicians, and he has examined the plaintiff in respect of workers compensation claims. He accepted that it was possible that exposure to the chemicals could have provoked a degree of asthma like symptoms, but was satisfied that these had resolved by the time of his examination in February 1997. In his later report he concluded that she suffers from asthma. He noted her family history of asthma. He says in his report that
“the doctor in Windsor Hospital considered it very likely that her chest symptoms then were due to possible exposure to ‘flowering trees’ and it is well known that exposure to certain plants can provoke an asthmatic like reaction, especially if a number of similar exposures took place previously. This is more likely to occur in a person who is predisposed to an asthmatic like reaction”.
On the preponderance of the evidence I am not satisfied that the plaintiff’s cough, which I accept developed on the Friday evening, was a symptom of Reactive Airways Dysfunction caused by the single exposure to the adhesive on Wednesday. While I accept that Dr Hurwitz says that this time gap still leaves it as a possible explanation, it is for the plaintiff to establish causation on the balance of probabilities, and this has not been established to my satisfaction. I note the report of Dr Chapman, an Ear Nose and Throat surgeon who examined the plaintiff in November 1995 and said in his report of April 1996 that the cause of the plaintiff’s condition “is not clear, but I felt that either an infection (probably viral) or an allergic response to some unidentified exposure would be the most likely diagnosis.” I note also that the Hawkesbury District Hospital report at the initial diagnosis took a family history of asthma, and made a provisional diagnosis of asthma and attributed flowering plants, it being spring time, as the likely cause. It seems to me that the claimed condition is one of a number of possible explanations, and that the plaintiff has not established the link to the requisite standard.
If I am wrong in this, it seems to me that the defendants are responsible for a Reactive Airways Dysfunction condition which was present from October 1995 to March 1996, by which time it had resolved.
It seems on all of the evidence that the plaintiff is no longer troubled by ongoing coughing symptoms. Dr Donohoe continues to assert that she suffers from RADS, but in cross-examination he accepted that he would defer to a specialist on this question, and I am satisfied on the evidence of Drs Hurwitz, Sutherland and Haber that she no longer has this condition, if indeed she ever did. Her substantive claim is that she has developed an ongoing fatigue condition. Her general practitioner, Dr Davis, has diagnosed this as “post traumatic stress syndrome”, in a report of 31 December 1996. There is a tendency for a diagnosis of post traumatic stress disorder to be readily made by general practitioners in accident compensation claims without proper regard to the diagnositc criteria for this condition, which are well understood and laid down in the Diagnostic and Statistical Manual of Mental Disorders, published by the American Psychiatric Association, and now in its fourth edition (DSM-IV). The single exposure in the workplace to an unpleasant smell could not, in my view, meet the proper criteria for post traumatic stress disorder, as properly defined.
The ongoing condition of fatigue has been diagnosed by Dr Donoghue as Chronic Fatigue Syndrome (CFS), which he attributes to the chemical exposure. Dr Donoghue is the principal doctor in the plaintiff’s case in this regard.
Dr Donoghue is a medical practitioner holding the normal undergraduate degrees, and holds himself out as a Fellow of the Australian Society of Environmental Medicine. He states that he has specialised in the study of CFS since the early 1990’s. He listed in his curriculum vitae having been Director of the Environment Medicine Centre at Manly Waters Hospital from 1989-1992.
Dr Donoghue’s qualifications were subject to attack in cross-examination, and in the report of Dr Sutherland. He agreed in cross-examination that he has had no specialist training. He stated that his Fellowship of the Australian Society of Environmental Medicine is “an honorary grant given to Doctors who had attended a certain number of scientific conferences held around Australia during a period of about 10 years.” He agreed that the Society was a group of like minded general practitioners and specialists who met and discussed issues concerning environmental medicine.
In the Australian and British medical professions the term “fellow” has a long and proud tradition, signifying that a person has undertaken a program of study and examination. A medical practitioner who is a Fellow of the Royal Australian College of Surgeons, for example, will have undertaken rigorous training and testing over many years before earning this title. It is a fact that the professions are largely self regulating in relation to these matters, but it is a matter of concern that a group of like minded general practitioners can form themselves into a society and then award each other a title of “Fellow” in that society, as the term seems to me to suggest a specialist qualification. I accept Dr Donohoe as a general practitioner, and a person with an interest in the condition of chronic fatigue syndrome and the effects of environmental factors on health. His “fellowship” I do not regard as a specialist qualification, a factor he properly conceded in cross-examination.
He listed a long list of publications, but agreed that only two of these were in peer reviewed publications, and that his one publication in the Medical Journal of Australia had been the subject of a contrary editorial in which it was described as “poorly conceived and written”.
Dr Donohoe was criticised by counsel for the defendant for confusing his role as an expert witness providing medico-legal reports with a treating role. Her general practitioner, Dr Davis, in a report of 15 February 2001 nominated Dr Donohoe as the specialist that she sees, but Dr Donohoe maintained at first in cross-examination that he was purely a medico legal expert and did not have a treating role. He later conceded that he did provide treatment, often in the somewhat unusual form of telephone consultations and advice on mineral supplements and the like, and acknowledged that he confused the two roles of treating doctor and expert witness.
Dr Sutherland was very critical of Dr Donoghue in his report and his evidence. His report of 7 September 2001 is a piercing critique of Dr Donoghues reports of July 1999 and August 2001. I will not set out the full report in these reasons, but it is appropriate for me to set out some extracts.
Dr Donoghue is of the view that the plaintiff continues to suffer from symptoms of RADS and a condition he describes as Reactive Upper Airways Dysfunction Syndrome. Dr Sutherland notes that Dr Hurwitz found that she did not suffer from these conditions in March 1996, and that his own examinations showed the same. He said
“Dr Donoghue offered no objective evidence in the form of abnormal tests from pulmonary function tests or bronchial challenge tests, to support his claims that Ms Lindbeck suffered from reactive airways dysfunction syndrome subsequently, and it is most unlikely that investigations of this kind would have yielded abnormal results had he initiated them.”
Dr Sutherland noted Dr Donoghues claim that she continues to complain of reaction to chemical exposure. He said:
“The next paragraph in Dr Donoghue’s account contains a very good example of how unscientific advice of this kind can be harmful to those receiving it. Dr Donoghue went on that “This has limited her activities and markedly reduced her enjoyment and quality of life. Minimising irritant and exacerbating chemical exposure has become a major part of Ms Lindbeck’s life. Inadvertent exposure leads to severe respiratory problems, illness and requires urgent medical management.” Unfortunately, it seems likely that Ms Lindbeck has been indoctrinated into the ideology and practices of a group known loosely as clinical ecologists, or practitioners of environmental and nutritional medicine. Once collusive and illness affirming behaviour of this kind has been entered into, there is little hope of a subsequent improvement and a return to good health, as long as it is continued. In fact, in many cases the perceived disability increases with time, with the affected individual coming to believe that he or she is reacting to an ever increasing range of otherwise innocuous environmental chemicals. This leads to social isolation, and in extreme cases, a retreat to a rural environment, where an hermit like existence is deemed to lessen the risk of further chemical exposures.”
It is apparent that there is a broad gulf between the medical experts in this case. Taking all of the evidence into account, it seems to me that Dr Donoghue has, at best, developed a hypothesis that could link environmental exposure to chemicals to chronic fatigue syndrome. His hypothesis suffers to some extent from the same weakness that the claimed link between this adhesive and RADS suffers, in that he has been unable to point in the scientific and medical literature to a link between the substance and the claimed condition, a point made by his critics.
Dr Sutherland in his report says
“Dr Donohoe continued his improbable claims by stating that “Mrs Lindbeck also suffers from chronic fatigue syndrome (CFS). This may have originally been caused by her respiratory difficulties and sensitisation, or may simply have been a direct result of her workplace chemical exposure and multiple chemical sensitivities. This has been reported to lead to CFS directly in a minority of people exposed”. Dr Donoghoe has made claims of this kind before, without any attempt to substantiate them. There is in fact no credible evidence to support these contentions.”
Dr Sutherland is also most critical of the treatment regime that has been followed by Dr Donohoe and Mrs Lindbeck’s local general practitioners. He says in his report that cognitive behavioural therapy is now regarded as effective in treating CFS. He notes, however, that a working party of the Royal Australasian college of Physicians in 1997 noted biases in examining persons who report chronic fatigue syndrome in self help group populations. Dr Sutherland says that
“it seems that her management has been complicated by her indoctrination into the beliefs and practices of clinical ecologists and practitioners of environmental and nutritional medicine. If she has been convinced that she suffers from multiple chemical sensitivities as well, then it is most unlikely that she will improve, while she continues to follow the demonstrably ineffective, and in my view unscientific advice offered to her by Dr Donohoe.”
Dr Haber also reported on the question of chronic fatigue syndrome. He stated :
“The diagnosis of chronic fatigue syndrome is based on symptoms and there are no available diagnostic tests as such. It requires four or more of the following symptoms to be concurrent and persistent for six months or more, namely:
. Impairment of short term memory or concentration
. Sore throat
. Tender cervical or axillary lymph nodes
. Muscle pain, or multi joint pain without arthritis
. Headaches of a new type, pattern or severity;
. Unrefreshing or disturbed sleep
. Post exertional malaise lasting more than 24 hours.
It must be noted that during the interview there was no obvious impairment of concentration, nor apparent impairment of short term memory, and in fact she was able to describe all her symptoms and date the events very well. She did not have any tenderness or pain in the cervical or axillary region, nor any lymph nodes were palpable. She suffers from muscle aches at times and they are not sustained. She specifically told me that she has been sleeping well, lately. She told me that she sleeps better than previously, falls asleep reading for a while, and does not wake up through the night, but on awakening in the morning does not feel refreshed. I understand that initially soon after the time of the alleged exposure to the fumes, she had severe anaemia and apparently this has been corrected since then. The anaemia was almost certainly related to her heavy menstrual losses and not to the exposure to the fumes. I have not been shown any results of recent tests, and in particular was not provided with chest x-ray, full blood count, serum electrolytes, or liver function tests, to exclude some underlying pathology. In my opinion therefore she does not fulfil the criteria required for the diagnosis of chronic fatigue syndrome.”
Dr Haber’s reference to being unable to exclude underlying pathology is consistent with Dr Sutherland’s assertion that chronic fatigue syndrome is a diagnosis of exclusion, that is , a condition that can only be properly diagnosed when other organic causes of a set of symptoms have been excluded, which I am not satisfied has occurred in this case.
Where there is a conflict in the medical evidence I prefer the evidence of Dr Haber and Dr Sutherland to Dr Donohoe. If I were wrong in my determination as to liability, I would not find that the plaintiff has any ongoing disabilities as a consequence of the exposure to the adhesive at work. I am not satisfied that the plaintiff has established, on the balance of probabilities, that there is any link between this exposure and any ongoing symptoms she may complain of. At the highest point of the evidence, it seems to me, Dr Hurwitz and Dr Haber state that the exposure to the adhesive might have lead to the asthma like symptoms that she reported some three days later. This is not sufficient, in my view, to establish that the exposure caused the symptoms.
Damages
As I have found that there was no breach of duty of care on the part of either defendant I have entered a judgment in favour of the defendants. I have also found that, if I am wrong in this, and there was a breach of duty of care, I am not satisfied that the plaintiff’s ongoing complaints, which mostly involve the condition of chronic fatigue syndrome, were caused by the exposure to the adhesive at the workplace. It would follow that, on this basis, I would award nominal damages only in respect of a short term irritation following the exposure to a strong smell at the workplace. I am satisfied that any asthmatic condition triggered by the workplace (and this is assuming, contrary to my findings, that the possible link set out by Dr Hurwitz was established on the balance of probabilities) would have resolved by early 1996.
The plaintiff’s case is that her chronic fatigue syndrome has had a catastrophic effect, and that as a consequence she will never work again, and requires considerable assistance in the home. I am not satisfied that this is so. I note the grave reservations expressed by Dr Sutherland in relation to the treatment regime developed by Dr Donohoe, and Dr Sutherlands evidence that patients with chronic fatigue syndrome can respond well to cognitive behavioural therapy, which has not been introduced here. I have grave reservations about Dr Donoghoe’s assertion that she will never work again given my doubts about his assertions as to the aetiology of her claimed condition.
In the normal run of personal injury litigation it is appropriate, even where a finding is made that liability is not made out, for the trial judge to nevertheless proceed to an assessment of damages. In the present case, given my findings that liability is not made out, and that the claimed condition of chronic fatigue syndrome has not been shown to be caused by any exposure to the adhesive, it seems to me that little would be achieved by a hypothetical assessment. Nevertheless, counsel for the plaintiff has prepared a detailed schedule of damages, which make the assumption that she will never work again, and that she will require considerable domestic assistance, in both cases due to the chronic fatigue syndrome which was caused by the defendants negligence. There was a report prepared by Macquarie Reporting Service setting out wage loss, superannuation and Griffiths v Kerkemeyer damages, but of course this was based on the above assumptions. If all of these matters were made out, it seems to me that the plaintiff’s approach to damages was appropriate. Counsel for the defendants did not criticise the plaintiff’s methodology, but of course stressed that the damages calculations were based on findings which they said should not be made.
As the plaintiff brings a claim against both her employer and the contractor, it is necessary to determine the degree of contribution by each party, and then assess the damages, because, as the alleged act of negligence occurred in New South Wales, I must apply New South Wales law in assessing damages, and this means that damages awarded against the first defendant, the employer, would be assessed pursuant to the provisions of the Workers Compensation Act 1987 (NSW) whereas damages awarded against the second defendant, the contractor, would be assessed at common law. The parties were in agreement that the correct approach to this type of matter is that set out by Allen J in Leonard v Smith (1992) 27 NSWLR 5, as endorsed by the court of appeal in Grljak v Trivan Pty Ltd (unreported, 19 April 1996)
In relation to the degree of liability, it seems to me that the employer would bear the greater degree of liability, in that it had control of the workplace, and it made the decision that the plaintiff and her colleagues could continue to work while renovations were taking place. I have of course found that there was no breach of duty of care, but if I were wrong, it seems to me that this factor of control of the workplace is significant. The contractors would, on this basis, also be negligent in introducing the adhesive, but it had no control over the workplace. I would have assessed the degree of responsibility at two thirds to the first defendant and one third to the second defendant.
The plaintiff’s schedule of damages, assuming the full claimed effect of the chronic fatigue syndrome were attributable to the negligence of the defendants, made a claim for general damages at 50% of a most severe case. On the assumed facts, this would seem appropriate. This would involve an award of general damages of $108,800. Treatment expenses were agreed arithmetically in the sum of $19,042. Past wage loss to trial was claimed in the sum of $83,549, and this was not disputed on the assumption, contrary to my findings, that the time off work was attributable to the negligence of the defendant.
Future economic loss to normal retirement age, assuming total inability to work, was claimed at $317,254, from which a discount for vicissitudes of 15% was allowed for a claim of $269,666.
Future superannuation loss, on the basis of the accountant’s report, was claimed in the sum of $40,507, and there was a Fox v Wood component of $5,027.
A Griffiths v Kerkemeyer claim for the past was calculated by the accountants at $64,350, and for the future at $291,600. This is of course on the basis of the assumptions in the report, that is that the plaintiff’s chronic fatigue syndrome was caused by the defendant’s negligence, will never resolve, and has created a need for the assistance there set out. If all of these assumptions were made out contrary to my findings (and in particular to the evidence that, with proper treatment, there is a favourable prognosis for recovery according to Dr Sutherland) then this would be an appropriate quantum. A claim for future treatment expenses was made in the sum of $10,368. This seems appropriate.
The plaintiff’s total claim against the first defendant was thus $892,909. This figure seems to me to be appropriate if all of the assumptions on which it is based could be made out. I would have awarded this sum, if satisfied about the assumptions. As I have indicated that I consider the first defendant to be responsible for two thirds of the condition, I would have awarded damages against the first defendant in the sum of $594,678.
The plaintiff’s schedule of damages against the second defendant, again based on the assumptions set out above, would have involved a higher sum for general damages under common law. The claimed general damages of $120,000 seems to me to be appropriate if all of the assumptions on which it is based were made out. This would lead to a total award of $904,109. As one third of this is the responsibility of the second defendant, I would have awarded, if all of the assumptions were made out, the sum of $301,973
I should add that this is purely indicative, and it seems to me that, if I am found to have been in error in relation to my findings as to duty of care and causation, it would be a safer course to assess damages rather than to rely on these figures, unless of course the Court of Appeal were satisfied that all of the assumptions upon which these figures were based could be made out.
I direct a judgement for the first defendant and the second defendant. I will hear the parties as to costs.
I certify that the preceding ninety two (92) numbered paragraphs are a true copy of the Reasons for Judgment herein of the Master, Mr T Connolly
Associate:
Date: 12 April 2002
Counsel for the Plaintiff: Mr Mahoney
Solicitor for the Plaintiff: Baker Deane & Nutt
Counsel for the First Defendant: Ms L. Gabriel
Solicitor for the First Defendant: Pricewaterhouse Coopers Legal by their Canberra agent: Deacons
Counsel for the Second Defendant: Mr J. Harris
Solicitor for the Second Defendant: Matthews Folbigg by their Canberra Agent: Smyth Burnett Bowden
Date of hearing: 17, 18, 19 & 20 September 2001 &
17 & 18 December 2001
Date of judgment: 12 April 2002
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