Chase v Workers' Compensation Regulator [2019] QIRC 195

QUEENSLAND INDUSTRIAL RELATIONS COMMISSION CITATION: Chase v Workers' Compensation Regulator [2019] QIRC 195 PARTIES: Chase, Claude (Appellant) v Workers' Compensation Regulator (Respondent) WC/2015/315 PROCEEDING: Appeal against a decision of the Workers' Compensation Regulator DELIVERED ON: HEARING DATES: 11 December 2019 28 March 2019 HEARD AT: Brisbane MEMBER: Industrial Commissioner Black ORDERS: 1. The appeal is allowed; 2. The decision of the Regulator dated 3 December 2015 is set aside; and 3. The Respondent is to pay the Appellant's costs of and incidental to this appeal to be agreed or, failing agreement, to be the subject of a further application to the Commission. CATCHWORDS: APPEAL AGAINST DECISION – physical injury diagnosed in May 2014 as the progressive transformation of germinal centres (PTGC) – appellant claimed that his condition was causally associated with his exposure as a firefighter to occupational carcinogens including perfluoroalkyl chemical components of aqueous foam firefighting compounds – consideration of other possible causes – appellant a heavy smoker – a history of neck lymphadenopathy associated with recurring dental infections. LEGISLATION: Workers' Compensation and Rehabilitation Act 2003 s 32, s 550 -- 1 of 27 -- 2 CASES: Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262 APPEARANCES: Mr D M Cormack of Counsel instructed by James Law Mr S A McLeod QC of Counsel, for the Workers' Compensation Regulator. Decision Overview [1] The appellant had been actively engaged in various fire fighting capacities between 1994 and 2002. A summary of the appellant's employment history is included in Dr Brandt's 27 May 2015 report. In terms of firefighting involvement, the appellant's areas of employment included the following: • February 1994 to January 1996: Regional Training Officer – Rural Fire Service; • January 1996 to September 2002: District Inspector – Queensland Fire and Rescue, Rural Fire Service. [2] During the course of this employment, the appellant was actively engaged in the duties of fire suppression and extinguishment, and in training in fire suppression and extinguishment. [3] In the course of performing these duties, the appellant was exposed to various carcinogenic substances including smoke, combustion products and fire extinguishment products including Aqueous Foam Fire Fighting Compounds (AFFF) containing the perflouroaklyl chemicals, perfluorooctanyl sulphonate (PFOS) and perfluorooctanoic acid (PFOA). The exposure included chemical foam exposure at the appellant's neck region. [4] Some time after his firefighting activities had ended, and in 2009, the appellant developed neck lymphadenopathy associated with a bacterial infection which arose during a dental procedure when the appellant was hospitalised due to sepsis.1 I understand that "lymphadenopathy" is a generic term for lymph node enlargement of any aetiology, benign or malignant. The painful lymph node was localised and resolved at the time. [5] An ultrasound scan of the appellant's neck taken on 14 February 2013 indicated several prominent lymph nodes. A biopsy was recommended for further evaluation. [6] An MRI scan of the appellant's neck taken on 18 December 2013 identified mild nodal enlargement, however over the next three months the appellant noticed a relatively quick increase in size in the submental and left mandibular nodal regions2. [7] The appellant's general practitioner, Dr Grigg, arranged nodal excision biopsies on 24 April 2014 and referred the appellant to Dr Robert Hensen, Consultant Haematologist, who first saw the appellant on 21 May 2014. 1 Exhibit 2 – report of Dr Hensen, 21 May 2014. 2 Ibid. -- 2 of 27 -- 3 [8] In a report prepared for Dr Grigg on 21 May 2014 (Exhibit 2), Dr Hensen stated that biopsies results were consistent with PTGC (progressive transformation of germinal centres) and reactive hyperplasia. Dr Hensen also commissioned PET/CT scans which were undertaken on 23 May 2014. These scans did not detect any node enlargement in any other body site.3 [9] Dr Hensen also said in his 21 May 2014 report, that there had been no bone pain or infections in the appellant's teeth, ears or neck region. He noted that the appellant had no prior history of cancer although he had "been a heavy smoker of twenty per day for greater than thirty years". [10] In letter to Dr Grigg on 4 June 2014, Dr Hensen said that the appellant's "suspicion is as you know that the chemical foam that the (sic) he has been exposed to as a fire fighter at the particular region of his body has been causative for these nodal changes which were quite significantly enlarged". A related concern for the appellant was a reported association between PTGC and lymphoma. [11] Given the concern at the rapid enlargement of one of the lymph nodes, and the known potential for PTGC to progress to lymphoma, Dr Hensen decided to treat the appellant with Mabthera monotherapy. [12] Dr Hensen said in a report to WorkCover on 10 April 2015 that this treatment was effective and led to a resolution of the lymph nodes which returned to normal size.4 Dr Hensen said that resolution of the lymphadenopathy was confirmed on ultrasound with normal sonographic appearances of the residual lymph nodes. [13] On 26 August 2014, Dr Griggs issued a workers' compensation medical certificate which included a diagnosis of Non Hodgkin's Lymphoma. On the same day, the applicant submitted an application for compensation to WorkCover Queensland. In his application form, the appellant said that his injury was caused by "exposure to toxic products eg Fire fighting foam" and he identified a diagnosis of "PTGC non specific lymphoma" and said that his treatment involved chemotherapy and pain management. [14] It is not known why Dr Griggs entered a diagnosis of lymphoma given that in May 2014 Dr Hensen had diagnosed the appellant's condition as PTGC. While for precautionary reasons the appellant may have been treated for lymphoma, the accepted diagnosis for the purpose of the proceedings was that entered by Dr Hensen in May 2014 of florid lymphoid hyperplasia and PTGC. [15] At the time of the proceedings in March 2019, while the appellant's condition may have remained under surveillance and while some treatment of Mabthera may have been ongoing, the appellant's condition had not altered, and it was not malignant. It is accepted that the appellant remains in the time window for the possible development of cancer, but at the time of the hearing his condition had not transformed into lymphoma. [16] On 4 February 2015, WorkCover asked Dr Hensen to provide an opinion in relation to the appellant's condition. In its communication to Dr Hensen, WorkCover had written: 3 Exhibit 5 - report of Dr Hensen, 10 April 2015. 4 Ibid. -- 3 of 27 -- 4 WorkCover Queensland is currently determining an application for compensation for Mr Chase. Mr Chase has sustained Non Hodgkin's Lymphoma which he attributes to his employment as a fire fighter, but particularly the exposure to foam chemicals. In your medical opinion do you attribute Mr Chase's exposure to foam chemicals whilst employed as a firefighter a significant contributing factor in the causation of Mr Chase's non-hodgkins lymphoma? [17] In his response to WorkCover on 10 February 2015, Dr Hensen said that the histology of the appellant's lymphadenopathy revealed PTGC which "would be consistent with exposure to chemicals or feasible to be a process driven by exposure to chemicals". He also said that the size of the lymph nodes and the high risk of transformation made intervention (treatment) of the appellant's condition appropriate. [18] In a further facsimile to Dr Hensen on 9 February 2015, WorkCover said that the appellant had reported that he had "sustained an injury as a result of exposure to Aqueous Foam Fire Fighting Compounds (AFFF) used to fight fires". WorkCover then asked Dr Hensen to provide a work-related diagnosis and asked whether the appellant's "exposure to AFFF whilst employed as a fire fighter" was a significant contributing factor in the causation of the appellant's work-related diagnosis. [19] In response to these questions, Dr Hensen diagnosed a work related injury of neck lymphadenopathy caused by PTGC, and opined that an association with occupational exposures seemed "quite likely" given that the location of the lymphadenopathy correlated with the chemical exposure site. He also said that there was a "plausible association" having regard to the case studies. [20] In a facsimile opinion prepared for WorkCover on 25 February 2015,5 Dr Hensen said that it was quite likely that the appellant's exposure to AFFF while employed as a firefighter was a significant contributing factor to the appellant's lymphadenopathy. [21] On 27 May 2015, Dr Brandt responded to a request by WorkCover to provide an opinion on the appellant's claim for compensation in relation to an injury which was "due to exposure to toxic products particularly exposure to firefighting foams whilst employed with the Rural Fire Service and Queensland Fire and Rescue between 1994 and 2002." It was Dr Brandt's understanding that the appellant claimed that his diagnosed condition (PTGC) was caused by exposure to AFFF firefighting foams (and specifically perfluoroalkyl components PFOS and PFOA) during active involvement in firefighting and training activities undertaken between 1994 and 2002. [22] Dr Brandt said in his 27 May 2015 report that in "assessing the medical probability" that the appellant's condition was causally related to exposure to PFOS and PFOA, the following questions needed to be addressed: 1. Have AFFF firefighting foams, and in particular the perfluoroalkyl components PFOS and PFOA, been classified as hazardous to humans? If so, what are the identified hazards? 2. Could Mr Chase’s exposure have led to an uptake of perfluoroalkyl chemicals? 3. What was the likely intensity and duration of Mr Chase’s exposure to perfluoroalkyl chemicals? 5 Exhibit 5 – report of Dr Hensen, 9 February 2015. -- 4 of 27 -- 5 4. Are perfluoroalkyl chemicals associated with the histopathological diagnosis identified, and if so is the site of the pathology consistent with the route of the uptake of the agents? [23] In essence, Dr Brant concluded that while the appellant had been exposed to firefighting foams during the relevant period, and while perfluoroalkyls can be absorbed through inhalation or by dermal contact, the appellant's claim should not succeed for the following reasons: • Human health effects associated with perfluoroalkyls have not been clearly established although studies have shown a potential relationship between elevated perfluoroalkyl levels and a number of health end points; • A review of the epidemiological literature disclosed that while there was an association between exposure to perfluoroalkyls and certain cancers including bladder, prostate; kidney; and testicular, there is no scientific evidence of a causal association between occupational or environmental exposure to perfluoroalkyls, and lymphatic cancer; • While perfluoroalkyls have been classified as hazardous, whether exposure leads to harm will depend on many factors including the exposure pathway, the dose and duration of exposure; • There is no scientific evidence supporting a causal association between exposure to perfluoroalkyls and the histopathological diagnosis of PTGC or any other lymphatic pathology. [24] In his 11 July 2016 report, Dr Hensen addressed the questions posed by Dr Brandt and responded to the effect that: 1. The chemicals PFOS and PFOA may be considered carcinogenetic and harmful to humans; 2. The appellant had a route and mechanism to allow high levels of chemical absorption; 3. The appellant experienced excessive levels of exposure to firefighting foams having regard to the prevalent use of foams during the relevant period (1994 to 2002) and the frequency of the active attendance in firefighting by the appellant; 4. The site of pathology (neck) is directly associated with the route of exposure (absorption by skin) and the histopathology of PTGC is entirely consistent with "a resident population of hyper-proliferative lymph nodes previously exposed to mutagenic chemicals". [25] On 16 June 2015, WorkCover determined that the appellant's claim was one for rejection. On 20 October 2015, the appellant asked the Workers Compensation Regulator to review WorkCover's decision. On 3 December 2015, the regulator confirmed WorkCover's decision. On 22 December 2015, the appellant filed a notice of appeal in the Queensland Industrial Relations Commission. -- 5 of 27 -- 6 [26] Whether the appellant's diagnosed condition was explainable by reference to any cause other than the occupational exposures was a matter for consideration. Dr Hensen had identified heavy smoking and dental infections as possible non-employment related causes: • The appellant was a heavy smoker for more than twenty years and did not stop smoking until 2014; • The appellant had previously developed neck lymphadenopathy associated with a bacterial infection from dental work in 2009. The Legislation [27] Section 32 of the Workers' Compensation and Rehabilitation Act 2003 (WCR Act) relevantly provides: "32 Meaning of injury (1) An injury is personal injury arising out of, or in the course of, employment if— (a) for an injury other than a psychiatric or psychological disorder— the employment is a significant contributing factor to the injury." Issue for determination [28] The respondent conceded that the appellant was a worker within the meaning of the WCR Act, and that he had suffered a personal injury in the form of florid lymphoid hyperplasia and PTGC of bilateral lymph nodes. [29] The ultimate matter for determination is whether the appellant's diagnosed condition of florid lymphoid hyperplasia and PTGC is causally connected to his employment pursuant to s 32 of the WCR Act. [30] It was the appellant's case that his injury was caused by his exposure to various carcinogenic substances including aqueous foam firefighting compounds during the course of his employment as a firefighter. Agreed facts [31] At the commencement of proceedings, the parties submitted an Agreed Statement of Facts in the following form: AGREED STATEMENT OF FACTS 1) The Appellant was born on 16 March 1957; 2) The Appellant was a firefighter with Queensland Fire and Emergency Services (the employer) between approximately 1994-2002; 3) The Appellant was a “worker” within the meaning of section 11 of the Workers’ Compensation and Rehabilitation Act 2003 (the Act), at all material times; 4) The Appellant was a “volunteer” within the meaning of sections 12, 14 and 15 of the Act, at all material times; 5) The Appellant was actively engaged as a firefighter with the employer and was engaged at all relevant times in the duties of fire suppression and extinguishment and training in fire suppression and extinguishment; -- 6 of 27 -- 7 6) As a firefighter with the employer, the appellant was exposed to various carcinogenic substances (combustion product and fire extinguishment products, namely smoke, foams and PFOS); 7) On or about 26 August 2014, Dr Alan Griggs, General Practitioner, issued a workers’ compensation medical certificate which diagnosed the Appellant with Non Hodgkin’s Lymphoma; 8) On or about 26 August 2014, the Appellant submitted an Application for Compensation to WorkCover Qld stating as follows: a) At question 15 – The nature of injury “suffering effects to whole of lymph system”; b) At question 16 – How did the injury happen – “exposure to toxic products eg. Fire fighting foam over period of employment”; c) At question 17 – Where did the injury happen – “at training at fire response emergencies – many locations”; d) At question 21 – Diagnosis – “PTGC non specific lymphoma’ and Treatment – “chemotherapy, pain management”; 9) Dr Robert Hensen, Consultant Haematologist, diagnosed the Appellant in or around May 2014, with florid lymphoid hyperplasia and PTGC (progressive transformation of germinal centres) of bilateral lymph nodes; 10) The Appellant sustained a personal injury, namely florid lymphoid hyperplasia and PTGC (progressive transformation of germinal centres) of bilateral lymph nodes in the neck region (the personal injury). [32] While the Agreed Statement of Facts confirmed that the appellant had been exposed to carcinogenic substances over a period of approximately eight years, the agreed statement did not include any agreement in relation to the frequency of the exposure or the intensity of the exposure. Nor did the statement clarify whether there was scope for a difference of opinion in relation to the harmful effects of perfluoroalkyl chemicals. [33] Dr Hensen had formed an opinion about frequency and intensity by references to various statements or testimonials that had been prepared by supporters of the appellant's cause. This supporting material was not tendered into the evidence, but was referenced in some detail in Dr Brandt's 27 May 2015 report. Evidence [34] Oral testimony was provided by Dr Hensen, Consultant Haematologist, for the appellant, and by Dr Brandt, Consulting Physician, Occupational and Environmental Medicine, for the respondent. [35] In addition to the oral testimony, the evidence included a significant amount of documentary evidence. Documents tendered were either marked individually as Exhibits 2, 3, or 4, or were marked collectively as Exhibit 5. • Letter from Dr Hensen to Dr Grigg dated 21 May 2014 (Exhibit 2); • Letter from Dr Hensen to Dr Grigg dated 4 June 2014 (Exhibit 3); • Facsimile from Dr Hensen to WorkCover Queensland on 10 February 2015 (Exhibit 5); • Facsimile from Dr Hensen to WorkCover Queensland on 25 February 2015 (Exhibit 4); • Report of Dr Hensen prepared for WorkCover Queensland on 10 April 2015 (Exhibit 5); • Report of Dr Brandt prepared for WorkCover Queensland dated 27 May 2015 (Exhibit 5); -- 7 of 27 -- 8 • Report of Dr Hensen dated 9 September 2015 (Exhibit 5); • Report of Dr Hensen dated 11 July 2016 (Exhibit 5); • Report of Dr Brandt dated prepared for the Workers Compensation Regulator on 10 November 2016 (Exhibit 5); • Report of Dr Hensen dated 31 October 2018 (Exhibit 5); • Report of Dr Brandt prepared for Workers Compensation Regulator on 2 February 2019 (Exhibit 5); • Additional resource prepared by Dr Brandt dealing with perfluoroalkyls dated 30 October 2018 (Exhibit 5). Progressive transformation of germinal centres (PTGC) [36] Dr Brandt described PTGC as an uncommon benign reactive lymph node process of unknown cause which often presents as asymptomatic, persistent or recurrent abnormal lymph node enlargement.6 The condition presents most commonly in the head and neck area and most commonly presents in adult males. In his evidence, Dr Hensen said that PTGC had a preponderance to present in the neck, and was present in the neck in 50% of instances. [37] PTGC is seen most commonly in lymph nodes in association with reactive follicular hyperplasia. PTGC occurs in 10% - 15% of enlarged lymph nodes with reactive follicular hyperplasia.7 [38] The pathology (of PTGC) is characterised as a nodule which is 3-5 times the size of a typical reactive follicle, with mantle zone small B-cells infiltrating the residual germinal centre.8 [39] Dr Hensen noted in his 11 July 2016 report that "PTGC is an uncommon histology". He said that PTGC is a relatively rare condition and that, in his practice, only 2% to 3% of lymph node biopsies result in a diagnosis of PTGC. I understand that the term "histology" refers to the study of the microscopic structure of tissues. [40] Dr Brandt said that PTGC was a rare condition and that its aetiology remains obscure. An obscure aetiology suggests that the causes or origins of the disease are not known or are difficult to identify. Dr Hensen's evidence was consistent. He noted the idiopathic character of the condition, and said that there were very few known associations:9 So when other patients present, although not commonly, with this condition?---Yeah. Yeah. There are very few, you know, real known associations, and it’s largely just put down to being idiopathic. So you’re either saying it’s just occurred for a reason that no one knows, or you can ascribe it to some other – the presence of some other thing in the person’s history. [41] In this context, Dr Hensen said that the main challenge was in the identification of what it was that was driving the process in the lymph node:10 6 Exhibit 5 – report of Dr Brandt, 27 May 2015. 7 Chang. 8 Hicks et el. 9 T1-30. 10 T1-15. -- 8 of 27 -- 9 … you could look at two nodes and they could both have PTGC as a response to something and you couldn’t see what’s causing the response – what’s driving it, except by looking at the patient’s, you know, clinical findings and their other medical problems to surmise, you know, what might be causing the lymph node enlargement. But for things like the atypical lymphoid proliferation or the follicular hyperplasia that they mention in the report – that can be stereotypical responses in lymph nodes to many stimuli, so it’s considered, essentially, a reactive phenomenon, and the main problem is trying to ascribe, you know, what has driven the process in the lymph node. So that’s usually the assessment that we undertake from the beginning if you’re given the diagnosis of PTGC and florid hyperplasia, or follicular hyperplasia, and you’re trying to find out, well, what process is driving that. [42] In turning his attention to the appellant's circumstances, Dr Hensen noted that the appellant's clinical history included, relevantly, dental infections and a significant smoking habit involving up to 30 cigarettes a day. It followed for Dr Hensen, that causation was to be found by reference to these factors and the appellant's exposure to occupational carcinogens:11 So looking at the case in terms of what has Claude’s exposures been? You know, there’s the dental issue. There’s the fact he was a smoker and then there’s the firefighting exposures. And trying to find out which of these has really mostly likely contributed to the emergence of the pathology, that’s been, I guess, my perspective. Occupational carcinogens [43] It was an agreed fact that between 1994 and 2002, the appellant was actively engaged as a firefighter and that whilst so engaged he was exposed to "various carcinogenic substances (combustion product and fire extinguishment products, namely smoke, foams and PFOS)". [44] It was Dr Hensen's view that firefighter studies have demonstrated "taking into account confounding factors, that fire fighters have increased rates of numerous cancers and other health risks".12 He said that, on his appraisal of the literature, "there is a growing awareness and discovery of the danger posed by the 200 plus compounds that firefighters are exposed to". [45] Dr Hensen emphasised that the exposure is not a point in time exposure but can involve high levels of intense exposure on repeated occasions over a prolonged period of time13. It was his view that occupational protection was limited in its effectiveness, and that carcinogen exposure was inevitable14. [46] In his evidence, Dr Hensen said that firefighters were exposed to a wide range of toxic chemicals and he identified combustion products, inhaled particulate matter, diesel fumes, fire-extinguishing foams, volatile organic compounds, polycyclic aromatic hydrocarbons, polychlorinated biphenyls (PCB's) and brominated and fluorinated flame retardants .15 11 T1-25. 12 Exhibit 5 – report of Dr Hensen, 11 July 2016, page 2. 13 Ibid. 14 Ibid - report of Dr Hensen, 31 October 2018, page 3. 15 Ibid, page 1. -- 9 of 27 -- 10 [47] Dr Brandt acknowledged in his evidence that the appellant had been exposed to carcinogenic substances and that associations exist between firefighters' exposure to these substances, and particular types of cancer:16 We know that a range of firefighting chemicals [indistinct] are carcinogenic. The – it’s – it’s inconclusive as to – I think there’s still some inconclusive [indistinct] literature in relation to perfluoroalkyls themselves, but there are a range of other firefighting chemicals, polycyclic aromatic hydrocarbons, etcetera, benzenes, which are definitely noted to be carcinogenic, and there are a number of cancers in firefighters for which there has been a statistically significant association identified. [48] It was Dr Hensen's evidence that it was not possible to isolate any of the various carcinogenic substances that the appellant had been exposed to in determining causation.17 It was Dr Hensen's view that all the substances were carcinogens and any one of them, or all of them, could have caused the appellant's condition. [49] Dr Brandt's evidence was generally consistent with this. He said that the studies that had examined firefighters' exposures to carcinogens did not examine the individual components making up the exposures:18 … the epidemiological studies that have been done on firefighters have been done on firefighting as a population of workers. And the reason for that is that the – we’re looking back in time at historical exposures, and for that population of workers, they didn’t have specific occupational [indistinct] exposures, so they didn’t examine every individual chemical [indistinct] exposure. So they classed firefighting as a – as an – an occupation as a whole, and, you know, if a firefighter visited a – a scene of a fire [indistinct] exposure, they were classed as exposed, and they compared them with non-exposed members of the force or other occupations. [50] It followed that, while the appellant may have been motivated by a belief that his injury was caused by exposure to perfluoroalkyl chemicals, his appeal was not prosecuted on the basis that exposure to these chemicals was, in any exclusive sense, the cause of his injury. Rather the appeal was prosecuted on the basis that a cumulative exposure to a range of occupational carcinogens over a period of eight years was the likely cause of the appellant's diagnosed condition. Perfluoroalkyls [51] In his 27 May 2015 report Dr Brandt said that concerns about perfluoroalkyl chemicals have been held for some time, and have been acted on in a preventative manner by a number of authorities: Concerns over the health and environmental impacts of foams developed in the late 1990's, focusing on the Class B synthetic foams containing PFOS and PFOA. According to the US EPA, prior to 2001 perfluoroalkyls were used to manufacture aqueous film forming foam (AFFF) used in firefighting. Over the past several years, the presence of perfluoroalkyls in non-occupationally exposed populations and wildlife has raised concerns about the environmental and health effects of perfluoroalkyls. This has resulted in facilities ceasing production or changing manufacturing practices to reduce releases and the amounts of these chemicals in their products. 16 T1-42. 17 T1-33. 18 T1-42. -- 10 of 27 -- 11 [52] Dr Brandt said that while both PFOS and PFOA were classified as hazardous, the health effects of perfluoroalkyls had not been clearly established. I accept that this evidence is broadly consistent with the literature review outcome which is illustrated by the findings of the US Department of Health and Human Services over a long period of time. In a guidance prepared in 2009 the Department had reported that while perfluoroalkyl chemicals were classified as hazardous, whether exposure leads to harm will depend on many factors including the exposure pathway, the dose, and duration of exposure.19 A subsequent guidance prepared in 2017 reported on work of the International Agency of Research on Cancer (IARC) which classified PFOA as possibly carcinogenic, and on the conclusions of the US EPA to the effect that both PFOA and PFOS are possibly carcinogenic to humans.20 [53] It is noted that there is an inconsistency in the Agreed Statement of Facts and the conclusions of studies that perfluoroalkyl chemicals are "possibly carcinogenic". The effect of the agreed statement of facts is that it is not in dispute that both PFOA and PFOS are regarded as carcinogenic substances and that the appellant was exposed to these substances during the course of his employment. There is a significant difference between the two outcomes. [54] In his 27 May 2015 report, Dr Hensen had noted that SafeWork Australia had classified PFOS as a category 2 carcinogen and a "probable human carcinogen". Category 2 probable carcinogens were defined as substances for which there is sufficient evidence to provide a strong presumption that human exposure might result in the development of cancer. If this definition were adopted, then it would reasonable to conclude that the effect of the agreed statement of facts is that it is more a matter of probability than possibility that the appellant's exposure to PFOS might lead to the development of cancer. [55] Irrespective of the carcinogenic nature of perfluoroalkyls, the US Department of Health guidance reference above stated that while perfluoroalkyls were classified as hazardous, whether exposure leads to harm will depend on many factors including the exposure pathway, the dose, and duration of exposure. The effect of Dr Hensen's evidence was that this set of criteria for harm had been satisfied in the appellant's case. He said that in circumstances where the appellant would have experienced excessive levels of exposure to firefighting foams over an extended period, the appellant's risk of harm would be very significant and at the higher end of the spectrum. [56] It was accepted that firefighters were included in the occupational groups that had recorded high blood levels of perfluoroalkyls. The 2009 Draft Toxicological Profile had noted that while PFOA was found at low levels in the blood of most people living in the USA, high levels were observed in occupationally exposed workers. [57] According to Dr Hensen (11 July 2016 report), firefighting studies had identified high levels of perfluoroalkyl chemicals in firefighters. He referenced firefighter research in California (2013), the Australian Firefighters' Health Study (2014), and the Fiskville Study (2016). He said that the studies showed that firefighters had accumulated levels of PFOS of up to 17 times the background Australian population level, and levels which persist in the body over a period of decades. 19 2009 Draft Toxicological Profile for Perfluoroalkyls. 20 Agency for Toxic Substances and Disease Registry (ATSDR). -- 11 of 27 -- 12 [58] Dr Brandt acknowledged that studies had shown a potential relationship between elevated perfluoroalkyl levels and "a number of health endpoints".21 Dr Brandt confirmed in his 10 November 2016 report that a study conducted by Rotander et al (2015) documented elevated levels of PFOS in firefighters who were previously exposed to 3M AFFF. [59] Dr Brandt said that, on his review of the literature, there appeared to be an association, particularly in high-exposure occupational groups, between exposure to perfluoroalkyls and certain types of cancer viz bladder, prostate, kidney, and testicular. [60] Dr Brandt said that no studies had been located which considered the immunological and lymphoreticular effects in humans following inhalation, oral or dermal exposure to perfluoroalkyl compounds. [61] Dr Brandt also said that he could not find "evidence of a statistically significant causal association between occupational or environmental exposure to perfluoroalkyls and lymphatic cancer, in particular Hodgkin lymphoma which may be associated with PTGC". Firefighting studies [62] Consideration of firefighting exposures included a review by Dr Brandt of a number of firefighting studies which were referenced in his 27 May 2015 report: • Cancer risks among firefighters (Le Masters) (2006); • Study of cancer in California firefighters (2007) (Bates); • Evaluating causality for occupational cancers: firefighters (2007) (Guidotti); • Cancer incidence among male Massachusetts firefighters (2008) (Kang); • Queensland Fire Fighters' Cancer Incidence Study (2009); • International Agency for Research on Cancer (IARC) Monograph on the evaluation of carcinogenic risks to firefighters (2010); • Cancer incidence among firefighters (2014) (Pukkala); • Fiskville Firefighters Health Study (2014); • Australian Fire Firefighters' Health Study (2014) (Monash Centre for Occupational and Environmental Health). [63] These studies were predominantly concerned with the identification of elevated cancer risks among firefighters and did not include consideration of any association between exposure to occupational carcinogens and PTGC. [64] It was accepted that published studies and meta-analyses had observed a statistically significant association between firefighting (generically) and a number of types of cancer. Dr Brandt said that several studies had shown an increased risk of testicular cancer, prostate cancer, Non-Hodgkin lymphoma, and multiple myeloma. There was also some evidence that firefighting is associated with leukaemia, malignant melanoma, mesothelioma, and cancers of the buccal cavity/pharynx, stomach, colon, rectum, skin, brain and bladder. [65] While there was an association between occupational exposures and lymphatic cancers, it was relevant that the association was with non-Hodgkin lymphoma, and not Hodgkin 21 Exhibit 5 – report of Dr Brandt, 27 May 2015, page 28. -- 12 of 27 -- 13 lymphoma. The distinction was considered significant by Dr Brandt because it was accepted that PTGC was most commonly associated with an uncommon subtype of Hodgkin lymphoma, Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL) and that PTGC was more rarely associated with Non-Hodgkin lymphomas. [66] The exclusion of Hodgkin lymphoma from the risk profile of firefighters was, on Dr Brandt's evidence, supported by the provisions of presumptive legislation where it existed in Australia22. Dr Brandt said that presumptive legislation covered only one class of lymphatic cancer, non-Hodgkin lymphoma. He said that for non-Hodgkin lymphoma, a minimum qualifying period of 15 years was required which meant that, at the time of diagnosis, there needed to be a preceding history of exposure as a firefighter with substantial involvement at firefighting scenes over a period of 15 years. [67] While Dr Hensen saw a probable association between firefighting exposures and PTGC, Dr Brandt relied on the literature to conclude that the scientific evidence did not support a causal association between a firefighters’ occupational exposure to hazardous chemicals and a process which may result in absorption and antigenic stimulation within regional draining lymph nodes leading to hyperplasia/PTGC. [68] It is not in dispute that the transformation from PTGC might not occur for many years after PTGC was diagnosed, and potentially up to fifteen years. Statistically, and on the evidence provided by the case studies, there is a one in three chance that the appellant's diagnosed condition will progress to lymphoma some time over a period of ten to fifteen years and perhaps longer. The appellant's age is a factor contributing to this degree of likelihood. Literature review [69] In broad terms, the following areas of interest in the literature were reviewed: • A review of the literature considering the harmful effects on humans of perfluoroalkyl chemicals in either an environmental or occupational setting. More specifically the question to be answered was whether the literature review supported a finding that the appellant's condition could have been caused by exposure to PFOS/PFOA; • A review of the literature considering the harmful effects of occupational carcinogens on firefighters as an occupational group. The predominant focus of these studies was not to consider whether occupational exposures caused PTGC. Rather these studies identified the relative risk of firefighters contracting cancers in comparison with other occupational cohorts, or the population in general; 22 On 17 September 2015, the Queensland Parliament passed the Workers’ Compensation and Rehabilitation and Other Legislation Amendment Act 2015 (the Act). Amendments introduced by the Act provide that Queensland firefighters who have been diagnosed with one of 12 specified cancers (including non-Hodgkin lymphoma) and have been employed for the respective qualifying period in an active firefighting role, then their cancer will be deemed to be work related for the purposes of accessing workers’ compensation benefits. -- 13 of 27 -- 14 • A review of literature dealing with a potential association between PTGC and lymphoma, principally a subtype of Hodgkin lymphoma. [70] Predominantly, the research around perfluoroalkyls and firefighter studies was completed by Dr Brandt, while the studies dealing with a potential association between PTGC and lymphoma were for the most part studies included in Dr Hensen's 18 October 2018 report. [71] The appeal was primarily defended on the premise that the available scientific or medical evidence did not support a conclusion that the appellant's condition was caused by either a firefighters' generic exposure to occupational carcinogens, or to any environmental or occupational exposure to perfluoroalkyl chemicals. [72] For the respondent, neither the literature relating to perfluoroalkyls nor the literature relating to firefighters, provided any evidence of an association between PTGC and the appellant's exposure to occupational carcinogens. For the appellant, the literature in these areas was relied on to demonstrate that carcinogenic substances that firefighters were exposed to during the course of their employment were harmful, and to support a finding that carcinogenic substances could have caused the appellant's diagnosed condition. The association between PTGC and lymphoma was of interest to the appellant because Dr Hensen regarded PTGC as a potential precursor to lymphoma or an incipient lymphoma risk. PTGC and lymphoma [73] It was accepted that there was an association, although not a scientifically proven nexus, between PTGC and lymphoma, and most commonly with a subtype of Hodgkin lymphoma. It was also accepted that the appellant's diagnosed condition might progress to lymphoma. [74] There was also some level of agreement about an association between occupational exposures and lymphoma. It was not in dispute that firefighting studies indicated an association between generic occupational exposures and lymphoma, but there was a difference in the evidence about whether there was any association between perfluoroalkyl chemicals and lymphoma. [75] Dr Brandt stated at page 29 of his 27 May 2015 report that his review of the published epidemiological literature did not locate evidence of a statistically significant causal association between occupational or environmental exposure to perfluoroalkyls and lymphatic cancers (in particular Hodgkin lymphoma which may be associated with PTGC), 23 an association was shown to exist between the generic exposures of firefighters and lymphatic cancer. [76] Dr Hensen however said in his 11 July 2016 report that the C8 Health Project Study had found a probable positive link between PFOS/PFOA and a number of diseases including thyroid disease, cancer of the testes, and non-Hodgkin lymphoma. 23 Exhibit 5 – report of Dr Brandt, 27 May 2015, page 28. -- 14 of 27 -- 15 [77] Particularly given the high rates of transformation from PTGC to lymphoma in the appellant's age group,24 Dr Hensen saw PTGC as a precursor to malignant disease or a condition from which malignant disease evolved. [78] In his 11 July 2016 report, Dr Hensen opined that the appellant's PTGC could be considered an incipient lymphoma risk which was associated with firefighting exposures including PFOS and PFOA: PFOAS and PFOA exposures have been associated with lymphoma development, and Mr Chase’s nodal histology may be considered a potential pre-cursor or incipient lymphoma-risk in his age group, and nodal clinical size and behaviour: thus not necessarily a benign entity. [79] In was in this context that Dr Hensen proposed that the question to be answered should not be limited to whether there was a causal nexus between occupational carcinogens and PTGC, but might be more accurately framed as whether exposure to carcinogenic substances was likely to have led to "the evolution of neoplastic disease".25 [80] It was Dr Hensen's evidence that PTGC is a co-existing nodal pathology and lymphomas do emerge from it.26 He said that PTGC has been noted to either precede, co-exist with, or follow NLPHL in up to 30% of cases.27 He said that lymphomas can be detected in PTGC and that a recurrence of NLPHL can be detected after lymph nodes with PTGC had been treated.28 He also said that the histology between NLPHL and PTGC was "strikingly similar". It was his evidence that:29 … they have found lymphomas present in PTGC nodes of different kinds, and they’ve also shown an increased risk of those lymphomas – in the case of nodular lymphocyte predominant Hodgkin lymphomas they’ve shown that it will relapse more likely in the PTGC area of the node as well. So there’s this association between the conditions that causes us concern, and we know that there are transformative events occurring in the PTGC clones. So there are mutations that are happening in the genes that drive their growth and makes them dysregulated, but actually capturing the point when a particular cell becomes a lymphoma is very, very difficult. [81] Dr Hensen said in his 31 October 2018 report, that "there is evidence for clonal progression and lymphomagenesis occurring in lymph nodes that are previously diagnosed histologically as FH/PTGC or else both pathologies may be evident in the same sample". [82] This discussion raised the possibility that lymphoma and PTGC may share the same causal connection. Dr Brandt acknowledged the possibility, but said while there appeared to be an association between PTGC and a subtype of Hodgkin lymphoma, there was uncertainty about whether both conditions shared a "common causal connection".30 [83] While it was accepted that any association between PTGC and lymphoma was most commonly an association with a subtype of Hodgkin lymphoma, Dr Hensen described in 24 Ibid – report of Dr Hensen, 9 September 2015, page 1. 25 Ibid – report of Dr Hensen, 11 July 2015, page 2. 26 Ibid – report of Dr Hensen, 31 October 2018, including Table 1 – summary of literature. 27 Ibid – report of Dr Hensen, 31 October 2018. 28 T1-25. 29 T1-34. 30 T1-47. -- 15 of 27 -- 16 his 11 July 2016 report an evolution to B-cell and T-cell lymphomas, which are subtypes of non-Hodgkin lymphoma. Dr Brandt's 12 February 2019 report also noted a case of "occasional co-occurrence" between PTGC and in situ follicular lymphoma, which is a type of non-Hodgkin lymphoma. [84] The question to be answered in the appeal is whether, on the balance of probabilities, the appellant's exposure to occupational carcinogens has caused the development of PTGC. It is not in dispute that PTGC is a benign condition or that it is a condition or entity that is separately identifiable from lymphoma. While there is a possibility of a common causal connection, there is insufficient evidence to support a finding to this effect. Whether PTGC is a precursor to malignancy, or whether PTGC may progress to lymphoma, does not materially assist in answering the question of whether PTGC is causally connected with occupational exposures. Respondent's case [85] The respondent relied principally in its defence of the appeal on conclusions reached by Dr Brandt as a result of his review of the literature and which resulted in the formulation of four reports either at the request of WorkCover or the regulator. While not pressed with any vigour, the respondent also raised the possibility that the appellant's condition could have been caused by a dental infection or by smoking. 27 May 2015 [86] Dr Brandt's first report prepared on 27 May 2015 involved a review of the literature in relation to what he understood to be the appellant's claim at the time. That is, the appellant said that his diagnosed condition of PTGC had been caused by exposure to AFFF and specifically the perfluoroalkyl components of these firefighting foams. While this report was focused mainly on the harmful effects of perfluoroalkyl chemicals, Dr Brandt also included an extensive review of studies examining the incidence of cancer in firefighting cohorts. [87] In his report, Dr Brandt concluded, from his perusal of the literature, that he was not able to locate any published epidemiological studies investigating the association "between exposure to chemical hazards and the pathogenesis of PTGC". This result supported his mechanistic opinion that perfluoroalkyl chemicals were not associated with the histopathological diagnosis of PTGC. [88] In considering the harmful effects of perfluoroalkyls, Dr Brandt said that the literature showed that there appeared to be "an association between exposure to perfluoroalkyls particularly in high-exposure occupational groups" and bladder, prostate, kidney and testicular cancer. He said that there was no evidence supporting an association between occupational or environmental exposure to perfluoroalkyls and lymphatic cancers. [89] In terms of causation, Dr Brandt said, at page 29 of his report, that "based on literature review", a causal association between the appellant's exposure to foams and perfluoroalkyls, and PTGC, was unlikely. In so concluding Dr Brandt had considered the toxicology of perfluoroalkyls, the carcinogenicity of perfluoroalkyls, epidemiological studies on perfluoroalkyls, and other materials relevant to perfluoroalkyl chemicals. -- 16 of 27 -- 17 [90] Dr Brandt's review of firefighting studies resulted in conclusions that generic firefighting exposures were associated with a number of types of cancer including non-Hodgkin lymphoma. Dr Brandt agreed that elevated levels of PFOS had been found in firefighters who had been exposed to AFFF. Dr Brandt - 10 November 2016 [91] Dr Brandt had been asked by the Regulator to provide a supplementary report to his 27 May 2015 report which included a review of Dr Hensen's report dated 11 July 2016. In this report, Dr Brandt: • Concurred with Dr Hensen's description dealing with a dermal exposure pathway relating to the potential absorption by firefighters of perfluoroalkyl chemicals; • Noted the report of Rotander (2015) which had documented elevated levels of PFOS in firefighters who had been exposed to AFFF; • Deferred to Dr Hensen's subject matter expertise in his description of the pathological processes of PTGC and its potential pathway to lymphoma while noting that the published literature suggested that PTGC was an uncommon disorder for which the aetiology remains obscure; • Noted that the C8 Health study which investigated the association between the cumulative exposure to PFOA and increased rates of cancer, did not identify any probable link with cancers other than testicular and kidney cancer; • Questioned Dr Hensen's view that there was a probable positive link between PFOS/PFOA and non Hodgkin lymphoma on the basis that the research relied on did not provide a statistically significant result; • Noted that while the Fiskville Firefighters Study may not have been sufficiently powered to examine subtypes of lymphoid and haematopoietic cancers, there was no statistically significant excess of cases of lymphoid and haematopoietic cancers; • Noted that the final report of the Australian Firefighters' Health Study had not found any statistically significant elevation in the incidence of Hodgkin's disease and non-Hodgkin lymphoma in firefighters. [92] Dr Brandt concluded his report with a paragraph headed "Opinion". In expressing his opinion, he said that after reviewing Dr Hensen's report and reviewing his own report in the context of Dr Hensen's report: • He believed that there remained uncertainty as to whether or not the appellant's exposure to PFOS/PFOA has contributed to the pathogenesis of the appellant's PTGC. • Stated that he was unable to resolve from a pathophysiological and mechanistic process, the question of whether and how the chemical exposures "have resulted in the pathological change leading to PTGC" in the appellant's cervical lymph nodes; • Stated that there needed to be a clear pathological process, underpinned by supportive animal studies and/or human epidemiological evidence for the "putative specific chemical exposures to reach the threshold of being a significant contributing factor". -- 17 of 27 -- 18 Dr Brandt - 30 October 2018 [93] In this report, Dr Brandt included additional references related to perfluoroalkyls. These literature extracts do not appear to alter any opinion arising from the main body of work referenced in earlier reports. Dr Brandt - 12 February 2019 [94] In this report, Dr Brandt reviewed literature references included in Dr Hensen's 31 October 2018 report, and considered some additional literature dealing with the health effects on humans of perfluoroalkyl chemicals. Most of these additional literature items had been discussed in Dr Brandt's 30 October 2018 report and all items dealt with the potential harmful effects of perfluoroalkyls. [95] Dr Brandt reviewed twenty three pieces of literature referenced in Dr Hensen's 31 October 2018 report. Of these, he considered that two items of literature were not relevant to the matters in issue. On my review of the other twenty one items, all but two were principally focussed on the association between PTGC and a subtype of Hodgkin lymphoma. The remaining two items involved a general discussion about PTGC including its aetiology. [96] On pages 35 to 37 of the report, Dr Brandt summarised his opinion on the matters in issue. While principally considering the association between PTGC and perfluoroalkyls in his earlier reports, he correctly identified the broader question in this report when he said that the appellant attributed his condition to "hazardous chemical exposures during his front line firefighting/training activities between 1994 and 2002, including exposure to firefighting foams and in particular the perfluoroalkyls PFOS and PFOA". In this regard Dr Brandt proceeded to conclude that there was "no reported literature evidence of causal association between occupational or environmental exposure to perfluoroalkyls or firefighting activities (as a generic indicator of exposure) and PTGC". [97] Dr Brandt stated that no studies had been located regarding "immunological and lymphoreticular effects in humans following inhalation, oral, or dermal exposure to perfluoroalkyl compounds", and that no studies had been located regarding cancer effects in humans following dermal exposure to perfluoroalkyl compounds.31 [98] In terms of causation, Dr Brandt concluded that after reviewing all the documentary evidence, including Dr Hensen's reports, he was unable to locate "any scientific evidence in support of a (sic) medically consistent causal relationship" between the appellant's firefighting activities, including exposure to perfluoroalkyls, and the development of PTGC. [99] Dr Brandt said that "none of the cited articles provide information that could resolve from a pathophysiological and mechanistic process, the question of whether and how exposures to chemicals during firefighting activities (including perfluoroalkyls) resulted in the pathological change leading to PTGC in Mr Chase's cervical lymph nodes". 31 Exhibit 5 – report of Dr Brandt, 12 February 2019, page 35. -- 18 of 27 -- 19 Other possible causes [100] While Dr Hensen acknowledged that either smoking or a dental infection may have caused the appellant's diagnosed condition, he concluded that other factors could not "explain the PTGC in the neck nodes or could exert the same biochemical influence on Claude's neck nodes to cause PTGC in comparison to the fire combustion products and PFOS/PFAS foams". Dental infection [101] The appellant previously had neck lymphadenopathy associated with a bacterial infection from dental work in 2009. However, the condition had resolved relatively quickly and was not considered to have any ongoing relevance. There was some suggestion in the evidence of a further concern about dental infection, but in circumstances where neither Dr Grigg was called to give evidence in the proceedings and where neither his medical records nor any records of dental treatment were tendered into the evidence, I decline to attach any significance to this suggestion. [102] Dr Hensen said that it was possible that a dental infection could cause PTGC, but that it would not be a typical stimulus to cause PTGC. While he conceded that it was conceivable that dental infections could have been the source of the appellant's PTGC, he excluded dental infections as a possible cause of the appellant's PTGC for a number of reasons. [103] Firstly, he said that he had never seen significant dental pathology that led to lymph nodes of the size present in the appellant's case and which was not associated with tenderness. He said that tenderness was not present in the appellant's case. Dr Hensen said that the appellant's lymph nodes had resolved by December 2014 and had been consistently painless throughout. He said that the appellant never complained to him of soreness or pain. Secondly, he said that usually the PTGC resolves once the dental problem has been solved. Finally, he said that PTGC was not commonly reported with bacterial stimulation. Smoking [104] While Dr Hensen said that smoking introduces carcinogens into the body, and while it was feasible that smoking could have been causally associated with the appellant's PTGC, he discounted smoking as a factor because no evidence of an association between smoking and PTGC had been revealed in studies conducted into the harmful effects of smoking. [105] The effect of Dr Hensen's evidence was that given the size of the smoking population and the number of studies around the harmful effects of smoking, if there were an association, he would have expected that it would have been identified already. But he said that he could not find any evidence in the literature of an association between smoking and PTGC. The scale and size of the smoking studies was to be contrasted with the paucity of research into PTGC. -- 19 of 27 -- 20 [106] It was in these circumstances that Dr Hensen opined that the appellant's previous smoking habit was "not considered a significant contributing factor in the development of PTGC, but could conceivably lower the threshold for tumour development".32 [107] No evidence was adduced by the respondent to contradict Dr Hensen's fundamental conclusion that while smoking and dental bacteria may have caused PTGC, it was more likely that the condition had been caused by exposure to carcinogenic substances. [108] While the respondent submitted that it was inconsistent for Dr Hensen to question the reliability of the literature reviews around the association of PTGC with occupational carcinogens and yet to rely on the literature to support his reasoning that PTGC was not associated with smoking, I am not inclined to endorse the criticism. [109] Dr Hensen had identified many reasons why he considered that the literature review associated with PTGC and occupational carcinogenic exposure should not be considered determinative. It was consistent for him to differentiate smoking in that, unlike PTGC, this disease had been subject to extensive research and many studies. [110] There was no significant challenge to the veracity of Dr Hensen's evidence in discounting smoking and a dental infection as a cause of PTGC. The respondent adduced no evidence to support a conclusion that the appellant's PTGC may have been caused by smoking or a dental infection, nor did Dr Brandt advance any contradictory view in his written reports or in his evidence in the proceedings. Appellant's case [111] The appellant relied on two fundamental propositions. Firstly, that there were limitations on what conclusions could be drawn from the literature review and that the literature review should not be considered determinative. [112] Secondly that the specialist haematological evidence should be preferred to theoretical or mechanistic evidence. The effect of the appellant's position was that despite Dr Brandt's conclusions on a literature review, there was convincing haematological evidence of a process which most likely explained the appellant's condition and established a causal connection with his occupational exposure to carcinogens. [113] It was submitted that Dr Hensen was a clinically experienced haematologist who specialised in lymphadenopathy and cancers. Further, Dr Hensen was the only haematologist who had been called to provide evidence in the proceedings. Occupational exposures [114] Dr Hensen said that firefighters experience some of the highest levels of occupational carcinogen exposure "and when presenting with progressive nodal changes one is obliged to consider them differently".33 It was his opinion that the appellant's occupational exposures to carcinogenic substances were "likely causative agents in his nodal pathology". 32 Ibid – report of Dr Hensen, 31 October 2018, page 2. 33 Ibid – report of Dr Hensen, 11 July 2016, page 5. -- 20 of 27 -- 21 [115] Dr Hensen emphasised that the appellant's exposure to carcinogenic substances was not a point in time exposure, but involved high levels of intense exposure on repeated occasions over a prolonged period of time (11 July 2016). [116] Dr Hensen concluded in his 2018 report that there was "ample exposure to fire combustion products and PFOS/PFAS foams, and the balance of probabilities, this exposure as a firefighter was a significant contributing factor in the development" of the appellant's PTGC. [117] Dr Brandt accepted that the appellant had been exposed to a range of chemicals (other than perfluoroalkyls) which were carcinogenic and in respect of which associations with a number of cancers had been identified. Mechanism of injury [118] The effect of Dr Hensen's evidence was that firefighting PPE could not provide full or sufficient protection from occupational carcinogens. Dr Hensen explained that the typical protective clothing worn by firefighters "was relatively exposed at the neck allowing chemicals to enter at this site".34 [119] Dr Hensen said that there was a route and a mechanism for high levels of dermal absorption of chemicals. In his 11 July 2016 report, Dr Hensen said: The site of pathology (neck) is directly associated with the route of exposure (absorption by the skin) and the histopathology of PTGC and florid lymphoid hyperplasia is entirely consistent with a resident population of hyper-proliferative lymph nodes previously exposed to mutagenic chemicals. [120] Dr Hensen said that the location of the appellant's lymphadenopathy (neck) correlated with the "chemical exposure site". He said that the appellant's "history of recurrent exposure" in the neck region over an extended period "with a mechanism for increased cutaneous absorption is consistent with toxin exposure as the likely cause for the changes in his neck nodes".35 [121] Dr Hensen said that while dermal absorption generally occurs at a slow rate, the temperatures experienced in firefighting would have substantially increased the rate of absorption. In his 11 July 2016 report he said that "absorption increases by 400% for every 5 degree Celsius temperature rise especially through the permeable neck region where combustible products and soot deposit". [122] Dr Brandt agreed that the appellant was likely to have been exposed to PFOS and PFOA during his employment in the fire fighting field. He also accepted that perfluoroalkyls can be absorbed through the skin and accepted that dermal exposure was a potential pathway for firefighters who had used firefighting foams.36 Dr Brandt said that while dermal absorption of perfluoroalkyls was generally expected to occur at a low rate, he agreed that "in a thermally demanding environment", and an environment where a firefighter was working hard, the rate of absorption would increase.37 34 Ibid – report of Dr Hensen, 9 September 2015 at page 1. 35 Ibid. 36 Ibid – report of Dr Brandt, 10 November 2016, page 1. 37 T1-40. -- 21 of 27 -- 22 Reasoning [123] This is a case of significant complexity in which a determination has to be made about a condition of idiopathic character and obscure aetiology. It is not a case where determinations about causation to the scientific standard are possible. No medical or scientific proof is to be found in the literature review of the causal association claimed to exist by the appellant. However, the appellant's case is that the expert haematological evidence is sufficient evidence to support a balance of probabilities finding that his occupational exposure to carcinogenic substances did significantly contribute to the development of his diagnosed condition. [124] No studies have been conducted to examine associations between PTGC and potential causative factors. Further in studies which had considered relevant occupational and environmental hazards, PTGC had not been identified. The appellant's particular circumstances complicated matter further. The effect of Dr Hensen's evidence was that the "multitudinous exposures to different carcinogens over time" made it difficult "if not impossible to establish with scientific certainty the causal relationship between a given exposure and an emergent malignant process".38 [125] It seems to me that, in this context, some assistance or guidance is provided by the observations made by Spigelman CJ in Seltsam Pty Ltd v McGuiness39 in discussing the legal implications of a matter in which medical science was not able to give clear and direct evidence of a causal relationship:40 93 With respect to many diseases, medical science is able to give clear and direct evidence of a causal relationship between a particular act or omission and a specific injury or disease. There are, however, fields of inquiry where medical science is not able to give evidence of that character. There are cases in which medical science cannot identify the biological or pathological mechanisms by which disease develops. In some cases medical science cannot determine the existence of a causal relationship. Such a state of affairs is not necessarily determinative of the existence or non-existence of a causal relationship for purposes of attributing legal responsibility. Epidemiological evidence may be able to fill the gap. It is of particular potential utility in the field of what is often referred to as “toxic torts”, especially in case of diseases with long latency periods. 94 In circumstances where the aetiology of a disease is uncertain, or subject to significant scientific dispute, the Courts are not thereby disenabled from making decisions as to causation on the balance of probabilities. As Herron CJ said in EMI (Australia) Ltd v Bes [1970] 2 NSWR 238 at 242: "Medical science may say in individual cases that there is no possible connection between the events and the death, in which case, of course, if the facts stand outside an area in which common experience can be a touchstone, then the judge cannot act as if there were a connection. But if medical science is prepared to say that it is a possible view, then, in my opinion the judge after examining the lay evidence may decide that it is probable. It is only when medical science denies that there is any such connection that the judge is not entitled in such a case to act on his own intuitive reasoning. It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me that no medical witness states with certainty the very issue which the judge himself has to try." 38 Exhibit 5 – report of Dr Hensen, 11 July 2016, page 2. 39 Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262. 40 Ibid, 280-285. -- 22 of 27 -- 23 [126] Dr Brandt's literature review conclusions were not in dispute at least at the headline level in that Dr Hensen accepted that the literature review did not provide any evidence of a causal connection between occupational exposures and the subsequent diagnosis of PTGC.41 It followed in the respondent's submission that in circumstances where the medical or scientific literature had not established any association between PTCG and the appellant's exposure to occupational carcinogens, the Commission would be reluctant to accept Dr Hensen's opinions about causation. [127] The basic difference between the experts was that, for Dr Brant, the omission from the literature review of evidence of an association between PTGC and occupational exposures was sufficient to warrant a theoretical or mechanistic conclusion that it was unlikely that the appellant's PTGC was caused by the exposures. Dr Hensen however did not accept that the literature review adequately resolved the matters in issue. He considered that conclusions drawn from the literature review were not the result of extensive research into the pivotal issue, but rather was a result of inferences drawn from an absence of studies into that issue. From a haematological standpoint, Dr Hensen believed that there were sound reasons for a conclusion that occupational exposures were the most likely cause of the appellant's condition. [128] The effect of Dr Hensen's evidence was that it was not unexpected that the literature did not include any consideration of the association between PTGC and occupational exposures, nor that studies into associations between PTGC and occupational carcinogens had not been conducted: 42 PTGC is considered a benign condition and not a malignancy in itself which explains why there has not been a great deal of interest in the condition in terms of scientific studies. It would explain why PTCG is under represented in the literature series. It is also not a major focus for the registries that are conducted for firefighters. The condition is also transient and it does not necessarily get reported and captured. [129] Dr Hensen also questioned the viability of future studies to resolve the issue in dispute for a number of reasons. Firstly, because PTGC was a rare condition and not considered a malignant condition, there was not a lot of interest in conducting studies. Secondly the efficacy of any studies started was doubted because of the transient nature of the condition. Finally, even if some studies were commenced, he thought it unlikely that sufficient studies would be completed to enable statistically significant scientific benchmarks to be met. [130] Dr Brant acknowledged that because PTGC was a relatively rare condition there was a lack of specific literature. He said that when he reviewed the firefighting studies he did not find any reference to PTGC. It was not identified as a condition associated with the occupational hazards of firefighting and he did not know of any study commissioned to investigate the incidence of PTGC in firefighters. He said because it was a benign condition it had not been included in the studies on occupational cancer. He agreed that in cases where PTGC was found to have co-existed with Hodgkin's lymphoma, correlation and causation would be more difficult to ascertain. 41 T1-10. 42 Ibid. -- 23 of 27 -- 24 [131] Dr Hensen said that the likelihood of a study being powered adequately to detect an association with PTGC was low given that PTGC was not a common diagnosis and because of the transient nature of the condition. In this latter respect, Dr Hensen said that PTGC may "either resolve spontaneously or develop further to other lymphomas which are more established morphological entities that will completely efface the nodal architecture erasing the histological presence of PTGC". [132] Dr Brant said in his evidence that he could not find any evidence in the literature which identified an exposure to chemicals as an accepted cause or pathway for PTGC. In his 10 November 2016 report, Dr Brant opined that there remained uncertainty as to whether or not the appellant's exposure to PFOS/PFOA "has contributed to the pathogenesis of the appellant's PTGC". He said that he was unable to resolve from a pathophysiological and mechanistic process, the question of whether and how the chemical exposures "have resulted in the pathological change leading to PTGC" in the appellant's cervical lymph nodes. [133] In his 12 February 2019 report, Dr Brant reiterated this proposition and said that the literature did not include information which could resolve whether and how exposures to chemicals (including perfluoroalkyls) during firefighting activities resulted in the pathological change leading to PTGC in the appellant lymph nodes. [134] While it is accepted that the literature did not provide the answers to the questions raised by Dr Brant, Dr Hensen did address the same or similar issues in his 31 October 2018 report and in his testimony in the proceedings. In so doing Dr Hensen accepted that he was expressing opinions which had not been endorsed in the literature and in respect of which there had not been scientific findings. However, despite the absence of studies on the subject and despite the absence of scientific and medical evidence of an association between occupational exposures and PTGC, he believed that the idea that exposure to occupational carcinogens might lead to the appellant's nodal pathology was sound at a mechanistic or theoretical level. 43 Further, Dr Hensen opined that these circumstances do not prevent him from arriving at a conclusion that the exposures were the likely cause of the appellant's condition.44 … I can’t say that PTGC’s been found in the case series that – that have been put in the – in the folder, only that it makes perfect sense to me, as a haema – haematologist – that these carcinogen exposures lead to the mutagenic events in the node or to the constant antigen stimulation that leads to hyperproliferation of a node in a way that’s different to, for some reason, other things in Claude’s life. [135] In submissions, the appellant said that Dr Hensen had provided a sound mechanistic pathological explanation of the processes the lymph nodes undergo when reacting to the carcinogenic substances that the appellant was exposed to during the course of his employment as a firefighter. [136] There was significant discussion in the proceedings about whether anything turned on the potential association between PTGC and a particular type of lymphoma. For my part however the questions to be answered in determining the appeal do not require me do decide whether there was such an association, and if so, what implications should be 43 T1-10. 44 T1-29. -- 24 of 27 -- 25 drawn from the association. I accept that when it came to causation, Dr Hensen did identify the correct question when he said that the key challenge was in identifying what it was that was driving the process in the appellant's lymph nodes45 and that the question was whether the appellant's exposure to occupational carcinogens "was a significant contributor to his development of his lymph node histological changes …"46 [137] I also accept that in addressing these questions, Dr Hensen set out in significant detail his reasoning for concluding that particular pathological processes had contributed to or caused the development of PTGC: • It was Dr Hensen's evidence in the proceedings that: But, mechanistically, the exposures can quite conceivably lead to PTGC. It makes a lot of sense. It’s exactly how a lymph node responds reactively to different compounds, so it’s not a unique or a surprising idea that a lymph node, you know, would respond to these kinds of carcinogen loads in this way because it’s just a stereotypical response to different react – you know, a reaction to different stimuli.47 • Dr Hensen said in his 31 October 2018 report that in a context of the appellant's "considerable and repetitive carcinogen exposure", he considered the appellant's emergent lymphadenopathy to be significantly contributed to by "his chemical exposures as a firefighter either by increased antigen stimulation of the lymph nodes or occult mutagenesis". • In the same report, Dr Hensen said that the carcinogenic nature of the compounds in firefighting work "cause DNA mutagenesis which cells rapidly work to repair, when these mechanisms fail and when the mutations are in oncogenes – those related to cell cycle control and DNA repair, lymphomagenesis is initiated and may require a number of oncogenes to become dysregulated to progress in evolution to malignancy". • The effect of his evidence in the proceedings was that frequent exposure to carcinogenic substances over a long period of time meant that carcinogens are present in the body for long periods and once absorbed they remain in the body "persistently stimulating the lymphocytes for a long time".48 • Dr Hensen further said that although PTGC is not fully understood in terms of aetiology, it was incorrect "to presume that the exaggerated lymphoid processes which are present and understood in terms of lymphoid responses to persistent stimulation are not being substantially influenced by a carcinogen load over time at the very site of absorption across the skin into lymph nodes draining this region". [138] The determination of the appeal involves a careful balancing of the literature review outcomes on the one side of the scales, and the reasoning of Dr Hensen to the effect that an association between PTGC and occupational carcinogens was sound and defensible, 45 T1-15. 46 Exhibit 5 - report of Dr Hensen, 31 October 2018, page 3. 47 T1-27. 48 T1-31. -- 25 of 27 -- 26 on the other side of the scales. In circumstances where the fundamental conclusions on the literature review were not in dispute, the focus turns to the reasoning of Dr Hensen and whether the medical or scientific explanations provided are sufficient to support a balance of probabilities finding that exposure to occupational carcinogens was a significant contributing factor in the development of the appellant's PTGC. In this regard it is significant that no independent specialist haematological evidence was called by the regulator and, in areas where the literature did not impose adequate restraint, the opinions of Dr Hensen were generally unchallenged. [139] On my appreciation of Dr Brant's approach, his opinions are constrained by conclusions open on the literature review. He does not directly take issue with opinions expressed by Dr Hensen except where he disagrees with Dr Hensen's interpretation on the literature. Everything is tested against it's consistency with the literature review or its endorsement by the literature. A consequence of this approach is that Dr Brant does not purport to be in a position to challenge opinions given by Dr Hensen which rely for authority on Dr Hensen's specialist expertise as a haematologist. These observations imply no disrespect to Dr Brant, but simply distinguish between the areas of speciality of the expert witnesses and demark the areas in which authoritative comment may be made. Conclusion [140] The omission from the literature review of studies establishing an association between PTGC and occupational exposures meant that the literature provided no definitive answer to the question to be answered in determining the appeal. [141] While I accept that the studies do not assist the appellant's cause, neither are they fatal to the appellant's prospects, and there are significant reasons why Dr Hensen's evidence around causation should be preferred to the conclusions drawn from the literature by Dr Brandt. [142] The idiopathic nature of the diagnosed condition, the rare and transient nature of the condition, and the non-malignant status of the condition, provide explanations for why PTGC had not been identified in the studies, particularly the firefighting studies. It is also a consideration that the efficacy or viability of conducting future studies specifically directed at examining the association between PTGC and carcinogenic exposures, is not clear. In the circumstances, there is a doubt around whether scientific or medical evidence to the required standard is likely to emerge in the near future which clarifies the nature of the association, if any, between PTGC and exposure to carcinogenic substances. [143] An absence of historical research and the improbability or impracticability of future research to remedy the historical deficiencies may call into question the extent to which the literature can be relied on as a legitimate or fair arbiter of the issues in dispute. [144] For the reasons disclosed herein, I am persuaded to prefer the evidence of Dr Hensen and to accept that it was more probable than not that the appellant's diagnosed condition of PTGC was causally connected with his employment as a firefighter. -- 26 of 27 -- 27 Order [145] The appeal is allowed and the decision of the regulator's review unit dated 3 December 2015 is set aside and replaced by a decision that the appellant’s claim for compensation is one for acceptance. -- 27 of 27 --