Clarke v Q-Comp [2007] QIRC 95 (2008) 187 QGIG 9

Extract from Queensland Government Industrial Gazette, Dated 11 January 2008, Vol. 187, No. 1, pages 9-17] QUEENSLAND INDUSTRIAL RELATIONS COMMISSION Workers' Compensation and Rehabilitation Act 2003 - s. 550 - appeal against a decision of the review unit Troy John Clarke AND Q-Comp (WC/2006/5) DEPUTY PRESIDENT BLOOMFIELD 24 December 2007 Appeal against a decision of the Review Unit, Q-Comp - pemphigus vulgaris - whether work a contributing factor - witness evidence - medical evidence - onus of proof - balance of probabilities - onus not met - appeal dismissed. DECISION Introduction This decision relates to an appeal by Mr Troy John Clarke pursuant to s. 550 of the Workers' Compensation and Rehabilitation Act 2003 (the Act) against the decision of the Review Unit, Q-COMP (Q-COMP) dated 19 January 2006 in which Q-COMP confirmed an earlier decision of WorkCover to reject Mr Clarke's claim for workers' compensation dated 2 September 2005. The claim related to an injury in the form of a debilitating skin disease, pemphigus vulgaris, said to have been contracted in the course of Mr Clarke's employment with J.J. Richards and Sons Pty Ltd (J.J. Richards), Waste Management Consultants, in Mackay. Pemphigus is a rare autoimmune disease which occurs in people with a genetic predisposition, but which is generally triggered by an environmental factor or factors. Relevant Legislation Section 32 of the Act relevantly provides: "32 Meaning of injury (1) An injury is personal injury arising out of, or in the course of, employment if the employment is a significant contributing factor to the injury. ... (3) Injury includes the following - (a) a disease contracted in the course of employment, whether at or away from the place of employment, if the employment is a significant contributing factor to the disease;". Onus The onus is on Mr Clarke to prove that his pemphigus vulgaris falls within the definition of injury as defined above. In particular, Mr Clarke is required to prove that his injury was a personal injury arising out of, or in the course of, employment and that the employment was a significant contributing factor to his injury. The onus of proof is to be established on the balance of probabilities. Appellant's Evidence Mr Clarke indicated that he became a professional footballer in approximately 1987 at the age of 17 and played professionally until approximately 1995 with 3 NRL clubs, and which included off-season in France and 2 years in England. In early 1995 he commenced work as a Training and Gaming Manager for the Cessnock Rugby League Supporters Club, playing football in the local competition for 1 year. In 1998 he moved to Mackay and worked for a period as a tradesman's labourer during construction of a wharf and sugar terminal at the Mackay harbour. Later, he worked for the Mackay Rugby League as a Sales Representative setting up charity matches for the NRL. In 2002 or 2003 he commenced his own sports promotion business which involved the co-ordination and conduct of a series of special coaching clinics - in a whole variety of different sports - for school children during school holidays. These coaching clinics were primarily conducted on school ovals and other dedicated outdoor sporting venues. Mr Clarke said he commenced work as a Sales Representative with J.J. Richards on 30 August 2004. On his first day of employment he commenced work at 11.00 p.m. at night and travelled with one of J.J. Richards' truck drivers to learn a bit more about the nature of the employer's business including truck access, where bins were located, types of clients and the like. During this 12 hour shift Mr Clarke said he assisted the driver in the performance of his duties by bringing some of the bins out of their enclosures, so that the forklift on the truck could lift the load into the truck, then placing the bins back into their enclosures. During this shift something of the order of 140 bins were cleared of which number Mr Clarke -- 1 of 9 -- 2 claimed he moved about 60% for the driver to empty. Mr Clarke also said that he scraped his arm while moving one of the bins during the shift. Over the next 10 days or so he travelled with J.J. Richards' other Sales Representative to "learn the ropes". Thereafter, he was left to his own devices. Mr Clarke said he also travelled with other relief drivers in the truck on 2-3 other occasions, to collect rubbish, when the regular driver was away or had called in sick, to show the replacement driver where to go. Whilst Mr Clarke's job description primarily required him to actively canvas for new commercial/industrial customers, provide service to existing customers to solve any problems they may have and systematically review customers' needs by personal contact to ensure that they were being provided with the most appropriate services, he also claimed that the role required him to do much more than that, including certain physical work. This included inspecting the areas where drivers were to pick up their loads, examining bins to make sure they weren't damaged, and, depending on the clients, to physically open certain bins and inspect them to ensure that no drums were placed in them. If there were, he was expected to remove them as they were not allowed to be placed in industrial bins. He said that on two occasions he had been required to physically take drums out of industrial bins. If a bin needed to be replaced, because it was damaged, he would assist the driver to shackle and lock the bin so that it could be lifted by a crane arm and placed on the truck. On other occasions he was also required to fit shackles and locks to bins, either in situ or at the Company's premises before a bin was delivered to a client. Mr Clarke also said that there were several locations - particularly the Mackay Marina and one building complex - where rubbish was often left beside the bins or where rubbish had fallen onto the ground because the bins were overloaded. Where this happened he was required to pick up the rubbish and place it back in the bins and generally tidy the area up. Whilst this rubbish was generally in plastic bags there was the odd occasion where the bags had split. On several occasions he had also been required to climb into the bin and jump on the rubbish to make room to put in additional rubbish bags that had been left on the ground or had fallen onto the ground. In addition, Mr Clarke claimed that he had been required to oversee and assist drivers whose responsibility it was to clear grease traps. At times he had assisted drivers with their hose lines and in lifting the lids of the traps. On one occasion he assisted a driver by using a knife-like implement attached to a long stick to scrape grease and other material off the inside of a grease trap. Overall, he believed that he had assisted in the clearing of grease traps on 6 or 7 occasions and had worn a mask on some of those occasions, but not others. However, virtually immediately after making this statement he said that the only time he probably did not wear a mask was at the hospital. Mr Clarke particularly emphasised his role in the collection and deep burial of rubbish collected from ships at the Mackay harbour as part of J.J. Richards' contract with AQIS. Mr Clarke said that his role in the collection of such rubbish was to stand with an AQIS Officer as the material was collected off ships in bags and loaded onto a Company truck. The driver would then place a tarpaulin over the load and place signs on the truck before driving to a dump. Mr Clarke and the AQIS Officer followed the truck to the dump where it was unloaded into a deep hole then covered with earth. Mr Clarke claimed that this task was undertaken once or twice a week, most particularly in the latter period of his employment with J.J. Richards. Mr Clarke also highlighted his involvement in the disposal of certain asbestos waste and waste product from sand blasting clients of J.J. Richards. He said it was his role to oversee the collection and transport of such product to the dump where it was also subject to deep burial. Whilst the asbestos was supposed to be double wrapped, on several occasions the plastic wrapping had split and there was "white powder everywhere". On two occasions, when he was on-call over the weekend, Mr Clarke was required to collect dead dogs and to transport them to the dump. On each occasion he was required to pick up the dog - one of which was in many pieces - and to wrap it in a tarp before placing it in the boot of his car for ultimate transport to the dump. He complained that he was required to use his company provided car for this purpose. He also complained that he was required to use his car to collect "big brown empty glass chemical bottles" from a particular client and take them back to the recycling plant. He said that he did not know what chemicals the bottles had previously held. Mr Clarke also said that contrary to a direction from management not to (because he had not been given "safety shots"), he had also gone "out the back" of the depot. He had done this for a variety of reasons including: to check the availability of bins, including the different sizes which might be available, in order to service new and existing clients; to cut chains to length so that they might be used by clients to lock their bins; to make several wheelie bins which were needed at a particular client's premises; and, to discuss with the workshop employees various matters including the repair of bins. Mr Clarke said that during his visits out the back he walked past areas where chemicals were being used to clean bins, walked past an open container which was used to store hospital waste, and walked near open conveyer belts from which rubbish, such as aluminium cans, glass and the like, was being sorted. -- 2 of 9 -- 3 Mr Clarke said that the clients of J.J. Richards included milk bars, newsagents, sporting clubs, restaurants, hotels, unit blocks, shopping centres, hospitals, the Mackay Marina and metal and engineering companies servicing the mining industry. He complained that he was expected to visit 75 or 80 of them every week and found this workload stressful. He also found it stressful that he was not assigned a desk or a computer and that he had to "borrow" a computer from the office staff, and sit at their desk, to do his paperwork. During December 2004 Mr Clarke developed a rash under his arm pits and his arm pits started to split. He visited his general practitioner on 29 December 2004 and was given some cream to treat what was then diagnosed to be a sweat and heat stress condition. However, the cream had no effect and during the course of January lesions started to form on his body. He sought a second medical opinion and was admitted to hospital for approximately 2 weeks in early April 2005 where he was diagnosed with Grosvenor's Disease. He was given steroid treatment, along with other medication, and released from hospital. However, his condition began to worsen and he went back to his original general practitioner who placed him in contact with a specialist at the Townsville hospital, a Dr Reid, and he was admitted to that hospital between 19 May 2005 and 9 July 2005. During his treatment by Dr Reid he was given a number of IVIg infusions which progressively settled his condition. Because his health fund withdrew support for his treatment program, Mr Clarke began to search for other ways to fund his treatment. In the course of searching the Internet for information about his condition, and its treatment, he came across a Dr Murrell at the St. George Hospital at Kogarah in Sydney and began a treatment program under her supervision. She was able to gain financial support from the John Hunter Hospital in Newcastle to fund his IVIg infusions. Mr Clarke said he was still receiving treatment for his condition at the time of the hearing. Medical Evidence Dr Sinha Dr Animesh Sinha is a physician specialising in dermatology and immunology. He is the Chief of Dermatology and Cutaneous Sciences and the Director, Center for Investigative Dermatology, Michigan State University USA. Dr Sinha indicated he had been involved in the clinical care and research investigation of patients with pemphigus over a number of years. His research started in 1986 and has focused primarily on the genetic basis of the disease and the factors leading to immune disregulation in this autoimmune condition. Dr Sinha is a Member of the Medical Advisory Board of the International Pemphigus and Pemphigoid Foundation. In a report dated 15 August 2007, Dr Sinha reported that in a 90 minute telephone discussion with Mr Clarke on that same day, Mr Clarke advised him that "his duties with (J.J. Richards) encompassed handling a wide range of waste materials involving animal carcasses, asbestos, sand blasting materials, sewerage and 'grease traps' that collected chemical and organic waste from a variety of industrial companies, including a fertiliser company. He states that he often worked in extremes of heat. Mr Clarke's work extended to repairing waste bins and exposure to the city waste dump.". Later in his report Dr Sinha indicated: "The full details regarding the etiology of pemphigus remain uncertain. What is clear is that autoimmune diseases such as pemphigus vulgaris are complex in nature - that is, they are multifactorial, requiring a combination of genetic susceptibility and environmental triggers. Genetic susceptibility to diseases is likely to involve multiple gene loci. While certain gene loci have been strongly linked by me and others (a considerable body of research was cited) with pemphigus, all the genetic risk factors are yet to be uncovered. Genetic elements, however, are necessary, but not sufficient - environmental factors are clearly required for autoimmune disease development and expression. While estimates vary, based on twin studies environmental elements appear to contribute 50-70% to disease development (further research cited). Moreover, it is well know (sic) that in a significant number of cases, autoimmune disease onset occurs in a precipitous manner that appears related to an environmental insult. For most autoimmune diseases, links to various environmental risk factors including medications, stress, infections, chemicals and toxins have been reported. Recently, there is accumulating evidence that pemphigus can develop subsequent to environmental exposures. A systematic review of the scientific literature (PubMed search) reveals numerous supporting citations (please see attached list). In fact, the term 'contact pemphigus' has been proposed to classify the sub-group of patients in which environmental exposures are implicated (International Journal of Dermatology (1994) 33:843). In one recent study, one in four male patients reported exposure to pesticides (Clin Expo Dermatol (2007) 32:256). -- 3 of 9 -- 4 Specifically, several components of gardening materials, pesticides and preservatives, along with metal vapors and other chemicals have been implicated as having a causal relationship with pemphigus (referenced in attachment): organophosphates (chlorpyrifos, phosphamide, diazinon), organochlorines (dihydrodiphenyltrichorethane (DDT) and 1,3 dichloropropene), Bayton, benzoin tincture, metal vapors (chromium, cadmium, berrlyium, nickel), pentachlorophenol (PCP). The mechanism by which particular environmental exposures contribute to, or trigger the autoimmune response is at this point unclear. Several possible explanations have been outlined in the referenced articles (see attached): 1) direct activation or dysregulation of the immune response; 2) direct injury to the skin and related structures that exposes normally sequestered self molecules (antigens) to the immune system; 3) interaction with skin associated structures to create altered self-proteins (neo-self antigens) that are then recognised by the immune system; 4) organochlorine pesticides are known to harbour estrogenic effects that directly activate the immune system; 5) organophosphate pesticides can block nictotinic acetylcholinesterase channels, potentially leading to increased acetylcholine at the acetylcholine channel and a decrease in muscarinic and nicotinic receptors that ultimately facilitate the loss of cell- cell adhesion between keratinocytes. Mr Clarke's employment duties related to waste disposal may have put him at increased risk of exposure to one or more of the above cited compounds that have been associated with disease in the literature.". In a subsequent email to solicitors for Mr Clarke, dated 17 August 2007, Dr Sinha added the following paragraph to his report: "Based on this scientific evidence, the balance of probabilities is that environmental factors contributed significantly to the development of his pemphigus vulgaris. Mr Clarke's employment duties related to waste disposal may well have put him at increased risk of exposure to one or more of the above cited compounds that have been associated with disease in the literature.". However, in the same email, Dr Sinha made the following comment to Mr Clarke's solicitors: "i attempted to orient my report to showcase the role of environmental factors in pemphigus in as positive a manner as the medical and scientific literature allows. but let me be clear. while the role of environmental factors in autoimmune diseases in general (and likely pemphigus vulgaris) is accepted, direct links backed by strong, reproducible, non-anecdotal data implicating specific specific (sic) environmental agents is lacking for most diseases, including pemphigus vulgaris. also, please keep in mind that environmental agents in this sense can refer to the broad universe of infectious, stress-related, and chemical/drug related substances/molecules. as such, in my opinion, no expert in the field could conclusively link a specific environmental agent to the development of (this) disease (pemphigus vulgaris), with the possible exception of the drug d-pencillamine. moreover, in this case, i have not seen any evidence that confirms mr clarke was directly exposed to any of the pesticides and other substances reported in the literature outlined in my report, either during the line of, or outside of work. do you have such documentation? even in this case, it would be difficult to conclude that a particular agent was the sole or primary cause of disease that no doubt also requires a genetic predisposition.". Under cross-examination Dr Sinha indicated that genetic predisposition to pemphigus, alone, was unlikely to lead to its development. Environmental factors and/or triggers were required for the disease to develop. In this respect, exposure to a particular environmental agent usually occurred weeks to months before the disease exhibited itself. However, exposure some 12 months before to a particular environmental factor could not be ruled out. Where there were several potential environmental exposures, where timing of a potential source was at issue, Dr Sinha's experience would lead him to go with the more acute exposure as the probably source, albeit that it may be more distant in time from the occurrence of the disease. Dr Murrell Dr Deidre (Dédée) Murrell, Head of Dermatology, St. George Hospital and Conjoint Associated Professor, University of New South Wales, is a specialist dermatologist working mainly in the public health system but with a right of private practice. Her main interest in dermatology is in blistering diseases, which are mainly either autoimmune, as in the case of Mr Clarke, or genetic, as in the case of children who suffer with a disease called Epidermolytis Spinoza. Dr Murrell said she was a founding member of the Medical Advisory Board for the International Pemphigus and Pemphigoid Foundation, based in the United States, and which started in 1995. She was also President of an organisation, founded in 2006, called the Australian Blistering Diseases Foundation. -- 4 of 9 -- 5 In a report, dated 14 December 2005, written shortly after Mr Clarke first visited her, Dr Murrell wrote: "Mr Clarke reports that his job responsibility includes moving waste from industrial bins, overseeing grease traps and when on call, he was also involved in the retrieval of dead dogs. He reports previously jumping on rubbish in industrial bins, picking up rubbish around bins and also previously cutting himself on an industrial bin. He reports his work vehicle was a Holden Commodore, in which he reports he has heard that dead kangaroos, dead dogs and dead cats had been collected in this vehicle. ... THE LINK OF PEMPHIGUS VULGARIS TO A POSSIBLE EXPOSURE Mr Clarke is concerned that he developed pemphigus after working at J. Richards & Sons Waste Management. A thorough literature search was performed using the Pub Med Search Engine. Concerning the induction of pemphigus and certain infections or environmental factors, there are two papers I would like to quote. The first being that from Sarah Brenner, published from Clinics in Dermatology, 2002; 20:114-118. This article mentions that several studies have demonstrated the importance of various exogenic factors in triggering an exacerbating disease (meaning pemphigus) 'including drugs, particularly those containing thiol and thenal, calcium, channel blockers, ultraviolet radiation, burns, x-rays, neoplasm, nutritional factors, emotional stress, hormones and pregnancy, viruses and vaccinations'. These also state 'to the best of our knowledge, infectious agents such as bacteria and fungi have not been reported as possible triggers of pemphigus'. Within this manuscript, there is a table, table 1, which does mention a number of cases in which patients exposed to viral disease in this particular table, herpes simplex or Epstein Barr virus or cytomegalic virus or human herpes viruses, have been associated with pemphigus vulgaris or pemphigus foliaceus. A second report I would bring to your attention to is that called 'Pemphigus Vulgaris, Environmental Factors - Occupational, Behavioural, Medical and Qualitative Food Frequency Questionnaire', published in the Internal Journal of Dermatology 2001, Volume 3, pages 526-569. These authors note that when comparing 126 pemphigus patients with 173 controls, that the risk for pemphigus vulgaris was lower for ex-smokers and current smokers than for patients who had never smoked. Exposure to pesticides and occupational exposure to metal vapour were associated with an increased risk of pemphigus. Pempigus patients had more pregnancy than controls. Further on in this article it states 'our finding that pemphigus patients were more often exposed to gardening materials and pesticides than were control subjects is supported clinically by reports of pemphigus induced by contact with pesticides'. It is also explained in this article that exposure to metal vapour was higher in pemphigus patients than in controls. However, the authors go on to state that without more specific information on the chemicals and level of exposure, they cannot adequately discriminate whether the observed effects are valid or whether biased reporting of exposure contributed to the observed elevated risks. Another form of pemphigus that is endemic in Brazil, pemphigus foliaceus, has been associated with poor rural areas and exposure to black fly bites, presence of rodents at home, exposure to fumes and insecticides (Lombardi et al Journal of Investigative Dermatology 1992 Jun 98: 847-50). So, one may gather, from these articles in the other manuscripts that are referenced in these articles, that there are a variety of factors which have been implicated in the development of pemphigus. In my literature search and readings, I do not see any specific references to exposure to dead animals or grease traps. In my clinical experience with pemphigus, I have two other patients whose disease may have occurred after exposure to chemicals. One had recently started working in the waste management industry with pick up work. The other was chronically exposed to pesticides via gardening. IN SUM AND IN SHORT I believe that Mr Troy Clarke has a difficult to control case of pemphigus vulgaris and, while the induction of this disease, and possibly exacerbation, may have been caused due to occupational elements he was exposed to during his previous employment at J. Richards & Sons Waste Management, to my knowledge, this association of dead animals or grease trap exposure has not previously been reported and he, of course, could have developed pemphigus independent of these factors. Further research in the future may clarify if exposures such that Mr Clarke reports having, may be a causative agent of pemphigus vulgaris.". By 9 May 2006 Dr Murrell had become somewhat more certain about the cause of Mr Clarke's pemphigus. In a letter of that same date to Mr Clarke's solicitors she wrote: -- 5 of 9 -- 6 "I reviewed Mr Clarke in my Bullous Clinic on Friday. He told me that you wanted a statement from me, that I believed his work was a significant contributing factor to the development of his pemphigus. I certainly do believe that. I also believed that on the balance of probabilities, his pemphigus was induced by the exposures he had to endure in his occupation involving collecting grease traps etc in Queensland. I have also reviewed his list of medications and none of these are contributing factors to his pemphigus.". In the course of her evidence in chief, Dr Murrell indicated that the incidence of pemphigus in Australia was quite rare, approaching something like one in a million persons. Although she hadn't added up the number of her existing patients with pemphigus vulgaris (because she mixed them in with her pemphigoid and other patients) she believed that she was seeing about 15 persons. In the whole of her career, including in the USA, she had come across possibly 50 patients as their primary treating doctor and had seen possibly another 10 patients during a period of study in New York. Dr Murrell said that she had expressed the view in her 9 May 2006 letter that work was a significant contributing factor to the development of Mr Clarke's pemphigus for several reasons, including:  he only started working in the waste management industry about 3 months before he developed pemphigus;  he described coming into direct contact - including by inhalation - with rubbish where bins were overflowing, the waste was not in the bins, the waste was not inside protective coverings and that he often had to pick this waste up with his bare hands and put it in the back of his car without having any proper protections;  he had to deal with grease traps and dead animals;  he had never worked in an industry where he had been exposed to those types of things before;  there is evidence that pemphigus can occur when people are exposed to various chemicals, phenols, pesticides etc; and  he had developed such a rare disease within 3 months of commencing a job which involved the above considerations. Dr Murrell also indicated that the reference in her letter of 9 May 2006 to an additional client who had recently started work in the waste management industry had also influenced her opinion with respect to Mr Clarke. This was because out of all of the patients she saw in one year she found it odd that she had encountered 2 men who were doing waste collection work in such a short time frame. As an aside, to reinforce the claimed link with the waste management industry, Dr Murrell indicated that she now had a third patient who had worked in the waste management industry. Under cross-examination Dr Murrell indicated that her opinion as to the link between Mr Clarke's work and the development of his pemphigus condition was based upon Mr Clarke's 3 months work in the waste management industry where he had regular exposure to inhaling and sometimes touching rubbish. When it was suggested that there was absolutely nothing in the literature to suggest touching rubbish or inhaling rubbish smells was a trigger for pemphigus she indicated there was some evidence that contact with chemicals induced pemphigus and there was also evidence that "consuming things" causing pemphigus. What these "things" were was not stated. Finally, Dr Murrell reluctantly agreed - by providing a qualified "yes" - with the proposition that there were situations where pemphigus has arisen but no environmental trigger has been found. Dr Brian Reid Dr Reid is a specialist physician and dermatologist to Townsville General Hospital and has been in private practice in Townsville for 31 years. Dr Reid said he first saw Mr Clarke on 6 May 2005 and that he had been referred by a Dr John Macintosh, in Mackay, for admission to hospital. Dr Reid opined that Mr Clarke's pemphigus condition was unrelated to his work in the waste management industry. He said that it was an autoimmune disease which is acquired sporadically and is not attributable to any infection. He said that the waste management was a huge industry in Australia, and internationally, and there was no evidence of occupational pemphigus. It was such a rare disease, relatively, that it was simply not sustainable mathematically to suggest that the waste management industry was a precipitating or aggravating factor for the condition. It just didn't happen. There was only about one case a year. Dr Reid was somewhat critical of the approach of Dr Murrell and suggested that she seemed "to have taken an oppositional view right from the start, and decided to go it alone. Most time, when we pass on a difficult case, we ring up the previous practitioner and ask for an overview of what he had done what he believed. That did not happen.". Dr Reid said that Dr Murrell had stated there was no definite evidence that Mr Clarke had pemphigus when she first saw him and she had sent him off for further tests. He said Dr Murrell was incorrect in doing that because the tests were positive for pemphigus from the middle of 2005. -- 6 of 9 -- 7 Dr Reid said the incidence of pemphigus in the general population was between 1 and 5 persons per million per year. At the moment he was treating 3 cases which were identical to that of Mr Clarke. Dr Reid also indicated that one needed to read the literature on pemphigus quite carefully because the disease came in different forms. The more common version was pemphigus foliaceus, which was common in certain areas in Brazil, whereas the rarer version was pemphigus vulgaris. In the Brazilian example cited, Dr Reid said that 55% of the general population in the area have the antibodies but not the disease. This compared to American citizens generally where 2% of them carried the antibody but not the disease. Even so, he said, there was a large body of people carrying the genetic predisposition who did not get pemphigus. Dr Reid also indicated the lapse of time between some environmental trigger and the development of the disease was "negotiable... it could appear after a long period of time or immediately on first contact.". Finally, Dr Reid indicated that Dr Murrell's evidence about 3 persons from the waste management industry having contracted pemphigus vulgaris was not a "landslide". It could also just be coincidence. Dr Reid also said that Dr Murrell had stated in one of her reports that Mr Clarke's condition may have been caused through occupational elements but later, in the same paragraph, she also stated that he could have developed pemphigus independent of those factors. On the balance of probabilities he was more inclined to adopt the latter view. Other Evidence Mr Kenneth Mackellar is the Central Queensland Manager for J.J. Richards and is based in Mackay. Mr Mackellar gave evidence about the normal duties of a Sales Representative and indicated they did not involve the physical handling of rubbish or grease traps, nor performing bin repairs or the like. He also indicated that Mr Clarke's role with the removal of quarantine from ships was to handle the paper work and either travel in the truck to the dump or follow the vehicle along with a representative from AQIS. This was a task that would only have happened every couple of months. Mr Mackellar also said that he never saw Mr Clarke out the back of the depot because that was not part of his job description. If Mr Clarke needed to find out something about an operational matter, including the need to fit a lock to a bin, he would have spoken to the operations manager. Mr Mackellar also rejected the proposition that there was an open container holding hospital waste, stating that it was actually an enclosed refrigerated storage facility. Conclusions There can be no doubt that Mr Clarke suffered a personal injury in the form of a debilitating skin condition called pemphigus vulgaris. There can also be no doubt that contraction of the disease has had a significant impact on Mr Clarke in respect of his overall health, energy levels, morale, motivation and self-esteem. However, notwithstanding the debilitating nature of the disease he has contracted, Mr Clarke has to show that his pemphigus vulgaris arose out of, or in the course of, his employment at J.J. Richards. This denotes a causal or consequential relationship between the employment and injury but it does not require a proximate relationship which would be necessary if the phrase used was "caused by" (Lackey v WorkCover Queensland (2000) 165 QGIG 22). Nonetheless, there is a requirement for a causal or proximate relationship between the injury and the work. In that sense, the Act requires that the employment has to be a significant contributing factor to the injury. For employment to be a significant contributing factor there must be a real or effective cause (Croning v Workers' Compensation Board of Queensland (1997) 156 QGIG 100). As to the question of whether work was a contributing factor to the development of his injury it is necessary to say something about Mr Clarke's evidence. Mr Clarke has undoubtedly discussed with his medical advisors, as well as read considerable literature about, the link between environmental factors and the development of pemphigus vulgaris. Not unsurprisingly, he has attempted to recount every possible event in his short employment history with J.J. Richards which might have been directly responsible for, or have contributed to, the development of his pemphigus condition. In that regard, he has mentioned handling dead dogs; travelling in vehicles where dead animals have supposedly previously been transported; working with drivers whilst they cleaned grease traps - sometimes giving them limited assistance; working near quarantine waste, asbestos waste and sand blasting waste; physically moving bins; picking up rubbish bags and throwing them into bins; climbing into bins and jumping on rubbish; handling large bottles which previously carried chemicals; taking drums out of bins; visiting metal and engineering plants where metal welding occurs; visiting a fertiliser storage facility; visiting hospitals and walking past J.J. Richards' hospital waste storage facility; walking past areas where bins were being cleaned with chemicals; handling clean and unclean bins; and, scraping his arm on a bin on one occasion while shifting it. -- 7 of 9 -- 8 Mr Clarke's recounting of his level of exposure to rubbish, chemicals and the like, as claimed above, seemed to have been exaggerated to a high degree. Whether this was deliberate or accidental is not important. What is important, however, is that even if Mr Clarke did come into contact with rubbish, and the like, as frequently as he claimed his evidence has not established any link between such contact and the development of his pemphigus condition. He has not, for example, provided any evidence that he came into contact with any pesticides, herbicides etc., nor the particular types of metal vapours which have been previously linked, in the literature, to the development of pemphigus vulgaris. In this regard, the evidence of Dr Sinha was particularly relevant. Even accepting Mr Clarke's claimed exposure to rubbish, dead animals, pesticides and the like (which I have found to have been highly exaggerated) Dr Sinha was only prepared to state that "Mr Clarke's employment duties related to waste disposal might have put him at increased risk of exposure to one or more of the above cited compounds that have been associated with (the disease) in the literature.". However, Dr Sinha qualified this statement by also stating that, with the possible exception of the drug d-pencillamine, no expert could conclusively link specific environmental agents to the development of pemphigus vulgaris. Further, he also indicated that he had not seen any evidence that confirmed Mr Clarke's direct exposure to any of the pesticides or other substances reported in the literature as causing, or contributing to, the development of pemphigus. Dr Murrell asserts that there was a link between Mr Clarke's employment and the development of his pemphigus condition but I have, with respect, treated her evidence on the point with some scepticism. Dr Murrell has been Mr Clarke's treating physician for two years and has obviously become very close to her patient. Furthermore, she has acted in the role of his advocate in making special arrangements for him to be able to have IVIg injections at the John Hunter Hospital in Newcastle. More importantly however, from my perspective, Dr Murrell appears to have convinced herself that there is a clear link between working in the waste management industry and the development of pemphigus vulgaris in circumstances where she has only encountered 3 such patients and there is nothing in the literature about any similar linkages anywhere else in the world. On this point, Dr Reid - who admittedly doesn't have as much experience with the disease as either Dr Sinha or Dr Murrell - is of the view that there is no established linkage between work in the waste management industry and in the development of the disease. As he put it, from what I consider to have been a very objective view point, the mathematics are simply not there to establish the link. Further, he said, there are many thousands of people who work in the waste management industry in the world and no linkage between such work and the development of pemphigus has been observed elsewhere. I regard this comment as particularly telling in my overall assessment of this matter. In an effort to address the clear absence of any link between the onset of Mr Clarke's pemphigus condition and a specific triggering event, Counsel for Mr Clarke, Mr Wiltshire, presented a detailed and well developed submission to the effect that notwithstanding the absence of such apparent link it was the case, on the balance of probabilities, that there was some environmental trigger, or triggers, which occurred during Mr Clarke's employment with J.J. Richards that led to his pemphigus condition. Rather than attempt to summarise Mr Wiltshire's submission on this point it is best to refer to it verbatim as follows: "5.8. The question then is whether, on the balance of probabilities, the environmental trigger for the disease was contact (direct, indirect, skin breakage or airborne contact) and/or stress that arose in the course of his employment, or whether the trigger arose from some other source not connected with his employment. 5.9. It is not possible for anyone to identify the exact trigger in the appellant's case. As he has a genetic susceptibility to the disease, it is reasonable to assume that he has been susceptible all his life. In that case, it seems likely that if there trigger were something he would have encountered in his everyday life then the disease would probably have been triggered earlier. Similarly, if the trigger was something related to his sporting activities then it is extremely likely to have been triggered earlier than it was. 5.10. Each of Dr Sinha and Professor Murrell identified temporal proximity to the development of the disease to be very relevant in identifying the trigger. The trigger is most likely to have occurred within the few weeks or months preceding the symptoms. 5.11. The only major thing that had changed in the appellant's life in the few months preceding the symptoms was that he had commenced work at JJ Richards. It is also particularly relevant that, in the context of a very rare disease, Professor Murrell has had three patients who have developed symptoms within a few months of commencing work in the waste management industry. 5.12. It is possible that the trigger was something outside of the appellant's employment but in view of the large array of waste products, chemicals and unsanitary conditions to which he was exposed in his employment, as well as -- 8 of 9 -- 9 the stress, it is far more likely (again considering temporal issues) that the trigger was something connected with his employment. ... 5.15. In all of the circumstances, it is submitted that on the balance of probabilities the trigger for the appellant's disease is far more likely than not to have arisen out of or in the course of his employment.". With great respect, I think that Mr Wiltshire's submissions somewhat understate the legal position. As Kitto J. observed in Jones v Dunkel [101 CLR 298 at 305]: "One does not pass from the realm of conjecture into the realm of inference until some fact is found which positively suggests, that is to say provides a reason, special to the particular case under consideration, for thinking it likely that in that actual case a specific event happened or a specific state of affairs existed.". Further, as Commissioner Blades observed in Ian James Johnston v Q-Comp (2007) 185 QGIG 86 "While (the) onus only has to be to the standard of the balance of probabilities, the tribunal of fact must feel an actual persuasion before those alleged facts can be found to exist.". Whilst the claimed link between Mr Clarke's employment with J.J. Richards and the development of his pemphigus vulgaris is plausible it, nonetheless, remains mere conjecture that his employment was linked to the development of his condition. It remains equally plausible, according to the evidence presented, that the condition developed from an earlier exposure to one of the recognised environmental triggers or because of some exposure to a particular trigger which occurred outside of, and totally unrelated to, the work environment. In the end result, I am unable to conclude that it is more probable than not that Mr Clarke's pemphigus vulgaris condition arose out of, or in the course of, his employment with JJ Richards or that his employment was a significant contributing factor to the development of his condition. In those circumstances I dismiss the appeal. I confirm the decision of Q-COMP dated 19 January 2006 and find that Mr Clarke's application for workers' compensation is one for rejection. I reserve the question of costs. The Commission determines and orders accordingly. A.L. BLOOMFIELD, Deputy President. Hearing Details: 2007 3, 7, 10 December Released: 24 December 2007 Appearances: Mr J.J. Wiltshire, Counsel, instructed by Mr P. Koutsoukis and Ms J. Keogh of Maurice Blackburn Cashman, for the appellant. Mr P. Rashleigh, Counsel, instructed by Ms L. Booth of Q-COMP for the respondent. Government Printer, Queensland The State of Queensland 2008. -- 9 of 9 --