STATE OF NEW SOUTH WALES t/a NEW SOUTH WALES DEPARTMENT OF AGRICULTURE v. ALLEN [2000] NSWCA 141

STATE OF NEW SOUTH WALES t/a NEW SOUTH WALES DEPARTMENT OF AGRICULTURE v. ALLEN [2000] NSWCA 141 - NSWCA 2000 case summary — Zoe

[8]

JUDGMENT 1 PRIESTLEY JA: In my opinion this appeal should be dismissed. 2 The decision at first instance is a paradigm example of a feature of fact finding often found in cases involving medical issues. That feature is the major cleavage between proof of a fact in non criminal court cases to the satisfaction of the fact finding tribunal on the balance of probabilities and proof of a fact for scientific purposes to the satisfaction of those expert in the particular field of science. The latter kind of proof is much more rigorous and demanding than the former. 3 The two kinds of proof are quite different in their objects and methods, but are frequently the cause of confusion when medical issues are concerned. In many such cases, experts in the field of the relevant medical science give evidence of their expert opinion concerning the medical issue. Trained in the scientific method of proof, some such experts find difficulty in adjusting themselves, when giving evidence in court, to the lesser requirements of legal proof, which, looked at from their scientific standpoint, they regard as inferior and unreliable. An expert who gave evidence for a party in litigation where there has been an adverse result reached by application of the legal standard of proof is quite likely to advise the party that the result is an unscientific and unsound one. Hence, many appeals by the indignant losing party: the various trials and appeals in Hocking v Bell, (see the decision in the Privy Council (1947) 75 CLR 125)), provide a classic example. 4 In the present case Powell JA in his reasons reviews the evidence before the trial judge in detail. In my opinion it is quite clear from the materials appearing in Powell JA's reasons that there was evidence before the trial judge on which he could properly arrive at the decision which he did. Recognition of that fact means that the main point in the appellant's appeal must fail. The dogged prosecution of the appeal seems to have been heavily influenced by the mistaken idea lying behind many of the submissions that the court should apply the scientific rather than the legal method of proof. 5 I agree with Powell JA's conclusions on the appeal, and generally with his reasons. 6 On the respondent's cross-appeal, I agree with Powell JA's reasons and conclusions. 7 Accordingly, I agree with the orders proposed by Powell JA in both the appeal and the cross-appeal.

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8 POWELL JA: This is an appeal and cross-appeal against a Judgment delivered and Award made by Armitage CCJ on 23 December 1998 in proceedings which had been brought by the Respondent/Cross-Appellant ("Mrs. Allen") seeking to recover against the Appellant/Cross-Respondent ("the Department") workers compensation following the death of her husband in May 1994. That death, so it was asserted, had ultimately been caused, or was, at the least, contributed to, by the nature and conditions of Mr. Allen's employment with the Department as a temporary stock inspector, it being asserted that, in carrying out his duties as such, Mr. Allen was exposed to carcinogenic and toxic substances, which exposure resulted in Mr. Allen contracting carcinoma of the pancreas which condition led to his death in May 1994. 9 The proceedings were brought by Mrs. Allen in two capacities, first, as legal personal representative of Mr. Allen - but whether as executrix of his will or as adminstratrix of his estate is by no means clear (see Black AB 2) - and, second, as a totally dependent widow on behalf of herself and of two of the three children of the marriage. In the proceedings Mrs. Allen claimed, in her first capacity, weekly payments pursuant to s.36 of the Workers Compensation Act 1987 ("the Act") from 6 December 1993 until 8 May 1994, lump sums pursuant to s.66 of the Act in respect of 100% loss of the efficient use or impairment of the right arm, left arm, back, neck, right leg, left leg, pelvis, penis, vision, hearing, speech, smell and taste - a total of $158,650.00 being claimed - a lump sum pursuant to s.67 of the Act for pain and suffering and expenses for medical and hospital treatment pursuant to s.60 of the Act. In her capacity as a wholly dependent widow Mrs. Allen claimed on behalf of herself and two children in question a lump sum of $223,850.00 pursuant to s.25(1)(a) of the Act and, in respect of the two children, weekly payments pursuant to s.25(1)(b) of the Act from 8 May 1994 during dependency. 10 The proceedings at first instance were protracted, the Application for Determination having been filed as long ago as 8 August 1994. The hearing before Armitage CCJ occupied some twenty hearing days spread over a period of some 2 years and 3 months, commencing in late February 1996 and concluding in late May 1998. That hearing was followed by lengthy written submissions which were filed on behalf of the Department in mid-July 1998 and written submissions filed on behalf of Mrs. Allen at the end of August 1998. 11 At the conclusion of the introduction to the Judgment which he was to deliver on 23 December 1998, Armitage CCJ wrote (RAB 21): "The issues were not defined at the commencement of proceedings but it is fair to say that in the manner in which the matter was fought the respondent denied injury, incapacity, impairment or loss and nexus or causal connection between incapacity or impairment or loss, together with the entitlement of the widow to a s.25 lump sum and the consequent weekly payments in respect of the dependency of her children upon the deceased. Dependency itself in respect of either the children or the widow herself was never admitted but it did not seem to me that at any stage any cross-examination occurred to suggest that the applicant widow and her three children were not totally dependent upon the deceased as at the date of death, nor was any evidence called to this effect. I propose so to find. As to the heads of the claim it was clear from the manner in which the matter was fought that the applicant alleged not only injury simpliciter within the meaning of the first 'leg' of the definition of injury in s.4 of the Act but also alternatively that the deceased had contracted a disease to which his employment was a contributing factor within the first part of the second 'leg' of the above definition in s.4 as well as that the deceased had suffered an aggravation, acceleration, or deterioration of a 'disease' within the second part of the second 'leg' of the definition of 'injury' in s.4 of the Act, to which the employment was a contributing factor. Needless to say the respondent in the manner in which the matter was fought denied that the deceased had suffered an 'injury' within any of these parts of the definition of that term in the Act."

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S.67(5) of the Act provided that no compensation under s.67 was payable after the death of the worker concerned. 16 It is the findings which I have earlier (para. 5 (above)) recorded and the Award made in favour of Mrs. Allen which are the subject of the appeal with which the Court is concerned to deal and it is the failure of his Honour to make an award pursuant to s. 66 of the Act - but not his failure to make an award pursuant to s.67 of the Act - which is the subject of the cross-appeal. 17 At the date of his death, Mr. Allen was 43 years of age, he having been born on 22 September 1950 (Black AB 3; Blue AB 35). At the time he was a temporary inspector of stock employed by the Department having commenced his employment on 8 February 1989 (RAB 2; Blue AB 1, 4), his duties as such inspector being - in broad general terms - associated with the control of cattle ticks in the Casino area. 18 Mr. Allen and Mrs. Allen - who was then 27 years of age - married on 12 July 1974. After their marriage, Mr. and Mrs. Allen moved to Moss Vale when they ran a dairy for about 5 years. It was during their time at Moss Vale when Mr. and Mrs. Allen's three daughters were born, the eldest Joanne Michelle having been born on 3 March 1976, the second eldest Narelle Colleen having been born on 22 April 1977 and the youngest Maree Elizabeth having been born on 2 September 1978. (Black AB 3) 19 In 1979, Mr. and Mrs. Allen, together with two other couples, purchased 500 acres of land at Leycester, which is said (Black AB 3) to be to the north of Lismore and on which land beef cattle were run until the property was disposed of in 1982. Although it is not entirely clear that this was so, it would seem (Black AB 6) that, during the time when Mr. and Mrs. Allen were involved with the property at Leycester, the cattle were dipped on an annual basis at sometime during the dipping season - which appears (Black AB 149) as if it may have been from the beginning of each year to May and, on occasions, June. 20 Following the sale of the property at Leycester in 1982, Mr. Allen leased a dairy business at Tatham, which appears to be to the south of Lismore and the south-east of Casino (Blue AB 442), which business he sold in November 1987 albeit that he continued to work on the property until May 1988 (Black AB 4). Since Tatham is located within the Tick Quarantine Area to which I will shortly refer, Mr. Allen was, at least in the last 2 years of his time on the property (Black AB 18), involved in dipping the dairy cattle on the property. 21 The disposal of the dairy business appears to have coincided with the acquisition by Mr. and Mrs. Allen of a coffee lounge in Casino where Mr. Allen appears (Black AB 4) to have assisted Mrs. Allen between May 1988 when he left the Tatham property and February 1989 when he commenced to work with the Department as a stock inspector. 22 Some indication of the duties of a stock inspector employed by the Department is provided by the Statement of Duties (Exhibit "DD" - Blue AB 3) which was tendered during the hearing before Armitage CCJ. It included the following: "RESPONSIBLE FOR: 1. Treatments and examination of livestock in accordance with registered circulars as required for the Cattle Tick Program. ……… 4. For dips under Departmental control manage the concentration of dipwash by regular submission of dip samples for laboratory analysis and carrying out rectifications as directed and supervise treatment of stock at these facilities. ………. 6. Maintaining fences, dipyards, buildings required for the Cattle Tick Program as directed. 7. Maintaining equipment allocated for official duties such as motor vehicles, tractors, chainsaws, pumps and sprays in good repair and condition. ………" 23 A further list (Exhibit 'EE" - Blue AB 4) recorded the following in relation to Mr. Allen: "INSPECTOR OF STOCK - CASINO AREA DUTIES INCLUDED: Examination run each year. Cleaning and patching dips -Promicide, Barricade S and Amitraz dips. This involved getting down inside the dip into contaminated dip sludge. Treating movement stock either dipping or spraying. Repairing dip covers which were still covered in dip poison and contaminated hair. This involved drilling the cement and welding mesh covers. Truck driver."

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24 It is convenient, here, to pause for the purpose of giving some further information as to the history, and the nature, of the Cattle Tick Prevention Program to which I have earlier referred so that one might more readily understand the duties which Mr. Allen was, from time to time, called upon to perform in his employment as a stock inspector. 25 Cattle tick is a serious threat to the beef and dairy cattle industries in New South Wales. The tick, which was introduced to Australia in about 1850, travelled from Darwin across the Gulf of Carpenteria and down coastal Queensland to arrive at the New South Wales border at the turn of the century, thrives in tropical and sub-tropical environments. It is a carrier of blood borne parasites which cause serious illness and mortality in susceptible cattle and, during its Southward migration, was accompanied by massive outbreaks of illness and death in cattle populations. 26 Since the introduction of cattle ticks into Northern New South Wales in the early 1900s their spread has been controlled by an eradication and containment programme which since 1920, or thereabouts, has been conducted by the Board of Tick Control on behalf of the Department. As best as I can judge it from the materials which are before the Court, the two essential elements of that programme have been the establishment of a Tick Quarantine Area and the imposition of a compulsory programme of dipping to prevent spread, suppress infestations and eradicate ticks from areas where possible. 27 The map (Exhibit "K" - Blue AB 442) depicting the Tick Quarantine Area in New South Wales would appear to indicate that the Tick Quarantine Area extends South from the border between Queensland and New South Wales for a distance of between 250 and 300 kilometres to a point south of Yamba on the coast and extends inland from the Eastern coast of New South Wales for a distance of approximately 150 kilometres. Casino, where, during the period of his employment by the Department, Mr. Allen lived with his family, is located about 100 kilometres to the South of the border between Queensland and New South Wales and about 50 kilometres inland from Ballina on the coast. 28 The Cattle Tick Program relied on the use of chemical dipping of cattle to prevent the spread, suppress infestations and, where possible, to eradicate ticks. As part of that program, over 1600 cattle tick dips were built in North-Eastern New South Wales both along the Queensland border and to the South of it. Those dips were widely distributed at strategic locations to minimise the distances cattle had to travel to receive treatment. The vast majority of those cattle tick dips were installed by the Board of Tick Control on land leased from private land holders. At the time of the preparation of the Report on The Management of Contaminated Waste Cattle Dip Sites in North-Eastern New South Wales ("the DIPMAC Report") (Exhibit "XX" - Blue AB 297) in March 1992, the Board of Tick Control administered 1014 cattle tick dip sites still in operation in the Tick Quarantine Area, whilst there were estimated to be a further 27 dips operated privately - thus, there were still some 1040 dip sites still operational. Some 556 dip sites which had previously been in use had, meantime, been decommissioned. Of those 1600 sites 288 - of which 257 were then operational - were located in the Lismore area, while 7 sites, all of which were still operational were located within the Casino area (Blue AB 317). 29 A Schematic Diagram of a Cattle Tick Dip site (Blue AB 364) which was part of the evidence at trial depicts a rectangular area with a primary division into approximately equal halves. Within one half there is located a holding yard which leads to a force pen and then to a cattle crush, the cattle crush ending at a point between the two halves of the rectangle. The diagram depicts, in the other half of the site, a dip bath, leading to a drain pen and then leading into a draining yard which occupies by far the greater part of the second half of the site. Alongside the dip bath, but outside the fence which encloses it on the external side, are depicted areas called "scooping mound" and "disposal pit" - the area of the scooping mound and disposal pit appear (Black AB 37-38) commonly to have been known as "the poison pit area". 30 A dip bath was, as it would seem (Black AB 29), approximately 9 metres in length and a little over a metre wide. At the point - apparently known as "the take off" - immediately adjacent to the end of the crush, the dip bath was approximately 8 feet deep. The base of the dip bath was inclined so that, at the far end, cattle which had been dipped were able to step straight into the drain pen. At each end of the dip bath was a sliding gate, the one at the take off to retain cattle in the crush until the bath was free and the one at the far end to restrain cattle which had been dipped returning from the drain pen. The base and the sides of the dip bath appear to have been constructed of concrete or rendered with cement (Black AB 194, 198-199). 31 The drain pen appears (Black AB 191) to have had a concrete or cement surface and to have been fitted with drainage holes directed to returning into the dip bath or discharging to the disposal pit any of the fluid from the dip bath which had drained from cattle standing in the drain pen. 32 In addition to the dip site associated with the Casino Cattle Sales Yards, dip sites within the Casino area at which Mr. Allen attended for the purpose of carrying out his duties included Teazie Dip in Theresa Creek Road, Cannibal Dip in Theresa Creek Road, Reynolds Road Dip in Reynolds Road, The Common Dip in Springrove Road and Petersens Dip also in Springrove Road (Black AB 30-35; Blue AB 436) The purpose served by the cattle dip site at the Casino Sale Yards - where sales occurred every Wednesday and quite often on Thursdays or Fridays (Black AB 46-47) - was to permit cattle which had been sold at the sales to be dipped so that they might then be taken out of the Tick Quarantine Area (Black AB 46). 33 Given the nature of what appears to have been the first case which was sought to have been advanced on behalf of Mrs. Allen, it should be recorded that the first tickicide used in dip baths was arsenic which was not replaced until 1955. Thereafter, DDT (dichlorodiphenyltrichloroethane) an organochlorine pesticide, replaced arsenic and was used from 1955 until 1962 - its use in Australia has since been banned. In the period from 1962 to 1996 (see Blue AB 420) a variety of chemicals was used in cattle tick dips. Those chemicals were as follows:

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It should, however, be noted that, in an article "DDT and Related Compounds and Risk of Pancreatic Cancer" by David H. Garabrant et al (Exhibit 1 - Blue AB 461-468) published on May 20, 1992 in Vol. 84 of the Journal of the National Cancer Institute, the following appears (Blue AB 466-467): "This study indicates that DDT is an independent risk factor for pancreatic cancer, which is not explained by either lifestyle factors or by the presence of other exposures. External evidence indicates that DDT can be carcinogenic in animal experiments. The evidence regarding Ethylan and DDD is not as strong. While each of these agents is clearly associated with pancreatic cancer in this study, the data are not adequate to determine if each is an independent risk factor because these exposures are correlated. In addition, there is no external evidence regarding carcinogenicity of these agents specifically, although they are structurally similar to DDT. ……… Previous studies have not shown evidence of carcinogenicity of DDT to humans. Two cohort studies of men involved in the manufacture of DDT were too small to examine the risk of pancreatic cancer. Other studies have indicated weak associations between DDT and soft tissue sarcomas, lymphomas and leukaemia. Animal studies indicate that DDT produces malignant liver neoplasms, lymphomas, and lung neoplasms in mice when it is given orally or subcutaneously and live neoplasms in rats when it is given orally. Working on production produces daily exposure to DDT which is hundreds of times more intense than it is for consumers. In humans, DDT is metabolised primarily to DDD which ultimately is excreted in the urine as isomers of 2.2-bis (4-chlorophenyl) acetic acid. Enteroahepatic circulation of metabolites of DDT has not been demonstrated in humans, although it has been demonstrated in rats (43). We do not propose mechanism by which DDT might cause pancreatic cancer. However, reflux of biliary secretions containing DDT metabolites into the proximal pancreatic duct should be considered as a potential route of exposure. More than 80% of pancreatic malignancies are of ductal epithelial origin, and most occur in the head of the pancreas (44).

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37 However, it would seem that, even if that had been so, a far clearer understanding of the position had been attained by the time the expert witnesses, who were later retained to provide reports, and to give evidence on behalf of Mrs. Allen at the hearing, had been retained. That this was so would seem to be demonstrated by the "Assumed Facts" (Exhibit "20" - Blue AB 555) that seems to have been forwarded to those witnesses for the purpose of enabling them to prepare their reports. 38 In light of the attacks made on the hearing of the appeal upon the evidence of two of the experts called on behalf of Mrs. Allen - Professors Levi and Stewart - (see Appellant's Written Submissions, para. 44-47) it is desirable that I set out part of the "Assumed Facts". The relevant part (Blue AB 555-557) was as follows: "Duties as Stock Inspector: As part of his duties as a stock inspector he was responsible for the supervision and control of pests, specifically ticks, in cattle. This required responsibility for the management of cattle dip sites involving construction and maintenance of cattle yards at dip sites, dipping cattle, inspecting cattle by feeling the beast at pest-prone sites and the general maintenance and upkeep of the concrete cattle dip structures and the solutions in the dips themselves. Exposure to pesticides generally : When inspecting cattle, Mr Allen was required to feel about the beast with his bare hands to detect the presence of ticks and this was often done after the beasts had been sprayed for other pests such as buffalo fly with chemicals other than DDT or arsenic. This resulted in Mr. Allen's hands and arms coming into contact with that other chemical directly on the beast. These chemicals included substances with trad names such as: · sumafly · nucidol · grenade · stymoxin. In maintaining the dipyards, Mr. Allen was often required to replace old posts which had been in the ground adjacent the dip baths for many years. This involved digging the posts out by hand resulting in significant skin contact with the soil around the base of the post. Especially in posts adjacent the dips, there was significant residue of all chemicals used in the dips over the 40 or so years of use including: · arsenic, · DDT, · ethion, · promacyl, · barricade (chlordimeform, cypermethrin) · amitraz. You have been provided with 'fact sheets' for each of these chemicals. As a stock inspector Mr. Allen was required to physically dip cattle at various sites including the Casino Saleyards which may have involved up to 3,000 head of cattle in the day. At the sale yards Mr. Allen operated a gate adjacent to the dip bath and, was regularly splashed in the face and eyes with dip bath solution. The chemical used in the Salesyards bath had the trade name Barricade (active ingredients Cypermethrin and Chlordimeform) up to May 1994 - ie, during the whole of Mr. Allen's employment. Mr. Allen would become wet from head to toe throughout the day when dipping cattle. At other dips, similar activity regularly occurred (although numbers of cattle were less), but the dip solution varied between amitraz and Barricade. At other sites, there was frequently dust and cattle hair blown from mesh topping the dip and the sides of the race through which the dip was constructed. This matter was deposited during previous dippings by cattle splashing dip solution. On windy days this material became airborne and was in the air breathed by the inspectors. Specifically, Mr. Allen was required to clean out the dip bath by pumping the dip solution from the bath into storage tanks and then getting into the bath to bucket the remaining slurry and shovel the remaining solid out of the bath to an area immediately adjacent. The dips are a concrete trench about 2.5 m deep from ground level and about 1.5m wide. They are about 9m long to enable cattle to be immersed and swum along through the pesticide that the baths are designed to contain. Mr. Allen regularly wore gum boots at the commencement of this task while the slurry was still present in the bath. He did not wear protective clothing and wore short pants and sleeveless shirts when doing so. Apparently protecting clothing, breathing apparatus, gloves or other material was not provided or regularly utilised by Mr. Allen and his co-workers. A dip could take 1-2 days to clean. The applicant worked in alternate shifts with a partner down in the bath of up to about an hour each, but would spend up to a total of four to five hours per day in those conditions when the baths needed cleaning or repairing. Mr. Allen regularly became soaked with the slurry and residue being cleaned out of the dip. Samples taken from the site adjacent to certain dip baths which are known to have been cleaned by Mr. Allen in this fashion have indicated concentrations between 2.4-9,579 mg/kg DDT and 3-3,050 mg/kg arsenic. Total organochloride concentrations of these samples are in the range 4-10,722 mg/kg. These samples were collected and reported on by A/Prof David McConchie of Southern Cross University. The analysis of the samples occurred during July/August 1995. The samples were taken from the site at which Mr. Allen and his co-workers dumped the slurry and soil from the baths as they removed it and reflect the concentrations to which Mr. Allen was exposed while working in those baths or digging around posts adjacent to the baths. The concentrations at Teazie dip, at which Mr. Allen worked, were 3,050 mg/kg arsenic, 9,579 mg/kg DDT (total OC 10,722 mg/kg). For Cannibal dip the concentrations were 578 mg/kg arsenic, 6039 mg/kg DDT (total OC 6,653 mg/kg). Another notable dip sample was Petersens dip having 170 mg/kg arsenic, 55 mg/kg DDT (but notably 1,361 mg/kg total OC, indicating a rapid decomposition of DDT into its by products, DDD and DDE). Non specific chemical soil analyses data is also published by DIPMAC suggesting residues of: · arsenic dup to 3,000 mg/kg · DDT up to 100,000 mg/kg · ethion up to 20,000 mg/kg Apparently Mr. Allen cleaned more than 30-40 such dips in this way over the period of time he worked as a stock inspector. Although some dips may not have had significant presence of either DDT or arsenic, several did. Mr. Allen also replaced hundreds of posts (all possible prior chemicals) adjacent various dips between February 1989 and December 1993. He attended the Casino salesyards (barricade) and dipped thousands of cattle each day 2-3 times per week during his employment."

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39 That part of the material contained in the "Assumed Facts" dealing with the nature of the duties of a stock inspector and dealing with the circumstances in which Mr. Allen would have been exposed to pesticides, for the most part, is derived from the evidence of three lay witnesses, Mr. Murphy (Black AB 26-108), Mr. Draper (Black AB 148-186) and Mr. McClenan (Black AB 189-216), all of whom had, from time to time, worked with Mr. Allen in one or other capacity. Mr. Murphy had been employed by the Department since about 1965. Between 1965 and 1977 Mr. Murphy had acted as a stock inspector. Then, between 1977 and 1989, Mr. Murphy had worked, first, as a labourer and, later, on the tick gates on the border between Queensland and New South Wales. Between 1989 and the date of hearing Mr. Murphy was again employed on duties as a tick inspector. Mr. Draper, who, by the time of the trial, had taken a voluntary redundancy package and was then an organic market gardener, had formerly been employed by the Department between February 1989 and February 1996, as a yard repairer, that position involving the maintenance and repair of stock yards and surrounding cattle dips, in particular, the Casino Sale Yards. Although, prior to the trial, Mr. McClenan, too, had taken a voluntary redundancy payment, he had been employed by the Department from January or February 1981 until January 1996 as a full-time stock inspector, from about 1988 working in the Casino area. 40 Although Armitage CCJ's Judgment makes it clear that a robust and sustained attack upon the credibility as a witness of each of Mr. Murphy, Mr. Draper and Mr. McClenan was made, his Honour's Judgment equally makes it clear that, as a general rule, he regarded each of them as an acceptable witness. 41 Although, in the circumstances, I do not consider it necessary to incorporate in these reasons the detailed record and analysis included by Armitage CCJ as to the evidence of Mr. Murphy, Mr. Draper and Mr. McClenan, some aspects of his Honour's Judgment in that respect might conveniently be noted. 42 The first passage - which provides an explanation for the existence of residues of Arsenic and DDT in the draining yard at dip sites was as follows (RAB 29-30): "Mr. Murphy then described the procedure for cleaning of sites up to 1977. There was an objection as to relevance, but I took the view that the question was admissible because it may indicate the likely composition of soil surrounding dip sites if evidence later emerged that the deceased had come into contact with those soils. So it proved, and I shall deal with that later. Mr. Murphy's evidence as to the procedure until 1977 was that they (the tick inspectors) would go to the dip and set up a pump and pump it out into the yard, indicating the dip as the part of the site that would be pumped out. He said it would be pumped out into the holding yard onto the ground, the surface of which simply consisted of dirt. He said, in response to a question by myself, that he saw this activity taking place between 1965 and 1977. A change occurred in the system after 1977, which was to take a fibreglass tank, place it in the draining pit and pump the solution into it. This change in fact did not occur until 1991, according to Mr. Murphy's answer to a question asked by me. Mr. Murphy confessed that he did not do the 'pumping out' work between 1977 and 1989, but said that when he returned to doing that sort of work in 1989, the system had by then changed and the procedure of pumping the waste material into a tanker (sic), as described above, had been implemented."

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43 The second passage which explains in some detail the procedure for cleaning out dip baths when Mr. Murphy and Mr. Allen worked together was as follows (RAB 30-32): "Mr. Murphy said that when he was working with Mr. Allen, the procedure for cleaning out the dip baths was to set up the tank in the draining pen so that the water would run back in through the hole into the dip. A sludge pump was then obtained and the solution was pumped out of the dip into a tank which had a capacity of approximately 3,000 litres, and then when the pump would not take any more solution out they would go in with a bucket on a rope and a shovel, and one of them would go underneath and under the childproofing [mesh] and one would work on top using a bucket and rope. The person underneath would put the solution into a bucket and the person on top would lift it up and throw it 'over the side' to the 'poison pit area' being the area described in the diagram as the 'scooping mound site'. He said that the material cleaned out of the bottom of the dip would come out as solid material like concrete. He said that once the solution was taken off the top, it being about 6 to 8 inches in depth, the solid material would be between 1 and 3 feet thick. The solid material he said was mud and hair. Controversy occurred at that point where (sic) the word 'lime' had been used by the witness. I indicated that my note did not so indicate, and a dotted line appears in the transcript at the point where the respondent's counsel Mr. Poulos said that the word 'lime' was used. I am not satisfied in these circumstances that it was used by the witness. The witness was then shown Exhibits O, P and R and he identified a build up of medicament on the site of the dip baths and on the walls. He said that the medication washed off as the cattle come through the cattle dip. Mr. Murphy then gave more specific evidence as to his participation in work with the deceased. He said that when the deceased started as a tick inspector in 1989, he and the deceased were instructed to carry out certain work in the Casino area, and in particular to clean out dips in that area by pumping them out. He said that during the 30 years he had been with the Department of Agriculture he had never cleaned out the same dip more than once, except for one that was leaking. He said that it took a day or two to clean such a dip out if it was really dirty, and a day if it was not. In particular, he said that when he and the deceased were doing the work, the deceased went down into the dip because he was 'a big strong young fella and I wasn't quite as big as what he was by a long way'. The work was done by somebody climbing down into the dip and removing the sludge and the harder material and somebody else staying on top, and according to Mr. Murphy's evidence, which I accept, it was the deceased who entered the dip. Apparently first of all the sludge was removed by using a bucket and then there was a hard packed material under that which was removed by using a pick, a mattock and a post hold spit. Once the first few inches of this material were removed, it was dry. Mr. Murphy noticed that as the material was dug up it was dusty and had a foul smell. Mr. Murphy also said that to gain access the pit for this purpose it was necessary to remove the childproof mesh referred to earlier in his evidence. To remove the mesh it was necessary to throw one section of it back up to enable the man going down to get into the dip. There was difficulty in doing this because the mesh was covered with the 'stuff' that was on the walls. The sections of mesh would be tight and there would be plenty of dust as they were removed. Mr. Murphy also mentioned that there was dust about the holding yard when cattle were in it, which made it difficult to breath (sic) on hot or windy days. Mr. Murphy said that the deceased would generally wear 'Wellica boots' (this may be a misprint for Wellington boots) when he was removing the sludge, and then when he got down to the solids he would generally put his ordinary boots on, and that otherwise he generally wore a shirt and shorts. I take the 'Wellica boots' (Wellington boots?) to be large rubber boots and the ordinary boots used by the deceased to be the ordinary type of leather work boots with or without laces commonly worn in agricultural and industrial occupations. A bucket and rope apparently was used to remove the solution from the dip bath and as the bucket was employed for this purpose the solution would cause splashing all over the place. Mr. Murphy said that Mr. Allen looked like 'a little kid playing in mud' when he had finished doing the work on the bottom of a dip bath that was being cleaned out. Mr. Murphy said that it was necessary to clean the dip bath 'right out', because if there were any cracks in it, they had to be chased and mended to stop the dip bath leaking. He said that to mend a crack 'you'd have to get the Kanga gun and cut it out with it, or a crowbar or a hammer and chisel' and that the deceased would generally be on the 'Kanga'd and that he, Mr. Murphy, would be on the chisel and a lot of dust was created on the bottom of the dips in this process. He said the dips were then patched with cement. It would render this judgment of unacceptable length if I traced in its entirely the evidence in chief of Mr. Murphy about cleaning and patching the dips. It is sufficient to say that when this process took place the deceased was exposed, in my view, on the evidence of Mr. Murphy which I accept, to large quantities of both wet and dry material which both adhered to his skin and were very likely inhaled by him, and this material consisted not only of substances which had been used in the dipping process immediately before the dip was cleaned, but also of material which had been deposited over the many years that the dip has been used. This was inevitable by reason of the manner in which the cleaning process took place, involving as it did the patching of leaks in the dip, which in turn necessitated the removal of dry material below the wet material which had been deposited during the immediately preceding use of the dip. Thus, in order to determine the chemical composition of the dry material, one would have to look in my view to evidence as to the substances used in the dip over many years, and not only to those which were employed in the dipping process immediately before the cleaning operation took place. I shall come to that question later."

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44 The next passage, which deals with other aspects of the work of cleaning and maintaining dip site was as follows (RAB 32-33): "Mr. Murphy also said that he and the deceased, during the period the deceased was working for the respondent department, also had to maintain dip sites in the Casino Area, which firstly involved digging out old rotting posts and putting new ones in, which in turn I involved digging a hole a foot in diameter and about 3 feet deep to remove the post. This created dust and a smell which was described by Mr. Murphy as 'not a real nice smell'. He was unable to identify it, he said, but it was 'a foul smell'. It seems to me to be an obvious inference that medicament used for dipping cattle over the years would accumulate around the posts surrounding the dip and cause them to rot, and that it was this material which caused the 'foul smell' upon which Mr. Murphy commented. It is, of course, impossible to determine from Mr. Murphy's evidence the precise source of the 'foul smell', but it seems to me an inescapable inference that on the probabilities the rotting process in the posts was contributed to by liquid material in the soil from the dip, and that therefore in the process of removing the posts with Mr. Murphy, however frequently that took place the deceased was exposed to whatever materials were in the medicament used for dipping cattle over many years at the various dip sites, in the form of residues in the soil surrounding the posts. Thus once again it is relevant to inquire as to the chemical composition of medicaments used in the dip sites over many years, not only in the years of the deceased's service. I will come to that question later. Mr. Murphy said that it was also necessary to clean out the drains from the drain pen. This involved cleaning the drains out with what was described as a 'pneumatic', presumably a pneumatic drill or hammer, and shovel. He said that both he and the deceased did this work, although the deceased would do a lot more than he did as 'he was bigger, stronger young fellow'. This too, it seems to me, would inevitably have exposed the deceased to whatever materials had built up in the drain pens and in particular in the actual drains thereof over the years that these had been used, not simply in the immediately preceding period during which the dip had been used during the period of employment of the deceased. Returning to the posts surrounding the drain pen, Mr. Murphy said significantly that those along the side of the bath and the drain pen would rot out a lot more frequently than the ones around the yard, and consequently would require more frequent replacement. This seems to me to confirm the inference I have already drawn that it was the liquid material used to dip the cattle which caused the posts to rot, and which on the probabilities accounted for the 'foul smell' described by Mr. Murphy when removing the posts. He commented that this varied from dip to dip and that he could not identify it precisely."

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45 The conclusions which Armitage CCJ drew from these aspects of Mr. Murphy's evidence, which conclusions are ultimately reflected in his Honour's conclusion on the whole of the evidence, were as follows (RAB 33-34): "It is appropriate to remark at this point that I regard the work in cleaning and maintaining the dips drains and fences as described above which was performed by the deceased as of much greater potential significance in this case than his actual work dipping cattle, because of the different composition of the tickicids (sic) used in the tip medicament some years before the deceased commenced employment with the respondent as compared to what would appear to be the more innocuous composition of these same tickicids (sic) during the deceased's employment with the department. In the view I have taken, as I shall reveal later, it is unlikely that the deceased's contraction of pancreatic carcinoma was contributed to significantly by the exposure he had to the tick medicaments used during his period of employment with the respondent in cattle dips, it is rather his exposure to more noxious substances used at an earlier time in the operations of the respondent that is in my view of critical significance in contributing to the onset of his pancreatic carcinoma. It is for that reason that Mr. Murphy's evidence and that of the deceased's other workmates as to the working conditions of the deceased and thus his likely exposure to medicaments used at earlier times in the cattle dips of the respondent becomes of critical significance and must therefore be carefully analysed. Nevertheless the evidence of Mr. Murphy as to current practice at dip sites at which he and Mr. Allen, the deceased, were employed, is of some significance although I shall not analyse it in detail because of the view I have formed that the substances currently used at the respondent's dip sites are unlikely to have been of significance in producing the deceased's pancreatic carcinoma. This evidence establishes that the process of dipping cattle, at least in the experience of Mr. Murphy at dip sties where he and the deceased were involved in the process, is a messy one, or at least it was during Mr. Murphy's period of employment alongside the deceased. The cattle entering the dip would create a splash, and they were of course dipped in large numbers. It was consequently inevitable that persons working at the dip sites and operating in the process of dipping cattle experienced some splashing of the dip medicament on their bodies. This evidence also establishes that during the period of Mr. Murphy's employment with the deceased, dip medicament would splash around the whole area of the dip and its surrounds. This to my mind, in the absence of any evidence indicating any change of system from earlier times except for the different chemical composition of the actual dip medicament, makes it overwhelmingly likely that this same splashing effect would have occurred during the time when different tickicides were used at dip sites became contaminated with these medicaments. This would appear to be corroborated, to some small extent at least, by the 'foul smell' Mr. Murphy described in the soil surrounding the posts adjacent to the dip sites."

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46 The material in the "Assumed Facts" relating to the pesticide concentrations in samples taken "from the site and adjacent to certain dip baths which are known to have been cleaned by Mr. Allen" is derived from a report (Exhibit "G" - Blue AB 435) prepared by Dr. D. McConchie in August 1995. After he had taken those samples from the scooping mound and the disposal pit at each of the Teazie Dip, the Cannibal Dip, the Reynolds Road Dip, the Common Dip and Petersens Dip, each of those samples was then analysed for the purpose of determining the concentrations of Arsenic, DDT, DDD, DDE, the concentrations for each of the latter three then being combined to provide a total concentration of organochlorines. Having described his methodology and recorded the analytical data obtained Dr. McConchie continued (Blue AB 438-439): " DISCUSSION Because the scooping mounds, and the drainage depressions near the mounds, are the areas of the dip site that are likely to have been exposed most directly and frequently to large quantities of the pesticides used in the dips, it is expected that residue concentrations at these sites will be higher than elsewhere in the dip yards; this expectation is confirmed by the data in Table 3 of the DIPMAC (1992) report. Furthermore, because the mound is elevated above the surrounding area, it is expected that the drainage of liquid from the mound to the adjacent depression will result in higher concentrations in soil samples from the depression than in samples from the mound itself; this expectation is confirmed by the data in Table 3 of this report. The data in Table 3 of this report also show that, at the dip sites examined, samples with particularly high arsenic contents (>500mg/kg) also have particularly high DDT contents. Of the five dip sites sampled in this study, Teazie Dip and Cannibal Dip (see Table 1 for locations) stand out as having notably high pesticide residue contents. In particular, the arsenic concentration in the depression at Teazie Dip (3,050mg/kg) is above the upper level of the range for all dips reported in Table 3 of the DIPMAC (1992) report and the DDT content of this soil is roughly twice the average value reported for disposal pit or scooping mound samples. The DDT concentration in the sample for the depression at Cannibal Dip is also higher than the average value reported for disposal pit or scooping mound samples (DIPMAC, 1992). Both organochlorine pesticide residue and arsenic concentrations in samples from the Reynolds Road Dip and The Common Dip (see Table 1 for locations) are among the lowest values found at cattle tick dip sites. At Petersens Dip, arsenic concentrations are clearly elevated above regional background values and above the 20 mg/kg investigation threshold, but they are well below average values for disposal pit or scooping mound samples (see DIPMAC, 1992). DDT concentrations at Petersens Dip are low, but curiously the DDD (a decomposition product of DDT) concentration in the sample from the scooping mound is much higher than would normally be expected to be associated with such a low DDT concentration; the high DDD value relative to the DDT concentration suggests that decomposition of the pesticide residues has been particularly significant at this site. The decomposition of the organochlorine pesticides indicated by the DDD/DDT ratio at Petersens Dip reflects the fact that these pesticides do decompose over time (the rate depends on many biogeochemical and climatic factors) and emphasises the point that organochlorine pesticide concentrations at all the sample sites would have been higher in the past than the values recorded in this study. Overall, the two dip sites examined that would pose the greatest risk to human health are Teazie Dip and Cannibal Dip and of the pesticide residues at these dip sites, the arsenic concentration at Teazie Dip would be of the greatest concern because arsenic is a known carcinogen (e.g. see DIPMAC, 1992)."

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47 The first witness to give evidence on the hearing, which hearing, as I have previously indicated, commenced in late February 1996, was Mrs. Allen. Mrs. Allen's evidence in chief was comparatively brief. At the outset she gave evidence in general terms of her marriage and the life which she and Mr. Allen had had together (see paras. 11-14 (above)). Having done so, she then gave some brief evidence as to Mr. Allen's personal habits - in particular, that he was a non-smoker and that he did not take alcohol - and of his general health which, seemingly, prior to 1992 was, on the whole, good despite occasional bouts of ill-health. Having done so, Mrs. Allen said that, after Mr. Allen had commenced to work with the Department, when he would return home his clothes were very very soiled, often with a muddy substance which had a very strong smell about it and that on many occasions his arms and legs appeared to have been caked in that muddy substance - having previously lived on farms Mrs. Allen identified the smell as that of the types of chemical which were used for dipping cattle. 48 According to Mrs. Allen, from about the beginning of 1992, Mr. Allen began to complain of headaches and tightness in the chest and, on occasions, would develop a rash around his legs and body - the headaches and tightness in the chest appear to have coincided with days on which Mr. Allen was engaged in dipping cattle (Black AB 7-8). As time went by, Mr. Allen's complaints became more frequent and the headaches and pains worse. In late September 1993, Mr. Allen complained of upper abdominal pain and nausea and a feeling of fullness after eating meals and consulted his general practitioner Dr. Chappell. However, although Dr. Chappell had various investigatory tests carried out, no specific abnormality was disclosed. Despite the continuing pain and discomfort which were becoming more and more severe, Mr. and Mrs. Allen and their children took a family holiday to New Zealand in November from which trip they appear to have returned in late December. 49 As Mr. Allen's pain continued he again consulted Dr. Chappell who, after having further tests carried out, referred Mr. Allen to a consultant gastroenterologist Dr. Hope for further assessment. Dr. Hope arranged for Mr. Allen to be admitted to Lismore Base Hospital where an abdominal CT scan was performed on 7 January 1994. That scan demonstrated enlargement of the spleen and an abnormal appearance of the pancreatic body and tail either due to pancreatic inflammation (pancreatitis) or pancreatic tumour. By the time Mr. Allen was referred to Dr. Hope, Mr. Allen's condition had progressed to the stage where the gastric pain tended to radiate toward the left shoulder and Mr. Allen had lost one and a half stone over the previous two months - these symptoms, so Professor Levi, who both provided reports (Exhibit "KK" - Blue AB 47, 552) and gave oral evidence on the hearing, was later to observe (Blue AB 50), were "relatively typical of that seen for carcinoma of the body and tail of the pancreas and the duration of time is consistent with the evolution of the disease prior to diagnosis". 50 Because the results of the further tests which Dr. Hope had arranged to be carried out were suggestive of a carcinoma of the pancreas, Dr. Hope arranged for a general surgeon, Dr. Buddee, to carry out a laparotomy for the purpose of exploring the pancreas and obtaining biopsy material and also for the purpose of determining whether, if the provisional diagnosis of a tumour were confirmed, resection was possible. That laparotomy was carried out on 24 January 1994 and established, first, that Mr. Allen was suffering from Pancreatitis and, second, that he had a well differentiated ductal adenocarcinoma of the pancreas. Dr. Buddee, having consulted with (inter alia) Dr. Strong, a gastroenterological surgeon at the Princess Alexandria Hospital in Brisbane, then considered that resection of the pancreatic mass was not feasible. 51 Mr. Allen was accordingly discharged to home on 1 February where he remained until his death on 8 May 1994. During that period of three months or thereabouts, Mr. Allen became very weak and, according to Dr. Chappell (Blue AB 56), "toward the end he could not support his weight unaided", "he became barely able to hold a cup of tea", "he retained some consciousness but visual perception was poor to the end" and "his voice became weak and was reduced to a whisper in April 1994". 52 The lay witnesses who, in addition to Mrs. Allen, gave evidence in support of the claim made in the Application for Determination were Mr. Murphy, Mr. Draper and Mr. McClenan, the substance of whose evidence can be ascertained from what I have earlier written (see paras. 35-38 (above)) and thus need not be repeated here. 53 The experts who both provided reports and gave oral evidence in support of the claims made in the Application for Determination were Professor Stewart, a research scientist, Professor Levi, to whom I have earlier referred, a specialist oncologist, Associate Professor Winder, a toxicologist and Dr. McCullagh, an immunologist, the object of the tender of Dr. McCullagh's evidence, as I understand it having been to establish that Mr. Allen was immunosupressed as a result of his exposure to DDT and thus contracted pancreatic carcinoma in a shorter period that the Garabrant article had suggested. In the result, Armitage CCJ was not prepared to accept Dr. McCullagh's thesis (RAB 78) and, that being so, I limit my record of the evidence of the experts who gave evidence in support of the claim to that of Professor Stewart, Professor Levi and Associate Professor Winder. 54 The first of the expert witnesses to give evidence in support of the claim made by Mrs. Allen was Professor Stewart, the Director of the Children's Cancer Research Institute at the Sydney Childrens Hospital at Randwick and a Professor in the School of Paediatrics at the University of New South Wales. Professor Stewart holds the degrees of Bachelor of Science and Master of Science from the University of New South Wales and Doctor of Philosophy from the Middlesex Hospital Medical School within the University of London, his thesis being entitled "Effect of Inhibitors of Nucleic Acid and Protein Synthesis on Nitrosimine Carcinogenesis". 55 The Childrens Leukaemia and Cancer Research Centre is a "Major Research Centre" of the University of New South Wales. The Centre's research director is responsible for the definition, progress and integration of laboratory research by a team of eight senior investigators and the associated technical assistants, graduate students and clerical staff. The Centre's research activity is integrated with that of the staff of the Department of Haematology/Oncology, Prince of Wales Childrens Hospital. 56 In addition to his position at the University of New South Wales, Professor Stewart has also acted as a member of consultative committees convened by such Authorities as the International Agency for Research on Cancer (IARC), the National Health and Medical Research Council (NHMRC), the Australian Cancer Society (ACS), the New South Wales State Cancer Council (NSWCC), the Clinical Oncological Society of Australia (COSA) and the National Occupational Health and Safety Commission (Worksafe). 57 Despite Professor Stewart's qualifications, on the hearing before Armitage CCJ, objection was taken to the tender of Professor Stewart's report and to his giving evidence upon the ground he was not appropriately qualified, an objection which his Honour overruled. 58 In his report (Exhibit "JJ" - Blue AB 532 et seq), in a part entitled "DDT as a Cause of Cancer in Humans", Professor Stewart wrote (inter alia) as follows (Blue AB 536-538): "Despite the various studies which have been conducted, and some suggestive data, clear evidence that DDT causes cancer is humans was not recorded until 1992. Assessing the previously available studies of cancer in humans associated with exposure to DDT, the International Agency for Research on Cancer (IARC) concluded, in 1990, that the evidence fell short of an association which is categorised as 'limited evidence of carcinogenicity in humans'. Rather the epidemiological data for DDT were appraised by the Agency as 'inadequate' to establish carcinogenicity. Evaluations of carcinogenicity data by IARC, which involve a specially convened international panel of experts, constitute the most authoritative assessments available. In ranking human and experimental carcinogenicity data which is not wholly negative (ie. includes at least some suggestion of cancer causation), the Agency distinguishes between 'sufficient' and 'limited' evidence. 'Sufficient' evidence is indicative of definitive findings: 'limited' evidence is indicative of definitive findings: 'limited' evidence falls short of this standard. In circumstances of less than 'limited' evidence, the data are said to be 'inadequate' for evaluation of carcinogenicity. Once evaluations of the available 'human' and 'experimental' data are determined, the findings are combined in determining the carcinogenic hazard which the agent in question poses to humans. There are four categories: Group 1 - chemicals or occupational environments definitively established as causing cancer in humans (eg tobacco smoke, astestos (sic)); Group 2A - chemicals or environments which probably cause cancer in humans; Group 2B - possibly cause cancer in humans and Group 3 - chemicals or environments for which data are not adequate to establish causation of cancer in humans. Since the 1990 IARC review of the 'human' data regarding the possible carcinogenicity of DDT, certain relevant findings have been published. The most important of these is an investigation prompted by a cohort mortality study among 5,886 chemical manufacturing workers which was completed in 1987 and which showed increased mortality due to pancreatic cancer. Twenty eight cases of pancreatic cancer and 112 matched controls were then subject to further study. DDT was associated with pancreatic cancer, the risk ratio for 'ever exposed' compared with 'never exposed' being 4.8 (Garabrant DH, Held J, Langholz B, Peters JM & Mack TM: DDT and related compounds and risk of pancreatic cancer. J Natl Cancer Inst, 84: 764-771, 1992). Among subjects who had a mean exposure to DDT for approximately 4 years, the risk was 7.4 times that among subjects with no exposure. The duration of exposure for all industrial chemicals included in this study was 2 years or more. Two DDT derivatives, Ethylan and DDD, were additionally associated with pancreatic cancer. Smoking was identified as an independent risk factor, but controlling for smoking (and other potential confounders) did not appreciably alter the risks seen for DDT, DDE or Ethylan. A second report concerning the human carcinogenicity of DDT has involved monitoring the level of DDT breakdown products (metabolites) in the blood stream of breast cancer patients and matched controls. Mean levels of the major metabolite of DDT were statistically significantly higher in the breast cancer patients. These reports do not definitively establish that DDT causes cancer in humans. However, it is likely that IARC evaluation of the epidemiology data as 'inadequate' would be revised upwards to at least the 'limited' category when the compound is again considered. ……… Overall evaluation of carcinogenicity data for DDT Taking the epidemiological and experimental data together, the IARC considered that DDT is a 'possible' cause of cancer in humans (Group 2B). Epidemiological data since published would have likely resulted in (at least) Group 2A classification: chemicals considered a 'probable' cause of cancer in humans."

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60 Professor Stewart concluded his report as follows (Blue AB 551): " CONCLUSION It was noted at the outset that evidence of carcinogenicity is to be taken with evidence of exposure in assessing the likelihood of an individual's cancer being caused by particular agents. The exposure of the deceased to chemicals used in, and accumulating around, cattle dips has been discussed extensively in other reports. Such reports specify a range of pesticides whose cancer-causing potential (in humans) is largely unknown. Arsenic-containing compounds and DDT are the only implicated agents for which a substantive body of carcinogenicity data exist. Arsenic and its compounds cause cancer in humans: studies involving insecticide exposure, smelting and contaminated water are consistent in implicating skin cancer, lung cancer and, more recently, bladder, kidney and liver cancer. Pancreatic cancer has been implicated in directly one study and inferentially in others. On the basis of experimental data, DDT is strongly suspected of causing cancer in humans. The strongest evidence that it does cause cancer in humans involves an association with pancreatic cancer. Since both DDT and arsenic-containing compounds have been independently implicated as causing pancreatic cancer, the notion of these compounds acting synergistically is a reasonable conclusion in general terms, and is obviously relevant to the present case. Few environmental factors have been established as contributing to increased risk of pancreatic cancer. First amongst these is cigarette smoke - which is irrelevant to the present case. There appears to be no basis to attribute the deceased's disease to alcohol drinking or any other dietary factor. In view of all considerations in this Report, and noting the content of Dr. Winder's report and other information concerning the deceased's occupational history, I conclude that it is reasonable to attribute his malignancy to the combined effect of arsenic-containing compounds and DDT: chemicals to which Mr. Allen was exposed in the course of his employment as a stock inspector."

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62 Having considered Professor Stewart's report and his oral evidence - and, in particular, various matters which had been raised with him in the course of cross-examination - Armitage CCJ concluded (RAB 58-59): "At the end of the day (or several) Professor Stewart never resiled from his essential hypothesis, which was that the Garabrant study, notwithstanding its limitations and the criticisms that may be made of it, supports in this case a probable association between this man's exposure to DDT, in the manner described above in my summary of the evidence of Messrs. Murphy, Draper and McClenan and of the report of Dr. McConchie, and his contraction of pancreatic cancer. What must be remembered, I think, in relation to this Court, is that as I have already said, I am not called upon to determine this question as a matter of scientific certainty. To be trite, the test is whether in this case it is proved on the balance of probabilities. In an endeavour to resolve that question, one may look at the whole of the evidence and not just that of the scientist or other expert expounding such a connection, and what I, as a 'mind uninstructed in pathology' to quote again Sheller JA in MLA Holdings ((1996) 13 NSWCCR 224, 231), find in this case is the evidence of three lay witnesses who are eloquent as to the dusty atmosphere in which the work of cattle dipping and repair and maintenance of tick dip yards was conducted by the deceased and others, involving as it did stock inspection and dipping and the digging up of soil and the replacement of posts and other fencing, which dust, it is fair to infer, was impregnated with substances which had been used over many years at the sites concerned. Then there is the evidence of Dr. McConchie in report form as to the high DDT concentrations and to a lesser extent arsenic concentrations at many of these sites in the very areas where the deceased had to work, at least on my interpretation of the evidence. Professor Stewart provides what is to my mind a plausible and rational hypothesis based to an extent, though not entirely, on an article in an international journal of high repute suggesting a strong association between pancreatic cancer and exposure to DDT. The evidence, it is fair to say, in relation to arsenic is much less strong, being based on one study which is very small of vineyard workers in Moselle Valley in Germany. Professor Stewart was cross-examined also to suggest that the deceased had pancreatitis and that this was alone sufficient to account for his development of pancreatic cancer. In reply Professor Stewart suggested that there is experimental data to suggest that pancreatitis itself may interact with DDT exposure to be a promoter of pancreatic cancer. It was the respondent's case (see above) that the applicant had pancreatitis. He probably did. The fact nevertheless is that Professor Stewart never departed from his essential hypothesis in relation to exposure to DDT in particular, which was that the deceased's pancreatic carcinoma was caused or (more likely) promoted by his DDT exposure in the respondent's employ, and exposure to DDT in this case is amply proved, in my view, so far as the deceased is concerned. Subject to other medical evidence, which I must consider in due course, I therefore accept Professor Stewart's opinion that there is in this case a probable connection between the deceased's exposure to DDT in the manner described and in the course of his employment with the respondent and his contraction of pancreatic cancer. That is, as I have said, a rational hypothesis and one strongly suggested by the lay evidence in relation to exposure and the report of Professor McConchie, but in any event it is, on a proper construction of Professor Stewart's evidence without more, a probable association in my view." 63 The second expert witness called in support of the application was Professor Levi, a Professor of Medicine at the University of Sydney and Director of the Department of Clinical Oncology at the Royal North Shore Hospital at St. Leonards. Professor Levi had, at the time he gave evidence on the hearing before Armitage CCJ, been a practising medical oncologist for 27 years and had been involved in treating a wide variety of malignancies, including cancer of the pancreas and other gastrointestinal cancers, as well as having been actively involved over that period of 27 years in both clinical and laboratory cancer research emphasising gastrointestinal and urinary cancers. 64 Professor Levi prepared two reports, the first dated 31 August 1995 (Exhibit "KK" (part) - Blue AB 47) and the second dated 27 June 1996 (Exhibit "KK" (part) - Blue AB 552), the terms of which reports, as Armitage CCJ pointed out (RAB 60, 62) were of themselves insufficient to support an association between Mr. Allen's exposure to Arsenic and DDT and his contraction of pancreatic cancer on the balance of probabilities, an observation which he based on the Judgment of Hope A-JA in Sydney County Council v. Furner (1991) 7 NSWCCR 210, 214. 65 In his first report, Professor Levi, after having referred (inter alia) to the material contained in Dr. McConchie's report, wrote (inter alia) (Blue AB 51): "With regards to the question as to whether exposure to these chemicals increased potential risk for the development of Mr. Allen's carcinoma of the pancreas. Evidence is available that ingestion of arsenic is associated with an increased risk of malignancy including skin cancers, carcinoma of the bladder, kidney, lung and liver (ref. Bates MN et al Arsenic Ingestion and Internal Cancers: A Review. American Journal of Epidemiology 135: 462-476, 1992). Other reports I have reviewed which support this association between arsenic and specific internal cancers and therefore raises the question of the potential carcinogenicity in relation to pancreatic cancer and arsenic exposure. It is appropriate however to indicate that no available report that I have reviewed specifically demonstrates an increased risk of pancreatic carcinoma with arsenic ingestion. Nevertheless, as arsenic has been demonstrated to be a proven human carcinogen and considering the very heavy concentrations of arsenic to which Mr. Allen was likely exposed, the potential for this exposure to have an influence of his ultimate development of carcinoma of the pancreas cannot be entirely excluded . With regards to DDT exposure and the potential development of Mr. Allen's carcinoma of the pancreas, several reports I have reviewed are of particular pertinence. A study by Garabrant DH et al, DDT and Relation (sic) Compounds and Risk of Pancreatic Cancer. Journal of National Cancer Institute 84: 761-771, 1992 is a well conducted nested case-control study of 28 verified cases of pancreatic carcinoma and 112 matched controls. The study was well controlled for potential bias and confounding influences including smoking and demonstrated that exposure to DDT and relevant metabolites resulted in a relative risk for the development of carcinoma of the pancreas of 4.8 times normal and this risk was associated with a dose response relationship, i.e. the longer and greater the exposure the greater the risk. It is appropriate however to indicate that in view of the relatively small number of pancreatic carcinoma cases studied, the confidence intervals for this study are wide (1.3-17.6) which diminishes at least to some extent the strength of the association between DDT exposure and the potential development of carcinoma of the pancreas."

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(in each case, my emphasis). 66 In his later report, Professor Levi wrote (inter alia) (Blue AB 552-554): "With regards to the question of latency and the potential of Mr. Allen's carcinoma of the pancreas to have initiated and therefore arise within a 4½ year period from the beginning of February 1989 when he commenced employment with the NSW Dept of Agriculture as a stock inspector, until October 1993 when he first developed symptoms indicative of his carcinoma of the pancreas, I make the following points. Latency is the period of time from initiation of the carcinogenic process until with the ultimate clinical development of a specific cancer, in this case pancreatic cancer. This duration can be varied in time and not uncommonly has been documented to be up to 25-30 years. Nevertheless, individual cancers vary and the precise duration of time from initiation of carcinogenesis to actual clinical appearance of the cancer in any one person cannot be precisely defined. Accordingly therefore in Mr. Allen's case, while it is appropriate to indicate that a latency of period of between 4-5 years would be on the shorter side of consideration, it is still biologically plausible and indeed it is well documented that such a duration of time would be sufficient for the entire process of initiation of the carcinogenic process to clinical development to occur. I am therefore prepared to state that this duration of time of employment until diagnosis of pancreatic cancer in Mr. Allen's case does not preclude its association with carcinogenic processes that may have occurred from exposure during employment. ……… Finally in other reports it has been suggested that the study by Garabrant DH et al, DDT and Related Compounds and Risk of Pancreatic Cancer. Journal of the National Cancer Institute 84: 761-771, 1992 can be discounted on the basis that compounding variables were not adequately taken into account. I would certainly dispute this as the study was in fact well conducted and there is clear indication that known confounding variables such as smoking, diet and possible occupation are all taken into account in the conduct of this study. Accordingly therefore this study remains a sound one. The principal limitation of this study however is the fact that the number of cases of pancreatic cancer is relatively small i.e. 28 verified cases of pancreatic carcinoma compared with 112 matched controls. This results in wide confidence limits to the demonstrated risk of pancreatic cancer (1.3-17.6) which diminishes to some extent the strength of the association between DDT exposure and the potential development of carcinoma of the pancreas. Accordingly further studies would need to be conducted to verify this apparent association and I understand this is presently being undertaken."

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68 Having recorded in his Judgment the nature of the cross-examination of Professor Levi and some of the answers given by him in the course of cross-examination, Armitage CCJ continued (RAB 65-66): "What I think these questions and answers mean, although paraphrase is dangerous, is that one cannot as a matter of scientific certainty say that this man's pancreatic cancer was promoted in the presence of chronic pancreatitis by DDT or arsenic exposure. However these exchanges, and for that matter the other exchanges in cross-examination, do not to my mind derogate from the answer given in chief and quoted above, which answer caused Mr. Poulos to point to the alleged unfairness of the respondent's position in view of Professor Levi's strengthening of view as compared with his reports. That answer therefore to my mind remains Professor Levi's opinion. Thus there is support for the proposition advanced by the applicant on the balance of probabilities from Professor Levi as well, although it must be carefully noted that it is only on the basis of the second paragraph of the second leg of the definition of 'injury' in s 4 of the Act, namely aggravation, exacerbation, acceleration or deterioration of a disease (pancreatic carcinoma), to which exacerbation or acceleration in the employment is a contributing factor. ……… Applying that learning to this case, it is not necessary that the deceased's exposure to DDT or arsenic be the only contributing factor or even a substantial one to either his contraction of pancreatic cancer, or to the aggravation, acceleration, exacerbation or deterioration of that disease, within each of the sub-paragraphs of the second leg of the definition of injury above mentioned. Professor Levi's support for the applicant's case, if I accept it, is in this context therefore sufficient to make out the elements of the second paragraph of the above definition, because he supports the proposition on the probabilities, as is shown by his use of the expression 'likely' on two occasions which I have italicised in his answer in his evidence in chief as quoted above, that the deceased's pancreatic cancer was promoted in the presence of chronic pancreatitis by his DDT and arsenic exposure, particularly the former. Professor Levi's support for that proposition appears to be (as it must in my view) primarily based on the Garabrant article, which undoubtedly does not quite go that far, but it is clear from Professor Levi's quoted answer above that his view is based not only on that article but on his clinical experience. This seems to me to be a perfectly legitimate way in which to proceed from the point of view of a medical, as distinct from a purely scientific expert. For the reasons expressed above in relation to Professor Stewart's opinion and also because of the additional factor that Professor Levi is a medical expert and does have twenty seven years' clinical experience in treating carcinomas of the type under consideration, I am inclined to accept Professor Levi's opinion, as expressed in the answer at the end of his evidence in chief which I have quoted above; that is to say, I am impressed as a lay matter by the coincidences between the deceased's development of pancreatic cancer and his performance of very dusty work dipping cattle and replacing posts and the like and dipping cattle in and around dip baths in the course of his employment with the respondent, that dust to which he was exposed being, on the probabilities in my view, created in part by soils contaminated by DDT and arsenic residues (see Dr. McConchie's report) and that to me makes Professor Levi's opinion, as expressed in the last answer in his evidence in chief (see above), more cogent, although I hasten to add this does not in my view amount to a conversion of 'possible' to 'probable' in the manner of Forst's case and the authorities which follow it because Professor's Levi's opinion appears in the end to be offered on the balance of probabilities rather than as a possibility. This is as I have said is (sic) made clear by the preceding question which asks for his opinion on the balance of probabilities, and by his use of the word 'likely' twice in his answer from which as I have said, in my view he never resiled from significantly in cross-examination."

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69 The third expert witness called to give evidence in support of the application was Associate Professor Winder, who held the degrees of Bachelor of Arts in Biology and Psychology from the Open University in the United Kingdom, Master of Science in Neurophysiology from the City of London Polytechnic and Doctor of Philosophy in Toxicology and Pathology from the Royal Post Graduate Medical School in the University of London and who was at the time of the hearing before Armitage CCJ an Associate Professor in the Department of Safety Science at the University of New South Wales. Among the various appointments which he had earlier held, Associate Professor Winder had been principal toxicologist in the Commonwealth Department of Health in Canberra, Visiting Research Fellow at the Australian National University, Director and Chief Toxicologist in the Chemical Section, Worksafe Australia and had held various teaching positions including one as Senior Lecturer in Occupational Health in the Department of Occupational Health at the University of Sydney. Since the mid-1980s Associate Professor Winder had been reading, researching, teaching and providing advice on cancer and occupational cancer. 70 In a report (Exhibit "F" - Blue AB 496) which he provided in December 1995, Professor Winder, under the title "The Toxicology of DDT" wrote (inter alia) as follows (Blue AB 503): "DDT is an industrial chemical which has had widespread dispersion in the environment. DDT has a low solubility in water, but a high solubility in fats. This means that DDT is preferentially stored in the body in the lipid phase, and mainly in fats. DDT also has a low vapour pressure, suggesting that in the occupational environment, skin contact is a much more important route of exposure than by inhalation. DDT is associated with a range of toxic effects in humans, including liver toxicity. Toxicological studies in mice show that administration of DDT produces lymphomas and malignant liver and lung cancers. Toxicological studies in rats show that administration of DDT produces malignant liver cancers. The potential of DDT to cause cancer in experimental animals is unquestionable. There are differences in the metabolism of DDT between animals and humans, for example enterohepatic circulation of the metabolites of DDT has been shown in rats but not humans. Once absorbed into the body, DDT is sequestered in the body in fatty tissues, and because of its high fat solubility, is mainly metabolised in the liver, where it can be excreted in the bile (which is itself a product of liver metabolism). The bile duct enters the small intestine adjacent to the duct from the pancreas. Here exists a credible mechanism for the access of DDT (and its metabolites) to the pancreas. Therefore, it can be hypothesised that DDT exposure may be associated with diseases in the pancreas. The evidence of cancer in people exposed to DDT remains equivocal. Some studies have not shown evidence of carcinogenicity of DDT in humans, while others report associations with soft tissue sarcomas, lymphomas, leukaemias, pancreatic cancer and breast cancer. Evidence continues to accumulate. Evidence for a specific mechanism for the carcinogenic effect of DDT is also available. DDT appears to inhibit the enzymatic processes involved in the replication of DNA. This suggests an effect on the development of genetic material. This suggests that DDT would be considered a non-genotoxic carcinogen. This means that DDT probably does not initiate cancer, but is rather a chemical which enhances or promotes the growth of pre-malignant lesions. This suggests that DDT is a chemical which can exacerbate existing non-life threatening tumours, or convert them into malignant cancers."

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(A footnote to the second last paragraph of this passage identifies as the study relevant to an association between DDT and pancreatic cancer as being the Garabrant article.) 71 Under the title "The Toxicology of Arsenic" Professor Winder wrote (inter alia) as follows (Blue AB 503-504): "Whereas DDT is a chemical which is found in fatty materials, Arsenic is a water soluble chemical. Arsenic is an element found in natural materials and therefore will be found at low levels in the environment. However, it is the manufacture of Arsenic compounds and the use of Arsenic as a pesticide which has increased environmental levels of Arsenic. Arsenic gets into the body through all routes of exposure. It is well absorbed from the gastrointestinal tract. It undergoes some changes in the body, and is mostly excreted in urine. Excretion can be quite rapid, with a half life in the body of about a day. It should be further noted that Arsenic is a cumulative poison. ……… There are a range of toxic effects from Arsenic exposure, including skin problems, liver effects, cardiac arrhythmia's, upper respiratory tract symptoms, neuropathy, gastrointestinal, cardiovascular and blood forming effects. Some of these effects would be dependent on exposures which can only be encountered during occupational settings. Arsenic also causes cancer of the skin, lung and liver, mainly in occupationally exposed workers. A dose response relationship has been described for lung cancer in arsenic workers. Non-worker populations living near point sources to air may also have increases in lung cancer, although the studies are not definitive. However, Arsenic is unquestionably a human carcinogen. Evidence is available for the mechanism of carcinogenicity of Arsenic. Arsenic does not appear to directly produce cancers in animals and is extremely weak in its ability to directly induce gene mutations (that is, act as a genotoxicant). However, it does cause gene amplification and may act as a tumour promoter. As well as a range of non-specific enzyme effects, Arsenic appears to reduce DNA repair mechanisms. As with DDT, Arsenic appears to be a chemical which acts indirectly with other agents to enhance specific genotoxic effects that lead to cancer. Arsenic is known to synergistically (multiplicatively) increase the rates of lung cancer in arsenic smelter workers who smoke. The possibility exists that synergistic interactions of Arsenic with other carcinogenic or potentially carcinogenic chemicals may occur."

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72 Under a heading "Epidemiological Studies of Pancreatic Cancer" Professor Winder wrote (inter alia) as follows (Blue AB 504-506: "The pancreas is an organ of both the gastrointestinal and endocrine systems. The endocrine pancreas is responsible for release of hormones into the blood which regulate carbohydrate metabolism, and the exocrine pancreas is responsible for the production of the digestive enzymes in pancreatic juice, which is secreted through the pancreatic duct to the duodenum. ……… A range of risk factors have been investigated which may affect the incidence of pancreatic cancer in humans, including: · cigarette smoking, which is the most agreed documented association of pancreatic cancer, with a relative risk of 2-6:1; · diet (particularly consumption of fats); · coffee as a beverage; · alcohol; · a number of medical conditions, including chronic pancreatitis, diabetes mellitus, gastric resection and pernicious anaemia; · occupation. Occupational groups where an association with cancer of the pancreas have been reported include: seafarers, chemists, coke oven workers, sawmill workers, exposure to metals, paper manufacturing, petrochemical manufacture, painting products, 'detergent, floor cleaning agents or polish', in municipal waste disposal, floor (sic) millers, farmers and in chemical manufacturing. One of these articles should be elaborated. The 1992 article of Garabrant and others was a cohort mortality study of 5886 chemical manufacturing workers. A decision to exclude subjects with less than ten years latency is arbitrary and is not demonstrated to affect the significance of the statistical analysis. After controlling for a range of factors, including tobacco, alcohol and coffee consumption, exposure to DDT was associated with increased death from pancreatic cancer. Among workers who had a mean exposure to DDT of 47 months, the risk was 7.4 times that amount control subjects with no exposure. The authors concluded that exposure to DDT was associated with pancreatic cancer, that this association was not explained by lifestyle factors, and the risk increased with both duration of exposure and time since first exposure. Additionally, exposure to two DDT derivatives (ethylan and DDD) also increased the risk by 5 times and 4.3 times, respectively. This paper provides direct proof that a clear association exists between exposure to DDT at work and subsequent development of cancer of the pancreas.

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73 Professor Winder recorded his conclusions as follows (Blue AB 511-512): "Mr. David Leslie Allen died from pancreatic cancer of an occupational cause. Supportive evidence for this conclusion comes from: · Mr. Allen was exposed to high levels of chemicals during the time of his employment as a stock inspector with NSW Agriculture; · the control of exposure and availability of safe systems of work for workers to do their job safety were all but absent where Mr. Allen worked; · some of the chemicals to which Mr. Allen was exposed are established or suspected cancer causing chemicals; · new evidence is available that suggests that one of these chemicals, DDT, is now known to cause pancreatic cancer in workers; · pancreatic cancer is a disease of old age, and is rare in individuals of Mr. Allen's age (43); · a report of an abdominal ultrasound on Mr. Allen in 1991 suggests an absence of cancer in that area at that time, whereas a report of an abdominal ultrasound on Mr. Allen in 1994 suggests a mass in the pancreas; · Mr. Allen's cancer has been described by a pathologist as a well differentiated cancer, indicating it grew aggressively, and suggesting it grew over a short period of time. There are three possible conclusions that can be drawn from this evidence: 1. On the balance of probabilities, the possibility of developing a cancer of a short latency (less than four years) occurring in a worker exposed to excessive levels of chemicals known to cause cancer (such as arsenic, DDT and possibly other as yet unidentified materials in a range of products) in the course of employment must be considered a possibility . 2. On the balance of probabilities, the possibility of a developing a cancer of a short latency occurring in a worker exposed to excessive levels of chemicals known to cause cancer in the course of employment, especially if those chemicals act on the process of development of cancer at different stages, where a synergistic interaction can occur, must be considered a distinct possibility . 3. It is possible that Mr. Allen had a pre-existing tumour in his pancreas before he started working as a stock inspector. It is this tumour which rapidly grew from after 1991 to the point that it was life threatening, eventually killing him. Because such cancers tend to occur in older individuals, it can be concluded that something else forced this cancer to grow and become life threatening in a 43 year old man. Mr. Allen's excessive exposure to chemicals during the course of his employment must be considered a highly probable promoter of this cancer (especially as both DDT and arsenic are considered tumour promoters). In such cases, it should also be considered that the pre-existing cancer, which was not initially life threatening, could have remained so for many, many years, perhaps never developing to the stage where it became life threatening (that is, Mr. Allen could have died of something other than pancreatic cancer in old age). There, the aggravation, acceleration, exacerbation or deterioration of pre-existing disease in this case could be considered entirely arising out of employment. On the balance of probabilities, as such, the possibility of a developing a cancer of a short latency occurring in a worker exposed to excessive levels of chemicals known to cause cancer in the course of employment, especially in those chemicals act to exacerbate and make malignant an already existing non-life threatening tumour, must be considered highly probable. However, there is no doubt that there is a distinct link between Mr. David Leslie Allen's exposure to chemicals at work, and his subsequent death from pancreatic cancer."

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84 The next expert witness called on behalf of the Defendant was Professor Kaldor, a Professor of Epidemiology at the National Centre in HIV Epidemiology and Clinical Research in Sydney, his principal qualification being a Doctorate in Statistical Procedures (Biostatistics) obtained from the University of California at Berkeley. In his report (Exhibit "!2" - Blue AB 688) Professor Kaldor, after recording his qualifications and experience, wrote (inter alia) as follows (Blue AB 689-690): " Assessment of cancer causation Before considering the specific case of Mr. Allen, I would like to make some general comments about assessing disease causation, and about cancer causation in particular. Disease causation can only be understood in terms of probabilities. There is virtually no disease-causing agent that will produce disease in every exposed individual, and conversely, there is virtually no disease that is always due to a specific causal agent. This probabilistic framework leads to a fundamental distinction in the notion of a factor being ' a cause' of a disease, versus the factor being ' the cause'. A factor is defined as ' a cause' of a disease if exposure to the factor increases the probability that the disease will occur. While some factors greatly increase the probability that the disease will occur, and others increase the probability only slightly, both types of factor can be considered to be 'causes' in this sense of the word. For example, a number of studies have shown that heavy long-term cigarette smoking increases a person's probability of sustaining lung cancer by about 20-fold compared to a lifetime non-smoker, and increases the probability of pancreatic cancer by a factor of 2 to 3. Nevertheless, cigarette smoking may be said to be a cause of both lung and pancreatic cancer. In contrast, it is never possible to state with 100% certainty that a specified agent is the cause of a given case of cancer, because it is possible for the cancer to occur even in the absence of exposure to the agent. In particular, the co-occurrence in the same person of the cancer and a history of exposure to the agent provides no evidence of causality in itself. It is, however, possible to estimate the probability that the agent was the cause of the disease. Once such a probability is estimated using the best available scientific information, it becomes a matter of subjective judgement as to what level of probability is to be considered high enough to act as if the agent was indeed the cause. For example, if the best available scientific information produced an estimate of 90% for the probability that the particular case of cancer was caused by exposure to the agent, most people would consider it reasonable to attribute the cancer to the agent. But what if the estimate was 50%, 40% or 20%? An estimate of less than 50%, in particular, means that it is more likely that the cancer was caused by something other than the agent in question. Estimation of the probability that a particular case of cancer was due to a specified agent is based directly on the increase in risk associated with exposure to the agent. If an agent increased the risk of cancer occurrence by a factor of 2, then the probability would be 50% that the cancer was caused by the agent in a person who had a history of exposure to it. Returning to the example of cigarette smoking, if a person developed lung cancer and had been a long-term heavy smoker, it could be stated that there was 95% probability that the lung cancer was due to smoking (a probability of 19/20 to be precise). On the other hand, if a person developed pancreatic cancer and had been a long-term heavy smoker, it could only be stated that there was a 50-67% probability that the cancer was due to smoking. The probability that a carcinogenic agent will actually induce cancer generally increases as exposure levels increase. Therefore the determination of whether an agent was the cause of a particular case of cancer in a person requires knowledge not only of the fact of exposure, but crucially, the level of exposure . For example, a person who only smoked one or two cigarettes per week may have an increased risk of cancer of a few percent, but if a lung tumour developed, there would be a very small probability that it was actually caused by the smoking. It would be much more likely due to other, perhaps unknown factors. Other factors that have a strong influence on the probability of cancer developing after exposure to an agent are the duration of exposure , and the latency (or time elapsed) since exposure. As with exposure level, the duration and latency of exposure to an agent can therefore have a very substantial influence on the probability that a case of cancer in a person was due to that agent."

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85 Later in his report, Professor Kaldor wrote (inter alia) as follows (Blue AB 691-693): " Evidence for causation in the case of Mr. Allen Following the steps outlined above, the first consideration is whether or not any of the agents in question are capable of causing pancreatic cancer. The specific agents referred to in evidence have been arsenic, DDT and cypermethrine. I will discuss each in turn. Arsenic has been investigated in a number of large-scale epidemiological studies. There has been a consistent finding of substantially increased rates of lung cancer, primarily in people exposed through copper smelting, and skin cancer in people exposed through medicinal solutions, leading to the classification of arsenic as a human carcinogen by the International Agency for Research on Cancer. Several of the studies that implicated arsenic as a lung or skin carcinogen have also looked at its effect o the risk of other forms of cancer. There has been no consistent finding in relation to any other form of cancer. DDT has been well established as a carcinogen in rodents for a number of years, and for public health reasons it has long been treated as if it were a human carcinogen, despite the lack of human studies until relatively recently. The study by Garabrant et al (1992), which has been extensively discussed by other witnesses, was the first to provide the suggestion of an association between exposure to DDT and cancer of the pancreas. This study, by well-recognised epidemiologists in the United States, used an appropriate design to attempt to identify whether any specific exposures were associated with pancreatic cancer in chemical workers. The main findings were associations between pancreatic cancer and exposure to DDT, DDD and ethylan, which are related compounds. The increase in risk was only assessed in workers whose latency of exposure (ie time since first exposure) was at least ten years. In assessing the report of this study, I have two concerns: · How specific was the method used for assessing DDT exposure? It seems that a worker was assessed as exposed if he worked in a building where DDT was recalled as being 'present', and if he had a job title that was considered by his co-workers to entail exposure. · How well were other potential confounding factors adjusted for? When the sample size of a study is small, and there are other potential risk factors present, it is difficult to ensure that the observed relationships are not due to confounding. The study also gives no basis for assessing the levels of DDT exposure that may have been present in the workers. Another relevant study has been published subsequently. In Michigan, where the factory studied by Garabrant et al was located, a larger case-control study was undertaken by Fryzek et al (1997). After interviewing 66 people with pancreatic cancer and 131 controls, the authors found that cases were significantly more likely than controls to have been exposed to insecticides in the period 1945-1955, and that there was a particularly significant association with ethylan exposure. The most frequently recorded organochlorine was DDT, which was associated with a 2-fold, non-significant increase in risk. The concerns expressed about the Garabrant study apply equally to this study, and there is a further, and potentially more substantial problem with the study: Only 30% of people approached as potential controls agreed to participate, leading to a large potential for bias. Case-control studies with under 60-70% participation are generally viewed as suspect. Apart from the two Michigan studies, there have been a number of studies of cancer risk in association with pesticide exposure in general, that may or may not have included DDT. To my knowledge, these studies have not found significant increases in the risk of pancreatic cancer. The evidence that exposure to DDT causes cancer of the pancreas in humans is certainly now stronger than it was when the International Agency for Research on Cancer last evaluated DDT in 1991. My opinion on the epidemiological evidence for a causal association is that it nevertheless remains limited, for the reasons outlined above. There is no perfect epidemiological study, and in general causality is not likely to be inferred from one or two studies. ……… There is now some evidence, albeit limited in quality and quantity, that DDT causes cancer of the pancreas in humans. If DDT is indeed a pancreas carcinogen, the next stop in assessing how likely it is to have caused Mr. Allen's pancreatic cancer is an estimation of the dose levels to which he was exposed, and the duration of his exposure. These estimates, and knowledge of the latency period would be used to calculate the probability that Mr. Allen's pancreatic cancer occurring within 4 years of his commencing employment was due to DDT. Although I do not have access to all of the information that I would ideally require for making this calculation, two aspects of the available information are highly pertinent: · Neither of the Michigan studies estimated any increase in pancreas cancer risk prior to ten years after first exposure. Indeed, even strong, well established chemical carcinogens do not generally produce measurable increases in cancer rates in the first 5 to 10 years following first exposure. Mr. Allen developed pancreatic cancer within 4 years of exposure, a latency period that would be extremely unusual in its brevity for any chemical carcinogen. · The exposure levels involved in the manufacture of a product have been generally held to be substantially higher than environmental exposure levels, particularly if they relate to time periods before there was an awareness of occupational hygiene and the prevention of cancer. It is therefore reasonable to assume that Mr. Allen's DDT exposure levels were substantially lower than the exposure levels of the Michigan factory workers, whose employment was largely in the 1950s and 1960s. Supposing that DDT is a pancreatic carcinogen in humans, and taking into account these two points, I consider it highly likely that the best estimate of the increased risk of pancreatic cancer associated with DDT exposure in the first four years of Mr. Allen's employment beginning in 1989 would be well below 2-fold, and would therefore translate into an estimate of the probability that Mr. Allen's pancreatic cancer was caused by DDT of well under 50%."

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86 In his Judgment, Armitage CCJ commented on Professor Kaldor's report as follows (RAB91-92): "It is not enough I think, in the case of Professor Kaldor simply to observe, as I did with Dr. Spence, that Professor Levi's expertise in the appropriate area is greater and that therefore I prefer Professor Levi's evidence as to the Garabrant study being well conducted to the evidence of Professor Kaldor criticising it. The fact is that Professor Kaldor is an epidemiologist of some eminence. The most I think that can be concluded about the Garabrant study in fact of the criticisms of Professor Kaldor is that it is the only one we have in relation to an association between pancreatic cancer and DDT exposure, and it is for me to determine whether the views on it expressed by Professor Stewart, and (particularly) Professor Levi should prevail over those of Professor Kaldor. Professor Kaldor does not consider the Garabrant study to be sufficient scientific proof as to a connection between DDT and pancreatic cancer and I readily agree that this appears to be the current and prevalent view in scientific circles on the whole of the expert evidence in this case. The question is whether, as I have reiterated on a number of occasions, the application has proved on the balance of probabilities upon the whole of the evidence, both scientific and lay, that the deceased's employment was a contributing factor either to the contraction of his pancreatic cancer or to the aggravation, acceleration, exacerbation or deterioration of it within s4 of the Act. Professor Kaldor's evidence really just seems to identify the limitations of the Garabrant study and to explain why it is not accepted in scientific circles generally as definitive. That does not, as a result of the legal approach I have taken (see the authorities I have referred to above) conclude the matter for me, and at the end of the day Professor Kaldor's views as to the unreliability of the Garabrant study do not derogate from the conclusions I have already formed as to the acceptability of the evidence of Professor Stewart and (particularly) Professor Levi, based in part (though not entirely) on that study, particularly in the case of Professor Levi, who relies on his clinical experience in the appropriate expert area."

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87 The fourth expert witness called on behalf of the Department was Dr. Garcia, a Clinical Senior Lecturer in the Faculty of Medicine, University of Sydney and Senior Staff Specialist in Immunology and Allergy in the Department of Immunology at Royal Prince Alfred Hospital, his evidence, as I have understood it, being primarily directed to countering the suggestion which had been made by Dr. McCullagh that Mr. Allen was immunosuppressed as the result of his exposure to DDT thus explaining the short latency period in the onset of the tumour, as compared to the time frame of his exposure to DDT in the employment of the Department. However, as Armitage CCJ, as I have earlier (see para. 46 (above)) indicated, was not prepared to accept Dr. McCullagh's thesis, I do not - nor did Armitage CCJ - think it necessary to deal in any great detail with Dr. Garcia's evidence. However, it is useful to add a reference to a comment made by Armitage CCJ at the conclusion of his discussion of Dr. Garcia's evidence which comment was as follows (RAB 95-96): "This illustrates the precise point I have made already, which was that the respondent's witnesses, perfectly legitimately in view of the nature of their disciplines, have approached the matter on the basis that a proposition is or is not proved as a matter of scientific certainty, with the possible exception of Professor Kaldor (see above). That is not the test at law. Insofar, as I have said, as Professor Stewart and particularly Professor Levi have offered an explanation expressed in their evidence on the balance of probabilities for the deceased's contraction of pancreatic carcinoma in his exposure to DDT, and to a much lesser degree to arsenic in the course of his employment with the respondent, by way of direct cause or, more likely, promotion of an existing pancreatic tumour by way of aggravation, acceleration, exacerbation or deterioration (probably acceleration), I find their explanation of this phenomenon more rational and acceptable than that offered by the respondent's experts, which is effectively no explanation at all. That is precisely the situation where, medical science offering no conclusion on the probabilities one way of the other, a lay inference upon the whole of the evidence may be permissible (see Forst's case and those following it, above) although whether it is to be made in the particular case is another matter. In this case I do not strictly have to engage in this exercise, as I have said, because Professor Stewart and particularly Professor Levi offer a conclusion on the balance of probabilities for me to accept or reject, but I have been assisted in accepting it by the lay evidence in the way that I have described above." 88 The fifth expert witness called on behalf of the Department was Professor Tattersall, Professor of Cancer Medicine in the University of Sydney, Clinical Academic at the Royal Prince Alfred Hospital and Honorary Consultant Oncologist at the Westmead Hospital. At the commencement of his evidence there was tendered his report (Exhibit "15" - Blue AB 653) and the article by Fryzek et al - the "others" included D. H. Garabrant - entitled "A Case-Control Study of Self-Reported Exposures to Pesticides and Pancreas Cancer in South Eastern Michigan" (Exhibit 16 - Blue AB 480), which had been referred to by Professor Kaldor in his report (see para. 77 (above)). 89 In his report, Professor Tattersall wrote (inter alia) as follows (Blue AB 658-660): "3. THE TECHNICAL INVESTIGATION 3.01 The causes of pancreatic cancer and pancreatitis, and the relationship between pancreatitis and pancreatic cancer. Mr. Allen had histological evidence of (chronic) pancreatitis (see surgical pathology report 24 January 1994) and in the few gland structures contained in the biopsy specimens, there was 'some cytological atypia', and 'a few architecturally and cytologically abnormal glands consistent with an adenocarcinoma'. This pathology report and the subsequent sequence of events leading to Mr. Allen's death in May 1994 confirmed that there was a pancreatic cancer, within the inflamed tissues of the tail of the pancreas. ……… There are few positive associations of pancreatic cancer with occupation, but a recent cohort mortality study among 5,886 chemical manufacturing workers showed increased mortality due to pancreatic cancer. A nested case-control study of pancreatic cancer among these chemical manufacturing workers was reported in 1992 (Garabrant et al, JNCI, 84 :764-771 - see Appendix 2). DDT was associated with pancreatic cancer (risk ration for ever exposed >10 years before death compared with never exposed = 4.8 [95% confidence interval 1.3-17.6]). Two DDT derivatives, Ethylan and DDD were additionally associated with pancreatic cancer with a risk ration of 5.0 and 4.3 respectively for those exposed >10 years before death compared with never exposed. There is no evidence that exposure 20 year exposure were associated with greater risk of pancreatic cancer than exposure for 10 years. The authors state: 'these results may indicate that DDT can cause pancreatic cancer in humans under circumstances of heavy and prolonged exposure'. The authors comment that more than 500 specific factors were examined in association with pancreatic cancer, and 'it is likely that some of the associations have been observed by chance. Adjustment using the modified Bonferroni procedures (Simes RJ. Biometrika, 73 :751-754, 1986) leads to none of the associations being statistically significant. ……… Arsenic exposure is a risk factor for lung and skin cancer, but no consistent associations with other cancer types have been reported though liver, bladder and kidney cancers have been found in excess in several studies. There is only one report of pancreatic cancer being increased in association with exposure to arsenic trioxide. Twenty-five years after insecticides containing arsenic trioxide were banned in German vineyards, a post mortem series demonstrated a significantly increased risk of lung cancer and an increased risk of some other cancers including pancreatic cancer (Luchtrath T.J. Cancer Res.& Clin.Oncol., 105 :173-182, 1983). 3.03 The plausibility that exposure to chemicals between 1989 and 1993 caused or contributed to the development or speed of progression of pancreatic cancer. Limited epidemiologic evidence of an association between DDT and arsenic exposure is notable for the long lead time between history of possible exposure and diagnosis of pancreatic cancer. As already mentioned, Garabrant et al (JNCI, 84 :764-771, 1992, SEE Appendix 2) reported no excess of pancreatic cancer in persons followed up for less than 10 years after DDT exposure . Similarly, the only report of pancreatic cancer after arsenic exposure reported an excess of pancreatic cancer deaths more than 25 years after the arsenic containing insecticide was banned. The lead times are in no ways surprising for an epithelial cancer after carcinogenic challenge. The follow-up of individuals irradiated at the Hiroshima bomb report no excess of this sort of cancer for more than 15 years after the bomb blast."

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92 The transcript record of the proceedings before Armitage CCJ records the following at the commencement of Professor Tattersall's evidence in chief (Black AB 859-860): "Q. Professor you have had access when you came to court today to an article which is authored by Fryzek and Garabrand (sic) and others which is published in the International Journal of Cancer in 1997. A. That is correct. Q. That is Exhibit 16. In reading that article did it occur to you that it may be of some assistance to any of the propositions that you have advanced in your report. A. I don't think it in any way changes the views I express in my report, if anything, I think it adds to the strength of the view that the lead time between the possible exposure during his employment by the Department of Agriculture and his development of pancreatic cancer is fancifully short, so short that it is fanciful to attribute a relationship between the exposures in that period and the cancer which he developed. That is because this case control study, although not perfect, nonetheless reports only a significant increased risk of pancreatic cancer in the case who were exposed on self report (sic) to DDT between 1945 and 1955 and this case summary I think is in 1995 to 1996 so basically what it is saying is that in that time frame there was a significant association between self reported DDT exposure but in all other time frames there was no significant association." 93 In light of Professor Tattersall's comment, it is necessary, in my view, to record part of the article - the abstract at its commencement, and its conclusions - and the manner in which, in his Judgment, Armitage CCJ dealt with the article, and Professor Tattersall's comment. 94 The abstract at the commencement of the article was as follows (Blue AB 480): "A case-control study of pancreas cancer in residents aged 30-79 years, of 18 counties in southeastern Michigan was conducted to investigate the risks of exposure to DDT and related materials in the general population. Sixty-six people with cytologically diagnosed pancreas cancer were identified using seven participating hospitals in metropolitan Detroit and Ann Arbor. One-hundred and thirty-one controls were frequency-matched to the cases on age, sex, ethicity (sic) and country of residence by random-digit dialling. All study participants were administered a questionnaire to assess life-time exposure to pesticides from both environmental and occupational sources, family history of cancer, past medical history, smoking history and demographic information. A statistically increased risk was found for self-reported exposure to ethylan … . Increased odds ratios were observed for self reported exposures to chloropropylate and DDT, as well as for the summary group of organochloride pesticides which included all these materials, though these associations were not significant."

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while the relevant part of the conclusions was as follows (Blue AB 485): "Our study has many strengths. This is one of the few studies based on direct interviews of cases of pancreas cancer. Due to poor survival, most studies of pancreas cancer have relied on surrogate interviews in which accurate exposure information is difficult to obtain. Our study was further strengthened by its strict case definition. All cases were required to have a psychological diagnosis of pancreas cancer. Pathology reports were reviewed by the study pathologist to ensure that diagnostic inclusion criteria were met. Finally, the study design incorporated important measures to reduce recall bias. Interviewer training, a structured interview and the inclusion of non-existent pesticides not only minimised recall bias but also allowed us to measure its potential impact. A number of organochlorine pesticides are persistent environmental contaminants with long biological half-lives. They are readily absorbed into the blood from the gastro-intestinal tract, through the skin or by inhalation of vapour or dust and distributed to tissues with a high fat content, where an equilibrium is established … The exact nature of the biological mechanism by which certain organochlorines may be involved in the etiology of pancreas cancer is not clear. It is possible that some of the organochlorine compounds we studied may accumulate in the pancreas as it is a lipid-rich organ and its ductal epithelial cells may have prolonged exposure even in the absence of continuous external exposure. There is also evidence that DDT and DDE are excreted in the bile … Thus, direct exposure of the pancreatic ductal epithelium to these materials is possible. The evidence provided by these analyses demonstrates that some organochlorines may be human carcinogens. Even though DDT was banned in the United States in 1972, DDT is still manufactured throughout the world and DDT-related compounds are still used in the United States. More than fifty years after its synthesis, the long-term health effects of DDT are unknown. Future studies are needed to clarify the associations between DDT-related compounds and pancreas cancer found in our study. One approach may be to investigate the association between DDT-related compounds and the pancreas cancer in different populations, especially those populations where pancreas cancer rates are high (eg African-Americans). Furthermore, the issue of latency and dose need to be more carefully evaluated to fully understand the relationship of pancreas cancer risk for different time periods and levels of exposure."

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96 At the conclusion of his discussion of Professor Tattersall's evidence, Armitage CCJ wrote as follows (RAB 100-101): "In cross-examination it is enough to say, I think, that Professor Tattersall did not deviate significantly from the view expressed in his report. The only possible concession is at page 35 of the transcript of 28 May 1998, that being the day on which Professor Tattersall gave evidence, when he conceded with attractive modesty that he would not currently nominate himself as an expert in gastrointestinal tract cancer. The theme of Professor Tattersall's evidence, as is the case of the respondent's other expert witnesses whose evidence I have already discussed, was that because the Garabrant study did not show a positive association between pancreatic cancer and DDT exposure with a latency period between exposure and diagnosis of the cancer of less than 10 years, it is unlikely that the deceased died of pancreatic cancer caused by his exposure to DDT in the circumstances of this case, the postulated latency period here, of course, being considerably less than 10 years. The problem I have with that proposition is that it inevitably does not address the central question raised by the law which I have attempted to summarise above, which is whether on the whole of the evidence, both medical and lay, the applicant has proved her case on the balance of probabilities. What I would have to do to accept the view the respondent's witnesses advance is to discount the evidence of Professors Stewart and (particularly) Levi that there is a probable association in this case between the deceased's exposure to DDT (and to a lesser extent arsenic) and his contraction of pancreatic cancer, on the basis that when one goes behind those opinions to the scientific bases on which they are based, those bases are defective. The trouble with that view is that on the one side there are learned experts who put together such papers as there are on the subject, principally the Garabrant study, with their own clinical experience, and express the view that there is a probable association, and on the other side there are equally well qualified experts who deny a probable association based essentially ono the same date, which they interpret essentially the same way. In this case it seems more reasonable and more in accord with the whole of the evidence, including the lay evidence, as I have said, to prefer the opinions of those experts who are able to assign a definite cause to the deceased's pancreatic cancer to the views of those experts who are unable to do so, particularly when the cause assigned by the applicant's experts seems sensible and rational and in accordance with the lay evidence, as I have said. For that reason, while accepting Professor Tattersall's evidence insofar as it establishes that there is no scientific proof that DDT causes pancreatic cancer, I do not think it is fatal to the applicant's case."

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97 The final expert called on behalf of the Department was Mr. Pickford an industrial hygienist who had provided a number of reports (Exhibit "17" - Blue AB 700) setting out "estimates of possible exposure of Mr. David Allen" to DDT and Arsenic "whilst he was undertaking work at cattle dips for the NSW Department of Agriculture for several years commencing in 1989", in which reports Mr. Pickford expressed the view - based on his estimates of Mr. Allen's exposure - that Mr. Allen's exposure to DDT and Arsenic was, by reference to standards established by such bodies as the World Health Organisation, the Unites States Environmental Protection Agency and the Australian National Occupational Health and Safety Commission, insignificant. It seems clear enough that the object sought to be obtained by the tender of Mr. Pickford's evidence as to demonstrate that, even if DDT and Arsenic were to be regarded was capable of causing, or contributing to, the initiation or development of pancreatic cancer, being exposed to either DDT or Arsenic at the levels estimated by Mr. Pickford would not result in the initiation or development of pancreatic cancer. 98 After referring to some of the evidence given by Mr. Pickford in the course of his cross-examination (Black AB 898-899), Armitage CCJ dealt with Mr. Pickford's evidence in the following way (RAB 102-103): "These and the other concessions made by Mr. Pickford at pp 25-26 of the abovementioned transcript satisfy me that Mr. Pickford's calculations make a number of unproven assumptions and are therefore not reliable. They may be the best guide we have, because they are the only guide in a scientific sense, to the deceased's DDT exposure, but they do not prove on the probabilities, to my mind, that it was insignificant as Mr. Pickford states. The onus question is a very difficult one in this case where the only evidence, apart from Mr. Pickford's testimony, as to the deceased's arsenic and particularly DDT exposure is anecdotal and comes only from the lay witnesses Messrs. Murphy, Draper and McClenan. Even accepting those witnesses as completely truthful (as I do within the limits of their recollection) they cannot prove how much soil adhered to the deceased's skin, which itself is only an incomplete measure of the amount of soil he inhaled which is the preferred method of promotion of pancreatic cancer from DDT and to a lesser extent arsenic exposure according to the evidence of Professor's Stewart and Levi, as I understand it, rather than dermal absorption. Doing the best I can however, on the evidence of the lay witnesses abovementioned, it seems to me proper to conclude that the deceased's work environment was very dusty, both because of the dust stirred up by digging up posts, when of course the soil was not wet, as it was on occasions, and because of the dust stirred up by cattle moving around in the cattle yards and by the activity of cleaning out the solid material from the bottom of the dips after the liquid material had been removed. This dust, for reasons I have already set out, was likely to have been impregnated, on the probabilities, not only with the tickicides currently used at the dips, but with those previously used over many years, including (as is not denied and indeed admitted by the respondent) DDT and arsenic. The exact level of such impregnation or contamination it is impossible to ascertain, and the same applies to the concentration of dust in the air which the deceased breathed. The best I can do, I think, in relation to the latter is to conclude that such concentration was relatively heavy, despite Mr. Pickford's conclusion to the contrary, which I regard as unreliable for the reasons set out above."

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99 Since it is the subject of the first ground of appeal taken on behalf of the Defendant, it is convenient that, before I record the conclusion to which Armitage CCJ came as to the effect of the totality of the evidence, I pause here to record what his Honour wrote as to the "correct legal basis on which (he) should approach the scientific evidence". It was as follows (RAB 46-48): " (i) Legal approach It is necessary before considering the scientific evidence to set out what I apprehend is the correct legal basis on which I should approach it, for that approach informs all I shall subsequently say about it. Firstly, causation in law is different from causation in science: March v. V & M H Stramare Pty. Ltd (1991) 171 CLR 506 per Mason CJ at 509; whether a causal connection exists is to be determined by applying commonsense to the facts of the case: March per Mason CJ at 515 and Deane J at 522, Stapley v. Gypsum Mines Ltd (1953) AC 663 per Lord Reid at 681, and Migge v. Wormald Bros Industries Ltd (1972) 2 NSWLR 29 per Mason JA (as he then was) at 44F, and see generally Kooragang Cement Pty. Limited v. Bates (1994) 35 NSWLR 452. As Lord Shaw of Dumferline said in Leyland Shipping Co. Ltd. v. Norwich Union Fire Insurance Society Ltd (1918) AC 330 at 362-3 (cited in another context by Sheller JA in HIH Casualty and General Insurance Ltd. v. Waterwell Shipping Inc (1998) 43 NSWLR 601 at 608): 'Causes are spoken of as if they were distinct from one another as beads in a row or links in a chain, but - if this metaphysical topic has to be referred to - it is not wholly so. The chain of causation is a handy expression, but the figure is inadequate. Causation is not a chain but a net. At each point influences, forces, events precedent and simultaneous meet; and the radiation from each point extends indefinitely.' I found this passage of considerable utility in understanding the phrase 'contributing factor' although it occurs in a different context, that of proximate cause in shipping law. A robust and pragmatic approach should be taken to the issue of causation; see Wilsher v. Essex Area Health Authority (1998) AC 1074 per Lord Bridge at 1090. The fact that medical opinions are not in accordance with the consensus of scientific opinion does not preclude their acceptance, as a matter of law. Commissioner for Government Transport v. Adamcic (1961) 106 CLR 292, cited by Powell JA at page 23 of his judgment in Zizzati Pty Ltd v. Ademovski (unreported Court of Appeal, 18/12/95), a case which illustrates the proposition that proof on the balance of probabilities on the whole of the evidence, medical and lay, is what is required in cases like the present one. It is not however sufficient for an applicant to demonstrate a possible connection between a particular work event and an injury, and the work must make a material contribution to the injury. St. George Club Ltd v. Hines (1961) 35 ALJR 106 AT 107 (Dixon CJ, Kitto, Taylor, Menzies and Windeyer JJ) following Bonnington Castings Ltd. v. Wardlaw (1956) AC 613. This is underlined by Sydney County Council v. Furner (1991) 7 NSWCCR 210 per Hope A-JA at 214 in which the trial judge's error was to conclude that evidence that a particular cause could not be excluded amounted to proof that such cause was operative on the balance of probabilities. However, that case was one where the trial judge erroneously came to that conclusion purely on medical evidence stating that a connection between work events and the contraction of a particular condition (in that case carcinoma as at present) was possible and could not be excluded. It is nevertheless open in law where the medical evidence only states a possible connection to form an inference on the probabilities that such a connection exists upon the whole of the evidence, both medical and lay in an appropriate case, according to the well known doctrine in Adelaide Stevedoring Company Ltd v Forst (1940) 64 CLR 538 per Rich A-CJ at 563-4. The same principle is affirmed in Australian Iron and Steel v. Connel (1959) 102 CLR 522, Tubemakers of Australia Ltd v. Fernandes (1976) 10 ALR 303 and EMI (Australia) Ltd v. Bess (1970) 2 NSWR 238 per Herron CJ at 242. In that case his Honour so concluded following what was said in Ramsay v. Watson (1961) 108 CLR 642 at 645 by Dixon CJ and McTiernan, Kitto, Taylor and Windeyer JJ where they said: 'That some medical witness should go into the box and say only that in his opinion something is more probable than not does not conclude the case. A qualified medical practitioner may, as an expert, express his opinion as to the nature and cause, or probable cause, of an ailment. But it is for the jury to weigh and determine the probability. In so doing they may be assisted by the medical evidence. But they are not simply to transfer their task to the witnesses. They must ask themselves 'are we on the whole of the evidence satisfied on a balance of probabilities of the fact?' In this case his Honour in his summing up instructed the jury that this was their task; and no ground is shown for impugning their conclusion. (Emphasis added)' Placing myself in the position of the jury referred to in that passage, that is the approach I have taken in this case. More recently I observe in conclusion that the dictum of Rich A-CJ in Forst (supra) was applied by the Court of Appeal in M L A Holdings Pty. Ltd v. Smith (1996) 13 NSWCCR 224 per Sheller JA at 231 where his Honour referred to the conclusion ' which the sequence of events would naturally inspire in the mind of any commonsense person uninstructed in pathology ', adapting the language of Rich A-CJ in Forst (supra). Handley and Beazley JJA concurred with Sheller JA in that case, and by implication of course with this approach, since it was part of the ratio decidendi of the decision. What emerges from these authorities I think is that this is not a trial of which scientific theory is correct in relation to the carcinogenicity of DDT or arsenic, or for that matter any other substance to which the deceased was allegedly exposed. That is a debate which must be conducted in scientific rather than in legal circles upon the basis of scientific proof. The law does not call for that standard of proof, but rather proof on the balance of probabilities on the whole of the evidence, both scientific and lay, and as the decision of the High Court in Ramsay v. Watson (supra) demonstrates, a tribunal of fact must not abdicate its task to the scientific and/or medical experts, albeit being guided by their evidence alongside the lay evidence in the case. Further, a conclusion naturally suggesting itself to a mind uninstructed in pathology (to paraphrase Sheller JA in MLA Holdings ), ie my own in this case, may legitimately be drawn from the lay as well as the scientific evidence, even though the scientific or other expert evidence alone may not form a sufficient basis for it on the balance of probabilities. That is a very different and contrasting situation from that which prevails in scientific circles in relation to proof of a hypothesis, but it is nevertheless the correct legal basis upon which to approach the causation questions in this case. The general approach I have taken above also gains support from what was said by Fitzgerald A-JA at pp53-4 in his judgment (with which Meagher and Beazley JJA agreed in this respect) in EM Baldwin & Son Pty Ltd v. Plane and Jsekarb Pty. Ltd. an unreported decision of the Court of Appeal handed down today."

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100 His Honour recorded his conclusion in the following way (RAB 103-104): " Conclusion In considering the evidence I have not referred to every exhibit or every part of the transcript of this lengthy trial, although I hope it goes without saying that I have studied the evidence carefully in its entirety. I have concluded, for reasons already set out, that the applicant has proved her case on the balance of probabilities in that it is more likely than not that her husband died of pancreatic cancer, which was promoted, ie aggravated and, more probably, accelerated or exacerbated, by his exposure to DDT and to a lesser extent to arsenic in the course of his employment as a stock inspector with the respondent. The greater part of that exposure was probably in the work of maintaining tick dip sites rather than inspecting cattle, but the inspection of cattle also involved the stirring up of dust in the tick dip yards, which was probably impregnated with DDT and arsenic as well as with the current tickicides used at the yards. In both of these ways the deceased was in a position to inhale, and probably did inhale, large quantities of dust impregnated with DDT and arsenic and thus, in my view, his pancreatic cancer was promoted, ie aggravated or accelerated or exacerbated. It is also reasonable to say, I think, that it deteriorated as a result and that his employment involving his exposure to DDT and arsenic in this way was a contributing factor to those effects. I prefer this explanation to the contention that the deceased's employment was a contributing factor to his contraction of pancreatic carcinoma, partly because of the relatively short latency period involved, and partly because the evidence of Professor Levi in particular in relation to promotion seems to me to be preferable to the view that the cancer was actually initiated by DDT or arsenic exposure. The promotion hypothesis better takes into account both the short latency period as I have said, and the fact that there were probably many other non-work related contributing factors to both the initiation and the promotion of the deceased's pancreatic cancer. That this is so is not fatal to the applicant's case (see particularly Treloar's case cited above) although it may well have been were this case affected by s.9A recently inserted in the Act, as it is not (see above))."

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This being so, it is appropriate here to consider which, if any, of the grounds of appeal sought to be taken by the Department are open to it. 105 In Azzopardi v. Tasman UEB Industries Ltd. (1985) 4 NSWLR 139 in which the Applicant/Appellant sought to challenge on appeal the conclusion of Burke J, sitting in the Workers Compensation Commission, that he (the Applicant/Appellant) had failed to establish that he had injured his knee on a periodic journey, Glass JA, after referring to passages in the judgments of Jordan CJ in McPhee v. S Bennett Limited (1935) 52 WN 8, 9 of Dixon J (as he then was) in Clarke v. Flanagan (1934) 52 CLR 416, 428 of Dixon J in Shepherd v. Felt and Textiles of Australia Limited (1931) 45 CLR 359, 379 and of Jordan CJ in DeGioia v. Darling Island Stevedoring & Lighterage Co. Limited (1941) 42 SR 1, 5 said at supra at 155-157: "It is clear from these extracts that numerous pejorative expressions in common usage possess a single meaning and are interchangeable. To say of a finding that it is perverse, that it is contrary to the overwhelming weight of the evidence, that it is against the evidence and the weight of the evidence, that it ignores the probative force of the evidence which is all the one way or that no reasonable person could have made it is to say the same thing in different ways. Upon proof that the finding of a jury is vitiated in this way, it will be set aside because it is wrong in fact. Since the Act does not allow this court to correct errors of fact, any argument that the finding of a Workers Compensation Commission judge is vitiated in the same way discloses no error of law and will not constitute a valid ground of appeal. It is also pointless to submit that the reasoning by which the court arrived at a finding of fact was demonstrably unsound as this would not amount to an error of law: R. v. District Court of the Metropolitan District Court Holden at Sydney: Ex parte White (1966) 116 CLR 644 at 654. A finding of fact in the Commission may nevertheless reveal an error of law where it appears that the trial judge has misdirected himself i.e. has defined otherwise than in accordance with law the question of fact which he has to answer. A possibility of this kind exists with ultimate findings of fact but not with respect to primary findings of fact such as whether the applicant suffered injury on a particular date. Further an ultimate finding of fact, even in the absence of a misdirection, may reveal error of law if the primary facts found are necessarily within or outside a statutory description and a contrary decision has been made, Hope v. Bathurst City Council (1980) 144 CLR 1 at 10; Australian Gaslight Co v. Valuer General (1940) 40 SR (NSW) 126 at 138; 57 WN 53 at 55. The decision here assailed is not of that character. To the legally uninitiated there is a spurious validity in a submission that it was not open to the judge to find that the applicant was not injured since there was evidence to that effect. If a respondent employer can argue a no evidence point why cannot the applicant worker? The answer is, of course, that alleged insufficiency of evidence to prove a fact always raises a question of law but alleged sufficiency of evidence to the point of conclusiveness cannot, since it assumes that the evidence has been accepted. The party not bearing the onus puts an argument, which assumes against himself that the evidence has been accepted, but submits that it is not capable of establishing the fact. The party saddled with the onus on the other hand cannot assume in his favour that the evidence is or ought to be accepted since this trenches upon the liberty of the tribunal of fact to accept or reject any evidence. Finally, the burden of proof to which the applicant is subjected cannot be masked by the use of double negatives. A purported ground of appeal which submits that there was no evidence that or it was not open to find that the applicant was not injured constitutes a futile attempt to convert a question of fact into a question of law by inverting the onus of proof. It has been suggested that since judges unlike juries are required to give reasons a perversity of result will or may suggest an error in some stage of the reasoning process and the perversity will then rise to the level of an error of law. It is important, I believe, to remember that whether an error is one of fact or law is determined by legal theory and the theory is the same whether the Tribunal be divided or undivided. Errors may be committed by a Workers Compensation judge at any one of three points viz determining the facts by way of primary findings and inferences, directing himself as to the law and applying the law to the facts found. At the first stage the determination of facts by a reasoning process marred though it be by patent error, illogicality or perversity will, as has been said, never be vulnerable to attack as an error or law by an applicant for compensation. At the second stage, any error made will by definition be an error or law. At the third stage when the law correctly stated is applied to the facts found in order to produce a conclusion error may intrude again. An erroneous conclusion that facts properly determined fail to satisfy a statutory test, for example, injury arising out of the cause of employment, substantial interruption to journey, or failure to provide suitable employment will ordinarily be an erroneous conclusion of fact. It is only in marginal cases that the statutory test is satisfied or not satisfied as a matter of law, because no other application is reasonably open: Hope v. Bathurst City Council (at 10); Australian Gaslight Company v. Valuer General (at 138; 55). Accordingly this Court will not entertain unexplained perversity of result as a ground for intervention although it will correct perverse or unreasonable applications of law to the facts found."

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but a submission that evidence, which is capable in law of supporting a finding of fact, ought to have been accepted, or ought to have been rejected, does not involve a question of law. 107 So far as the first of these conclusions is concerned if the submission is that the evidence, even if accepted, is incapable in law of supporting a finding of the relevant fact, that clearly raises a question of law (Azzopardi v. Tasman UEB Industries Limited supra). In a case in which the opinion of an expert witness has been tendered, the question whether the history upon which that opinion has been based has, or the hypothetical facts which the witness has been asked to assume for the purpose of giving his opinion have, been sufficiently established will raise a question of law although, if that question be answered in the affirmative, the weight to be given to the opinion is but a question of fact (Paric v. John Holland Constructions Pty. Limited [1984] 2 NSWLR 505, 509-510 per Samuels JA) 108 So far as the second conclusion is concerned, it is sufficient to record the following passage from the Judgment of Jordan CJ in McPhee v. S Bennett Limited supra to which I have earlier referred: "The question whether there is any evidence of a particular fact is also a question of law: Sittingbourne Urban District Council v. Lipton Ltd [1931] 1 KB 539 at 544 and Mersey Docks & Harbour Board v. West Derby Assessment Committee [1932] 1KB 40 at 110, 111. But if there is evidence of the fact, the question whether that evidence ought to be accepted in whole or in part, or ought to be accepted as sufficient to establish the fact, is itself a question of fact and not a question of law, unless, of course, there is some law which provides that the particular evidence, when given, is to be taken to establish the fact. If a tribunal which has exclusive jurisdiction to determine facts decides that it does not accept the evidence tendered as establishing a particular fact, its decision, apart from the exceptional case which I have just mentioned, is conclusive. In that case the party upon whom the burden of proving the fact lies must fail. There is no rule of law that such a tribunal must believe the evidence, because it is all one way. It can accept all, or some, or none of it."

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(see also Commissioner for Government Transport v. Adamcik (1961) 106 CLR 292, 303 per Menzies J 308-309 per Windeyer J 110 In the light of what I have written above, it is clear that ground 6 in the Amended Notice of Appeal, which was filed on behalf of the Department, does not raise a question of law, a fact which appears to have been recognised by counsel appearing on the hearing of the appeal for the Department as the Written Submissions which were provided by them contain no submissions directed to that ground of appeal. 111 No such simple conclusion is open in respect of the other grounds of appeal, the true nature of which can only be ascertained by reference to the submissions which were advanced in support of them. 112 In their Written Submissions, counsel for the Department sought to deal together with grounds 1, 2, 3 and 7. The burden of those submissions may be ascertained from the following paragraphs in them: "20. As to Ground 1 the Appellant submits that the onus was upon the Applicant in the court below to prove that it was more probable than not that on the evidence Mr. Allen's exposure exceeded the levels which were set as the appropriate standard by the medical experts. There being no evidence of sufficient probative value to meet or exceed this standard his Honour was not entitled to make an award in favour of the Applicant. 21. It is the Appellant's principal assertion that there was no probative evidence upon which his Honour could conclude that Mr. Allen was relevantly injured. The Respondent set out to prove and was required to demonstrate that Mr. Allen was exposed to dangerous chemicals in a sufficiently heavy concentration over a sufficiently long period of time in order for him to have suffered an injury within the meaning of s4 of the WCA Act. That is, whether or not the work performed by him constituted an injury in that it caused or alternatively aggravated, accelerated, exacerbated or lead (sic) to the deterioration of his pancreatic cancer. 22. The Appellant submits that his Honour misdirected himself as to the issues that he had to decide in the matter and that he failed to consider submissions that were put to him and to have regard to evidence that was before him which prompted and required another conclusion: Mifsud v. Campbell [1991] 21 NSWLR 725. If such evidence had been considered the evidence below was not sufficient to meet the standard which was proposed by the medical witness (sic)."

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the medical research - and, in particular, the Garabrant article - upon which the expert witnesses called on behalf of Mrs. Allen based their opinions as to the causal relationship between Mr. Allen's cancer and his exposure to DDT and, to a lesser extent, Arsenic, did not provide any basis for the opinions which were advanced, so that those opinions were of no evidentiary value; and, in any event, those opinions were outweighed by the opinions advanced by the experts called on behalf of the Defendant. 117 While it is true that there may be cases when there is such a disparity between the hypothetical material put before an expert witness for the purpose of obtaining his opinion and the facts proved in evidence as to render the opinion offered by that expert witness of no evidentiary value whatsoever, it is not every disparity between the hypothetical material and the facts proved which will produce that result. As was put by Samuels JA in Paric v. John Holland Construction Pty. Limited supra at 509-510: "We were referred to Wigmore on Evidence 3rd ed vol II s680 and foll at 6, in which this area of the law is discussed. In a footnote which I find in the 1940 edition (at 800) there is a reference made to a decision of Boardman v. Woodman (1866) 47 New Hampshire 135. I confess I have not looked at the original report, but the passage extracted by the learned author, which I would fully accept as accurate, is as follows: '… so proved as to resemble as near as may be the case under consideration; the jury can judge whether the case supposed is so far like the one they are considering as that the opinion of the expert on the supposed case is any guide to them.' Furthermore, there is another reference in a footnote to the same section, and this in the 1979 edition (at 942). This is a reference to a Wyoming case, Culver v. Sekulich (1959) 80 Wyoming 437 at 458. It is in these terms: 'From our analysis of the record it appears to us that there was some evidence to support every hypothetical question to which objection was made. Such evidence was not always complete, was sometimes hazy as to time, distance and other vital words, but in general, furnished a fair climate for the consideration of the views of the expert witnesses.' I would respectfully adopt that last statement as exactly in point and its application disposes of both aspects of the problem to which I have earlier referred. It is a question of whether the hypothetical material put to the expert witnesses represents a fair climate for the opinions they expressed. I do not think there is any requirement that the matter put is precisely consonant with the material provided; and certainly it cannot be contended there was no evidence upon which the opinions could be based. Discrepancies may be fatal; in some cases even slight discrepancies may be fatal; in other cases even broad departures are not likely to affect the force of the expert opinion. Moreover, it is for the tribunal of fact to assess this factual basis. In the present case it seems to me that there was a fair climate in which the expert views could properly flourish and certainly it was open to the learned judge to come to that conclusion."

[90]

I have set out in paragraph 31 (above) that part of the "Assumed Facts" which recorded Mr. Allen's duties as a stock inspector and the factual material as to his exposure to pesticides in the course of his performance of those duties. The facts found by his Honour - basing himself upon the evidence of Messrs. Murphy, Draper and McClenan which I have set out in paragraphs 35-38 (above) coupled with the material prepared by Dr. McConchie which I have set out in paragraph 39 (above) - in my view provide a sound basis upon which Professors Stewart and Levi could found their respective opinions insofar as they were based upon the nature of Mr. Allen's duties and his exposure to pesticides. 118 The attack which was made on behalf of the Department in respect of the reliance by the experts called in support of Mrs. Allen's case upon research material - and in particular the Garabrant report - was to the effect that, before those opinions could be accorded any evidentiary value, it needed to be demonstrated that the conditions of employment to which Mr. Allen was exposed were comparable with those to which the workers the subject of the Garabrant had been exposed and the period during which Mr. Allen had been exposed to those conditions had been comparable with that to which the workers the subject of the Garabrant report had been exposed. The argument then proceeded that, as the workers the subject of the Garabrant report had been engaged in the manufacture of DDT - which involved "daily exposure to DDT which is hundreds of times more intense than it is for consumers" - and had been so involved for periods in excess of ten years, there could be no comparison between the exposure to which Mr. Allen was subjected, and that to which the workers the subject of the Garabrant report had been subjected so that any opinion based upon that report was of no evidentiary value whatsoever. 119 I am unable to accept this argument. While it is true that each of Professor Stewart and Professor Levi referred to the Garabrant report as providing support for the views which they expressed, those views were not based solely upon the Garabrant report, the limitations upon which each of Professor Stewart and Professor Levi recognised (in the case of Professor Stewart, see para. 51 (above); and in the case of Professor Levi see paras. 55-59 (above)). This notwithstanding, Professor Stewart (as I have earlier noted) concluded (see para. 53 (above)) that it was reasonable to attribute Mr. Allen's malignancy to the combined effect of Arsenic containing compounds and DDT while Professor Levi, in his first report (see para. 58 (above)) wrote (inter alia) that evidence was accruing to support that industrial exposure to DDT is associated with the subsequent development of carcinoma of the pancreas, and, as I have earlier (see para. 60 (above)) noted, at the conclusion of his evidence in chief at trial, expressed the view that the initiating factor was Mr. Allen's chronic pancreatitis leading on to promotion or aggravation from exposure to either DDT or other pesticides or the combination of them. 120 The position thus was that two distinguished witnesses, Professor Stewart, a research scientist, and Professor Levi, a specialist oncologist, while aware of the views expressed by the expert witnesses who were to be called on behalf of the Department, which views were the contrary of those they expressed, nonetheless expressed the views which I have earlier recorded. In this situation it is appropriate to refer to what was said by the members of the High Court in Commissioner for Government Transport v. Adamcik supra. Although he would have upheld the appeal upon the basis that Dr. Haines' opinion was based at least in part on assumptions which had not been made out, Taylor J said supra at 298: "Under our existing system it is, of course, within the exclusive province of the jury in cases such as the present to determine which of two conflicting bodies of expert evidence they will accept. Accordingly, and in spite of the arguments to the contrary raised by the appellants, it was open to them to give such value to Doctor Haines' theory as thought fit. It was for them to regard it as impressive or to remain highly sceptical or to treat it as meretricious humbug so far as an attempt was made to link the development of the deceased's leukaemia to the negligence for the consequence of which the appellants are responsible. But apparently they accepted his general theory as probable despite the fact that it was opposed to weighty medical evidence and in the face of Dr. Haines' own statement that he had never known of a case where leukaemia had supervened upon traumatic injury. It should be emphasised that the trial of the issues between the parties did not involve a scientific investigation into the cause or causes of leukaemia. The issue to be determined was whether it was more probable than not that the deceased's death was caused by negligence for which the respondents were responsible. And, of course, in seeking to determine this issue the jury was limited to a consideration of the evidence adduced by the parties. Neither the court the jury was at liberty to seek other information or initiate enquiries of their own. In the result, therefore, the decision in no way resembles the assertion of a scientific truth; it represents merely acceptance of part of the evidence in the case as against other conflicting evidence. And, it may be said, the acceptance was by a body singularly unfitted to pronounce on matters involving consideration of medical or scientific theories. But as long as some members of the medical profession can be found to advance mistaken or erroneous medical theories in cases such as the present there will always be the danger that juries will accept their testimony. In the circumstances, it is necessary that we should approach this case on the basis that it was open to the jury to accept Dr. Haines' general theory. But acceptance of this theory cannot, in my view, alone dispose of the case for first of all there must be found in the evidence a sufficient factual basis for its application."

[91]

After referring to Dr. Haines' evidence that the injuries which the deceased had earlier suffered and the subsequent onset of leukaemia were probably causally related, Menzies J said supra at 302-303 : "It was argued, however, that Dr. Haines' evidence should as a matter of law be disregarded either because he was not qualified to express these opinions or because an examination of his evidence as a whole shows that it was self-contradictory and worthless. Dr. Haines was a Bachelor of Medicine, a Bachelor of Surgery, a Member of the Royal College of Physicians and was an honorary assistant at a large teaching hospital in Sydney. He carried on specialist practice as a physician. Proof of these qualifications did qualify him as an expert and warranted the admission of his opinion about the relationship, if any, of physical injury and emotional stress with leukaemia. From his cross-examination it appeared that although Dr. Haines had treated about twenty case of leukaemia, he had only treated one case of acute lymphatic leukaemia; but this is a matter that went to the weight of his evidence rather than to its admissibility. It would be going too far to say that any legally qualified medical practitioner is to be regarded as sufficiently qualified as an expert to express an opinion upon any matter of medical science, but in this case it is not necessary to go anything like that far. This is a case of a practising specialist physician with high qualifications and a hospital appointment expressing his opinion about the cause of a well-known disease, a subject upon which, despite investigation, there is as yet no positive knowledge. Had this witness said that in his opinion there was no relation between the deceased's injuries and the leukaemia which brought about his death - as did other doctors who qualified as experts by giving evidence of the same kind of qualifications as those Dr. Haines possessed - there could hardly have been a challenge to the admissibility of his evidence. It is only because his opinion was one that medical science seemingly does not accept as reliable that it is contended he lacked the qualifications necessary for expressing it; but the giving of correct expert evidence cannot be treated as a qualification necessary for giving expert evidence."

[92]

For his part, Windeyer J, in whose judgment Kitto J concurred, wrote (inter alia) supra at 306, 308 : "The case is not one in which a witness, posing as an expert, made assertions that are contrary to proved scientific facts or to the known phenomena of nature, thus exposing his ignorance of the learning he professed. To liken the doctor's statements, as counsel did, to the assertion of an eccentric person that the earth is flat is, even for argumentative purposes, mistaken. If there were any value at all in such a comparison - and there really is not - Doctor Haines would, no doubt, answer that he should be likened rather to those who first denied that the earth was flat. In the same way, it is a mistake to liken his evidence to mere superstitions by which curative properties are attributed to things that have been scientifically proved to have no such properties. The most that could be urged against Doctor Haines' evidence is that the cause of leukaemia is not, in a positive sense, known and that his view is thus unproven and not accepted by others: not that it can be scientifically established as false. He said of the present case that he, as a qualified physician, considered that it was not merely possible, but probable, that the leukaemia was the result of the accident. ……… Dixon J, as he then was, in his dissenting judgment in Adelaide Stevedoring Co. Ltd. v. Forst ((1940) 64 CLR 538, 569), said: '… I think that upon a question of fact of a medical or scientific description a court can only say that the burden of proof has not been discharged where, upon the evidence, it appears that the present state of knowledge does not admit of an affirmative answer and that competent and trustworthy expert opinion regards an affirmative answer as lacking justification, either as a probable inference or as an accepted hypothesis.' This proposition, on which the appellants relied, does not avail them, unless it be said that Doctor Haines' evidence must be dismissed entirely as incompetent and untrustworthy. His general competence as a physician was not contested. The jury could consider whether this opinion was honestly held. It was for them to consider whether, as counsel suggests, he was a charlatan. They might think so or they might regard him as an earnest but misguided proponent of an incorrect theory or as a discoverer and prophet or in some other way."

[93]

121 In my opinion this attack on the evidence given by Professors Stewart and Levi fails. 122 I therefore conclude that the Appellant's attempt to demonstrate that there was no evidence upon which Armitage CCJ could base a finding that it was more probable than not that there was a causal relationship between Mr. Allen's exposure to DDT and the promotion, acceleration or aggravation of his pancreatic cancer must fail. 123 The next attack made by the Appellant under this group of grounds of appeal was that Armitage CCJ misdirected himself as to the issues which he had to decide and as to the approach which he adopted in proceeding to determine those issues. As to this I do not feel it necessary for me to say any more than that the passage from his Honour's Judgment as to the legal approach adopted by him (see para. 91 (above)) and the conclusion which he recorded (see para. 92 (above)) in my view do not demonstrate any error on his Honour's part and I would reject this attack. 124 Insofar as in part of the submissions which it sought to advance in relation to this group of grounds of appeal the Appellant sought to submit that Armitage CCJ failed to consider submissions which were put to him and failed to have regard to evidence that was before him which prompted and required another conclusion, I think that question can be considered together with the attack sought to be raised by grounds 4 and 5 which also sought to assert that his Honour failed to have regard to and deal with the submissions of the Appellant and failed to have regard to and deal with evidence which was of a material nature so that his failure amounted to an error of law. 125 Despite the form in which these grounds of appeal were drawn, the manner in which the submissions directed to them was advanced involved an attempt to demonstrate that Armitage CCJ's findings of fact were erroneous and should be rejected. For the reasons which I have earlier set out, such an approach is not open to the Appellant in the present case. However, if the fact were that Armitage CCJ did fail to have regard to and deal with submissions advanced on behalf of the Department and did fail to have regard to and to deal with evidence which was of a material nature, it would be open to the Appellant to seek to persuade the Court that the trial miscarried and thus there was an error of law reviewable on appeal. That this would be so is made clear by the following passage in the Judgment of Samuels JA in Mifsud v. Campbell (1991) 21 NSWLR 725, 727-728: "Following amendments to the notice of appeal the plaintiff, as appellant, contends that the learned judge erred because his finding that the defendant was not negligent or, rather, that the plaintiff had failed to prove that he was, was made without regard to the evidence of consumption of alcohol by the defendant, of flight by the defendant, of the point of impact of the vehicles and of the fact that the lights on the defendant's vehicle were off shortly after the collision. It seems to me that this ground of appeal does not seek to establish that the learned judge's conclusion was necessarily wrong, or to seek to replace it by a finding that the plaintiff was entitled to judgment. It attacks the method by which the judge reached his conclusion. There is, I think, an analogy, which is of service in determining the present case, with those authorities which deal with the judicial obligation to give reasons. In Public Service Board of New South Wales v. Osmond (1986) 159 CLR 656, the High Court (at 667) said that it was right to describe the giving of reasons as 'an incident of the judicial process' although a normal but not a universal one. In Soulemezis v. Dudley (Holdings) Pty. Ltd. (1987) 10 NSWLR 247, McHugh JA (at 278) makes some comments upon that holding, and goes on to say (at 281) that the failure to explain the basis of a crucial finding of fact involves a breach of the principle that justice must not only be done but must be seen to be done. Similarly, in my opinion, it is an incident of judicial duty for the judge to consider all the evidence in the case. It is plainly unnecessary for a judge to refer to all the evidence led in the proceedings or to indicate which of it is accepted or rejected. The extent of the duty to record the evidence given and the findings made depend, as the duty to give reasons does, upon the circumstances of the individual case. Accordingly, a failure to refer to some of the evidence does not necessarily, whenever it occurs, indicate that the judge has failed to discharge the duty which rests upon him or her. However, for a judge to ignore evidence critical to an issue in a case contrary to an assertion of fact made by one party and accepted by the judge - as the defendant's denial of having consumed alcohol - may promote a sense of grievance in the adversary and create a litigant who is not only 'disappointed' but 'disturbed' - to use the words which appear in the New Zealand case of Connell v. Auckland City Council [1977] 1 NZLR 630 at 634. It tends to deny both the fact and the appearance of justice having been done. If it does as in my opinion is the case here, then it will have worked a miscarriage of justice and produced a mis-trial and resulted in what I would take to be an error of law which is reviewable on appeal. Whether it is an error of law or an error of fact, it seems to me a failure by the judge to do what the nature of the office requires."

[94]

126 It is true that, despite his lengthy and careful judgment, Armitage CCJ did not refer in terms to each and every of the submissions advanced on behalf of the Department at trial or to every piece of evidence to which attention was directed. However, those extracts from his Honour's Judgment which I have set out above in which he defined the issues for trial, analysed the evidence of the various witnesses - both lay and expert - recorded the legal basis which he should approach the scientific evidence and, finally, recorded his conclusions, are in my view sufficient to indicate that, in his Judgment, he discharged the obligation which was cast on him in a more than adequate fashion - a judge's duty to state his or her reasons for deciding does not exist in respect of every matter which is raised in proceedings (Kiama Constructions Pty. Limited v. Davey (1996) 40 NSWLR 639, 647 per Meagher JA). I would therefore reject these grounds of appeal. 127 There remains ground 8 which was to the effect that Armitage CCJ failed to give sufficient and proper reasons for rejecting the evidence of Mr. Pickford. Although the form in which the ground is drafted would suggest in error of law in the sense which I have discussed in relation to grounds 4 and 5, the submissions which were advanced in elaboration of this ground in reality involved an attack on his Honour's fact finding. That this was so is demonstrated by the following extracts from the Written Submissions directed to this issue: "85. What the Appellant sought to prove through Pickford was that even taking a worst-case scenario (weighted or biased against the Appellant), Mr. Allen could not have been exposed to anything remotely close to recognised, scientifically-acceptable levels of arsenic or DDT so as to make any difference to his disease. There was documentary evidence which tended to support Pickford's thesis in the form of ambient air studies and dermal absorptions rates (Blue 377-578 (sic)). ……… 87. It is submitted that when one looks at all the evidence, including the lay witnesses, relied on by the judge, the conclusion is that Pickford's opinions remain reliable and prove, on the balance of probabilities, that Mr. Allen's exposure to dust, if any, that may have been impregnated with DDT and/or arsenic (and to what extent this is unknown) was indeed insignificant and non-contributory to his illness. ……… 89. Essentially, the main reason that his Honour rejected Pickford's evidence is because of what his Honour felt were a number of concessions in cross-examination about the assumptions made by him in expressing his opinions. It is submitted that any 'concessions' as referred to by his Honour in fact do not deter (sic) from the main thrust of Pickford's opinion. It is submitted that his Honour placed too much emphasis on the cross-examination of Pickford and that, in reality, there were no material concessions made which required the rejection of his evidence. ……… 93. Therefore, it is submitted that his Honour should not have rejected Pickford's evidence in the way he did and that this evidence supports the evidence of submission about the non-contributory nature of Mr. Allen's employment with the Department in the (relatively) short period of time that he worked there."

[95]

This being the basis upon which the Appellant sought to support this ground of appeal, no question of law is involved and the ground of appeal should be rejected. 128 For these reasons, I conclude that the Appeal should be dismissed. 129 It is necessary then to turn to the Cross-Appeal which is directed to Armitage CCJ's failure to make an award pursuant to the provisions of s.66 of the Act. 130 Although I have earlier (see para. 8 (above)) recorded in outline the grounds upon which his Honour rejected the claim for an award pursuant to s.66, it is convenient that I now record in detail the basis on which his Honour proceeded. It was as follows (RAB 104-105): "It remains to formulate the award appropriate in the circumstances. Before doing that I should observe that the deceased (sic) has not in my view proved her case in relation to s.66 benefits. The reasons for this are twofold. The first is that I am not satisfied on the probabilities that the deceased had particular permanent percentage losses and impairments. The evidence for these comes from the report of Dr. Chappel dated 18 January 1996, part of Exhibit A, where Dr. Chappel asserts: 1. Mr. Allen's loss of power and strength in his legs represented 80% loss of efficient use of his legs. 2. Mr. Allen's loss of power and strength in his arms represented a 90% loss of efficient use of his arms. 3. Because of the deterioration of his visual perception, I would estimate that the (sic) lost 20%-40% efficiency of binocular vision. 4. Due to the weakness in his voice, he was unable to converse, other than in a whisper, and I would assess that he lost 50%-70% of the power of speech. These, as I am sure Dr. Chappel would admit (and he was not called) are very global estimates. They do not rely, as orthopaedic and other specialists (sic) assessments customarily do, on degrees of loss of movement in the affected parts, or an exact estimation of the precise pathology affecting respective parts. I simply do not accept them as accurate on the balance of probabilities, even though I fully appreciate that they are the only expert evidence on the subject. Despite this, it is open in law for me not to accept them (cf Poricanin v. Australian Consolidated Industries Ltd. (1979) (sic) NSWLR 419; (1979) WCR 147) and I do not. The second reason for rejection of the Applicant's s.66 claims is that, as I held in Hellier v. Gosford City Council ( No. 12293/96, unreported, 22.6.98) it is necessary for a loss of use to be 'permanent' within the meaning of s.65(1)(b) of the Act, which governs s.66(1), for such a loss of use to last, or be likely to last, indefinitely. I referred in that case to Rolfe v. Metropolitan Meat Industry Board (1958) WCR 135, where at 138 Wall J said: The dictionary meaning of 'permanent' as given in the Shorter Oxford Dictionary is 'lasting or designed to last indefinitely without change; enduring; persistent opp. to temporary'. It will be seen that this meaning falls short of the notion of a perpetual state of affairs, and that, while what is permanent may continue for all time, it need not necessarily do so. I also observed that the Concise Oxford Dictionary (8th ed) (1990, reprinted in 1991) defines 'permanent' as meaning 'lasting, or intending to last or function, indefinitely'. In this case, at the time that Dr. Chappel is speaking in his report (retrospectively because the report post-dates his death) the deceased had been diagnosed as suffering from inoperable cancer and had a very short life expectation, according to all medical opinion at the time. The various losses which he suffered therefore were not likely to last 'indefinitely' but were likely to endure only for a very short time until the deceased's unfortunate death, as indeed occurred. In those circumstances I do not think that it can be said that the various losses assessed by Dr. Chappel, even if I accepted, as I do not, were 'permanent' within the meaning of s.65(1). In those circumstances the applicant's claim under s.66 fails."

[96]

131 It is necessary first to deal with the second of the reasons assigned by Armitage CCJ, for, if that reason be held sound, no consideration of the first is called for. 132 Although in Borovac v. Corporate Ventures Pty. Limited (1995) 12 NSWCCR 84 there was some discussion by the Court (Mahoney, Clarke and Meagher JJA) as to the meaning to be attributed to the phrase "permanent impairment" in the factual context then under consideration, so far as I have been able to ascertain there is no decision of this Court as to the meaning of that phrase in a context such as that with which we are concerned to deal. However, although, in the cases to which I will now refer, the point presently under consideration was not raised for decision - the point at issue being whether or not a claim for an award under s.66 could survive the death of the worker under consideration - the decision in each case involved an award under s.66 in respect of injuries which led to the death of the worker within a short time after injury. The first of those cases was Bresmac Pty. Limited v. Starr (1992) 29 NSWLR 318 in which case the worker sustained an injury resulting in quadriplegia in October 1988, his death occurring in January 1991. On the application of the Executor of the worker's Will, Manser CCJ made an Award pursuant to s.66(2) of the Act in the sum of $119,250.00 - that sum being the maximum amount payable pursuant to s.66(2) of the Act in respect of injuries sustained after April 1991 - the Applicant's entitlement to an Award being upheld on an appeal but the amount of the Award being reduced on appeal to $85,200.00 - that being the maximum amount payable pursuant to s.66(1),(2) in respect of injuries sustained after 1 October 1988. The second such case was TNT Australia Pty. Limited v. Horne (1995) 11 NSWCCR 497 in which case the worker sustained an injury on 27 September 1990 which injury rendered him a quadriplegic as a consequence of which he suffered a total loss of the efficient use of both arms and both legs and from the effects of which injuries he died on 1 November 1990. Thereafter, on an Application for Determination brought by the worker's widow as Executrix of his Will, in which application the worker's widow claimed a lump sum of $92,450.00 - that being the maximum payable pursuant to s.66(1) of the Act in respect of injuries sustained after 1 April 1990 and before 1 October 1990, Duck J made an Award, apparently in the amount sought - that Award was upheld on appeal. 133 Although, as I have indicated, the question with which this Court is now concerned to deal is not concluded by the decisions of the Court in Bresmac Pty. Limited v. Starr supra and TNT Australia Pty. Limited v. Horne supra, I consider that the Award made in each case was in accordance with the provisions of s.66 of the Act and that, in the present case, Armitage CCJ ought to have made an Award pursuant to s.66 of the Act in favour of Mr. Allen's estate. Let it be assumed that the precondition to the making of an Award under s.66 of the Act is that there be a permanent impairment of the type provided for in the Table to Division 4 of Part 3 of the Act, and let it be further assumed that the word "permanent" postulates an impairment which will, at least, remain constant and may even deteriorate and which will be of an indefinite duration, the fact is that, as at 6 December 1993, Mr. Allen had sustained an injury, which injury Armitage CCJ held to be work related, the sequelae of which injury involved the deterioration in Mr. Allen's physical abilities and in his bodily functions, which deterioration would inevitably progress until at some - indefinite - time in the future, his death would ensue. Contrary to the view expressed by Armitage CCJ it seems to me that, in this situation, Mr. Allen was to be regarded as having suffered a variety of permanent impairments. 134 Given that Mr. Allen is to be regarded as having suffered a number of permanent impairments, the facts that Dr. Chappel's estimates for loss were "very global" and that they were not accepted by Armitage CCJ do not afford a reason for denying an award in respect of those impairments - a court's task in such a case is to arrive at a determination of the loss by reference to all of the evidence (see, for example, Manning Valley Senioir Citizens Homes Limited v. Cleveland Court of Appeal, 29 August 1995 (unreported)) 135 In these circumstances, I am of the opinion that the Cross-Appeal should be allowed. 136 The question then is whether, as a consequence, this Court should remit the matter to the Compensation Court so that Armitage CCJ, doing the best which he can in the light of the whole of the evidence might determine the extent of the permanent impairment and the appropriate award pursuant to s.66, or whether this Court - which by s. 32(2) of the Compensation Court Act 1984 "may make such other order in relation to the appeal as (it) sees fit" - should make that determination for itself and order the Award amended accordingly. 137 Although I was at first inclined to propose the former course, it seems to me that, given the approach taken by this Court in Bresmac Pty. Limited v. Starr supra and TNT Australia Pty. Limited. v. Horne supra, the Court should adopt the latter course. 138 If one were to adopt the percentage losses suggested by Dr. Chappel and apply those percentages to the amounts provided for by the Table of Disabilities for injuries sustained between 1 October 1993 and 1 April 1994 one would produce a total sum of between $407,729.00 (based on the lower percentage suggested) and $449,281.00 (based on the higher percentage suggested), sums which far exceed the maximum amount payable for multiple losses or impairments sustained in that period. That being so, it seems to me that it would be appropriate to order that the Award be amended by inserting an Award pursuant to s.66(2) of the Act in the sum of $158,000.00, that being the maximum amount payable for multiple losses or impairments flowing from injuries sustained in the relevant period. 139 My inclination is to think that that sum should carry interest as from 6 December 1993 (see, for example, Borovac v. Corporate Ventures Pty. Limited supra at 96 per Clarke JA). However, as the question of interest on any Award which might be made in the event that the Cross-Appeal were to succeed was not the subject of any submissions on the hearing of the appeal, the better course would seem to be to leave that question to be decided on an application pursuant to the liberty to apply reserved in the original Award. 140 For these reasons I propose the following formal Orders:

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