Estate of Gilchrist v Accident Compensation Corporation (Work Related Gradual Process Claim)

IN THE DISTRICT COURT AT WELLINGTON ITE KOTI-A-ROHE KI TE WHANGANUI-A-TARA [2019] NZACC 56 ACR 160/16 UNDER THE ACCIDENT COMPENSATION ACT 2001 IN THE MATTER OF AN APPEAL UNDER SECTION 149 OF THE ACT BETWEEN LOIS HEATHER GILCHRIST and CALEB HALL GILCHRIST as Executors for THE ESTATE OF RODNEY GILCHRIST Appellant AND ACCIDENT COMPENSATION CORPORATION Respondent Hearing: 27 February 2019 Appearances: Ms Woodhouse for the appellant Mr Bisley and Ms Harris for the respondent Judgment: 31 May 2019 RESERVED JUDGMENT OF JUDGE DENESE HENARE [Work Related Gradual Process Claim Section 30 Accident Compensation Act 2001] [1] This appeal concerns a decision of the Corporation to decline cover for adenocarcinoma of the oesophagus,! "because there is no medical evidence that Rodney had a physical injury or disease from exposure to asbestos", while working. [2] Sadly, Mr Gilchrist died on 19 February 2015. The application to appoint Lois Heather Gilchrist and Caleb Hall Gilchrist, executors of the estate of Rodney Adenocarcinoma of the oesophagus: a type of oesophageal cancer. Gilchrist as the appellant in this appeal is confirmed. I dispense with the formality of sealing and service of this order. [3] The central question turns on whether it is more likely than not that Mr Gilchrist's oesophageal cancer was caused by occupational exposure to asbestos. [4] Counsel provided a statement of agreed facts and an agreed list of issues in the appeal. Statement of Agreed Facts [5] Mr Gilchrist was born in 1962 and passed away, aged 53, on 19 February 2015. His cause of death was adenocarcinoma of the oesophagus. Employment History [6] Mr Gilchrist worked as an orderly at Oamaru Hospital from 1979 until 2000. During that time, he had some duties in the boiler room and as a general handyman. [7] In 2000, Oamaru Hospital closed. Mr Gilchrist remained on site as a caretaker and was involved in general cleaning duties. [8] In 2004, the buildings were sold, and demolition began. Mr Gilchrist was involved in cleaning up during this time. [9] In 2005, OSH performed a site inspection which noted asbestos in the building. [10] Following that report, the Oamaru Hospital was closed. When it re-opened, protective gear was issued to workers. [11] From 2008, Mr Gilchrist was employed in building work as a hammer hand. Mr Gilchrist's Oesophageal Cancer [12] On 21 October 2010, Mr Gilchrist had a CT scan of his chest revealing "minor linear fibrotic scarring involving the posterior and anterior aspects of the right lung base". The CT scan also showed that "the pleural spaces are clear with no pleural thickening or pleural plaques to suggest the presence of asbestosis related lung disease". [13] In around 2013, Mr Gilchrist began to experience a dry cough and complain of chest pain. In July 2014, he was diagnosed with adenocarcinoma of the oesophagus. [14] Mr Gilchrist died from this cancer on 19 February 2015. Asbestos Exposure [15] Most industrial building in New Zealand constructed before the 1970s, like Oamaru Hospital, contained asbestos in various forms. [16] Asbestos is also ubiquitous in the urban and rural environment. [17] The vast majority of asbestos-related pleural and peritoneal cancers develop in workers who generated dust from cutting, grinding and sanding asbestos materials with machine tools, or who worked next to others doing so. Risk Factors for Oesophageal Cancer [18] Smoking and obesity are major risk factors for the development of oesophageal cancer. Other Facts [19] Mr Rangi was a boilerman at Oamaru Hospital between 1978 and 1997. He contracted metastatic small cell cancer and had an ACC claim for work-related personal injury approved. [20] Mr Millar worked "on and off" at the Oamaru hospital from 1975. He contracted pleural mesothelioma in July 2009. ACC has accepted that his cancer was caused by asbestos. His claim listed Oamaru Hospital as "one of the many work places" he was exposed to asbestos. Agreed Issues [21] Counsel agreed the question for the Court is whether it is more likely than not that s 30 of the Accident Compensation Act 2001 (the Act), applies to Mr Gilchrist. This section, against the present facts, requires that Mr Gilchrist's adenocarcinoma of the oesophagus was caused in circumstances where: [a] He was employed in an environment (Oamaru Hospital) that has a particular property or characteristic (that is, the presence of asbestos) (s 30(2)(a)(ii). [b] That particular property or characteristic causes or contributes to the cause of the personal injury (i.e., adenocarcinoma of the oesophagus) (s 30(2)(b); [c] The risk of suffering the personal injury is significantly greater for persons who are employed in that type of work environment than for persons that are not (s 30(2)(c)(ii)). [22] That gives rise to the following questions: [i] Does the evidence establish, on the balance of probabilities, that there is a causal relationship between asbestos exposure and adenocarcinoma of the oesophagus? [ii] Does the evidence establish, on the balance of probabilities, that Mr Gilchrist was exposed to levels of asbestos in his work environment at Oamaru Hospital that caused, or contributed to the cause of, his adenocarcinoma? [ifi] Does the evidence establish that the risk of developing an oesophageal adenocarcinoma is significantly greater for people exposed to the levels of asbestos present at Oamaru Hospital in their work environment, than for people who are employed in other employment environments? [23] The issues between the parties concern: The effects of the epidemiological studies in assessing the causative relationship; Whether Mr Gilchrist was exposed to heavy doses of asbestos; and Whether asbestos played a causative role in Mr Gilchrist's death. [24] In summary, the issues are: Issue one: Is there a causal relationship? Issue two: Was Mr Gilchrist's asbestos exposure causative? Issue three: Was there a higher risk for this workplace? Issue one: Is there a causal relationship? [25] This issue addresses the state of the scientific knowledge. The epidemiological studies assist the Court in deciding whether asbestos exposure is capable of causing adenocarcinoma of the oesophagus. [26] In Seltsam,' a decision of the New South Wales Supreme Court, Spigelman CJ explained the use of epidemiology in assessing general causation: 59 Epidemiology is the study of the distribution and determinants of disease in human populations. It is based on the assumption that a disease is not distributed randomly in a group of individuals. Accordingly, subgroups may be identified which are at increased risk of contracting particular diseases. Epidemiological evidence identifies associations between specific forms of exposure and the risk of disease in groups of individuals. Epidemiologists do make judgments about whether a statistical association represents a cause-effect relationships However those judgments focus on what is sometimes called in the epidemiological literature "general causation": Whether or not the particular factor is capable of causing the disease. Epidemiologists are not concerned with 'specific causation": Did the particular factor cause the disease in an individual case? . . . Seltsam Pty Limited v McGuiness; James Hardie & Coy Pty Limited v McGuiness [2000] NSWCA 29. 67 Most epidemiological studies identify the strength of an association by a measure called relative risk (RR). RR is defined as the ratio of the incidence of disease in exposed individuals compared to the incidence in unexposed individuals. If the relative risk equals 1.0 the risk in exposed individuals is the same as the risk in unexposed individuals. If the relative risk is greater than 1.0 the risk in exposed individuals is greater than the risk in unexposed individuals. . . . 78 Epidemiology is, as I have noted above, concerned with the study of disease in human populations. It is not, of itself, directed to the circumstances of an individual case. For the purpose of determining whether exposure to a particular substance is the legal cause of a particular disease, epidemiology only provides evidence of possibility. Evidence of possibility, including expert evidence of- possibility expressed in opinion form and evidence of possibility from epidemiological research or other statistical indicators, is admissible and must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn. Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference is not open to be drawn. [Emphasis added] Background [27] Mrs Gilchrist provided the Corporation with a number of research articles on the health effects of asbestos. [28] Dr Monigatti, Occupational Physician, provided opinion on 5 May 2015 noting there are risks in relying on information found on the internet and he noted some of the problems with the research provided. He stated: Anyone can find articles on the internet that assert or imply the existence of a link between a specific agent and a particular cancer. What has to be determined, in each case, is whether the association is causative or spurious. A spurious association can arise from deficiencies or errors in the studies. [29] Dr Monigatti went on to consider the Asbestos Survey document forwarded by Mrs Gilchrist, noting the Great Britain survey and summary of the report regarding known associations between asbestos exposure and death from certain causes, of which oesophageal cancer was excluded. [30] Dr Monigatti referred to the International Agency for Research on Cancer (IARC) which is the World Health Organisation's authority for the evaluation of carcinogenic risks to humans. The IARC had found insufficient evidence that asbestos exposure causes oesophageal cancer. (31] Dr Monigatti noted the IARC found sufficient evidence that acetaldehyde (associated with consumption of alcoholic beverages), alcoholic beverages, betel quid with and without tobacco, tobacco, x-radiation and gamma-radiation cause oesophageal cancer. However, there is sufficient evidence that asbestos causes cancer of the lung, mesothelioma (pleural and peritoneal) and ovary, and limited evidence for an association with cancer of the pharynx, stomach, colon and rectum. [32] Dr Monigatti noted although some studies suggest a link may exist, that causal link has yet to be established, and further studies in the future might well come to different conclusions. That is why the IARC has not been prepared to recognise any causative relationship. He commented: In summary, there is some recent epidemiological evidence to suggest that workers who have high and prolonged exposure to asbestos may be at increased risk of developing adenocarcinoma of the oesophagus. However, it is neither strong nor consistent enough to permit a reasonable inference of causation in any occupation, as opposed to mere speculation about cause. This is not attributable to a lack of studies or to poor methodology but to the weakness of the evidence itself, as recognised by the IARC. [33] Dr Monigatti noted the study by Offermans et al,3 "supported the notion that asbestos entails an increased risk of oesophageal adenocarcinoma, but only at prolonged, high exposure levels". Dr Monigatti noted the strengths of this study included the large sample size of 58,279 men over 17.3 years and the adjustment for several lifestyle confounders such as alcohol and smoking. [34] In his final report of 27 July 2017, Dr Monigatti commented: ... They (IARC) found insufficient evidence for an association with cancer of the oesophagus because the results of the epidemiological studies on association with asbestos are mixed and animal experiments do not support biological activity of asbestos at that site. Offermans N, Vermeulen R, Burdorf A, Goldbohm R, Keszei A, Peters S, Kauppinan T, Kromhoul H, van den Brandt P. Occupational asbestos exposure and risk of oesophageal, gastric and colorectal cancer in the prospective Netherlands Cohort Study. Inl J Cancer. 2014;135(8). 1970-7. Doi: 10.1002/ijc.28817. [35] Dr Monigatti explained that background exposure to asbestos is common and does not cause any sort of asbestos related cancer. What is required to cause such cancers is heavy and prolonged exposure to disturbed asbestos containing material. [36] Dr Monigatti explained the nature of the study and meaning of Hazard Ratio (HR). An HR of 2.0 is the accepted threshold for causation on a balance of probabilities basis. He noted the strengths of the study including prospective design, large sample size, long follow-up, and adjustment for confounding factors. He commented: In the Offermans study, oesophageal cancer developed in 187 of the cohort population. No statistically significant results were observed, although the HR for "ever" versus "never" highly exposed and for the duration of high exposure (continuous variable per 10 years) was considered borderline significant [HR 2.22 (95% CI 1.00 to 4.94) and 1.45 (95% CI 1.00 to 2.10)], respectively. Results by histology of oesophageal cancer showed a statistically significant association with oesophageal adenocarcinoma, not only for "ever" versus 'never" highly exposed [HR 2.52 (95% CU 1.01 to 6.26)] but also for other asbestos exposure variables. This was after adjustment for age, family history of oesophageal cancer, smoking status, education level, body mass index and alcohol consumption. The authors concluded that their findings supported the notion that asbestos entails an increased risk of oesophageal adenocarcinoma, but only at prolonged, high-exposure levels. The strength of this good-quality study is its prospective design, the large sample size, the long and nearly complete follow-up of the cohort, and the adjustment for several lifestyle confounders such as alcohol and smoking. [37] Dr McBride referred to studies by Morgan et al,+ Offermans et al, and Boulanger et al, noting that these studies do not indicate causation, but the evidence is growing stronger. Dr McBride opined the risks shown in these studies, in high risk workers were in the order of twofold, which is consistent with a "more likely than not" hypothesis. In respect to the Morgan study he noted: One of the early meta-analyses was carried out by Morgan et al., including all the asbestos cohorts then known. The Standardised Mortality Ratio (SMR) for esophageal carcinoma (all types) was 214, 95% confidence interval (95% CI) 132.6-327.6 based on 21 cases observed, 9.8 expected. Morgan R, Folian D, Wong O. Asbestos and gastrointestinal cancer. A review of the literature. West J Med 1985; 143(1) 60-5. Boulanger M, Morlais F, Bouvier V, Galaleau-Salle F, Guittel L, Marquignon M, Paris C, Raffaelli C, Launoy G, Clin B. Digestive cancers and occupational asbestos exposure; Incidence study in a cohort of asbestos plant workers. Occup Environ Med. 2015.72(11):729-7. Doi: 10.1136/oemed-2015-102871. The study by Offermans et al. addressed the association between asbestos exposure and oesophageal, gastric and colorectal cancer. This group used the Netherlands Cohort Study, estimating asbestos exposure by job title and job exposure matrix (JEM). Sixty five cases were in the asbestos exposed group. The results in high exposure groups were interesting, a two-fold increase in risk for oesophageal cancer overall, and for oesophageal adenocarcinoma a Hazard Ratio (HR) of 2.52, 95% Confidence Interval (95% CI) Cl 1.01-6.26. Further evidence was reported by Boulanger et al. in 2015, based on a cohort of 2024 workers exposed in an asbestos re processing plant. In this case the JEM was based on asbestos exposure data. Based on 25 cases of oesophageal cancer with 14.9 expected (based on regional mortality data), the standardised incidence ratio (SIR) was 1.67 95% Cl 1.08-2.47. Based on a cumulative exposure index, the SIR was 1.9, 95% Cl 1.16-2.94. This cohort was exposed o 'mixed' dust including amphiboles and the smoking rates were thought to be comparable to the general population rates. [38] Dr Monigatti explained the key measure using Standardised Incidence Ratios in the Boulanger study: Of the 36% of the cohort available for follow-up, 25 of the men developed oesophageal cancer. A significant excessive risk was observed in men in general (SIR 1.67 (CI 1.08 to 2.47)) and in men with the strongest CEI [SIR 1.90 (955 CU 1,16 to 2,94)]. The SIR was also elevated and close to significant among men exposed to the highest asbestos dust atmospheric levels [SIR 1.63 95% CI 0.98 to 2.55)]. The authors thought their results suggestive of a relationship between asbestos exposure and cancer of the oesophagus in men. The strengths of the study are its prospective design and the measurement of atmospheric fibre concentrations enabling them to quantify the precise asbestos exposure for each participant. The weaknesses are lack of statistical power (small study with high loss to follow-up) and failure to adjust for confounding factors such as alcohol and tobacco consumption, dietary habits and body mass index on the assumption that they would be similar in the study and reference populations. [39] Dr Monigatti noted the study by Fortunato & Rushton referred to by Dr McBride is irrelevant because it is concerned only with the association between stomach cancer and the work-related asbestos exposure. [40] Two studies by Li et al' and the Institute of Medicines are referred to by Dr McBride. 6 Fortunato L. Rushton L. Stomach cancer and occupational exposure to asbestos. A meta-analysis of occupational cohort studies. Br J Cancer. 2015;112(1 1):1806-15 doi: 10.1038/bjc.2014.599. Li, B., Tang, S.P. and Wang, K.Z. (2016), "Esophagus cancer and occupational exposure to asbestos: results from a meta-analysis of epidemiology studies", Dis Esophagus, Vol. 29 No.5, pp 421-8. Institutes of Medicine (US) Committee on Asbestos: Selected Health Effects. Asbestos: Selected Cancers. Washington (DC): National Academies Press (US); 2006. Available from: https:// www.ncbi.nim.nih.gov/books/NBK20339. [41] Dr McBride stated: The Institute of Medicine (IM) Committee (institutes of Medicine, 2006) carried out a comprehensive review of 'asbestos and selected cancers'. In the JS, Oesophageal Adenocarcinoma (OA) makes up more than half of besophageal cancers in miles, the known predisposing factor being Barrett's esophagus, the predisposing factor being metaplasia caused by reflux of stomach acid in the distal oesophagus. In the 25 cohort studies reviewed by the committee, cases of oesophageal cancers were a few and of these few cases sub-types were not distinguishable. Two studies, of American insulation workers, (Selikoff 1979) and asbestos factory workers in the UK (Berry, 2000) showed strong evidence of an increased risk of OA with 'any' asbestos exposure, the former an SMR of 2.08, 95% CI 1.07-3.63, the latter an SMR of 253. The meta-analysis however failed to show an association. The three case-control studies reviewed failed to show consistent results. The committee's conclusion was that "Some studies have found an association between asbestos exposure and oesophageal cancer, but the overall results of epidemiologic studies are mixed. In addition, what little evidence there is from animal experiments about asbestos's carcinogenic potential specifically on oesophageal tissues does not support biological activity at this site. On the basis of those observations, the committee concluded that the evidence is inadequate to infer to the presence or absence of a causal relationship between asbestos exposure and oesophageal cancer". [42] In respect to the study by Li et al, Dr McBride reported: The most recent meta analysis is that of Li et al, (Li et al, 2016) who reported that "overall, occupational exposure to asbestos was associated with an excess risk of EC (SMR = 1.24, 95% CI: 1.13-1.38, P < 0.001), with little evidence of heterogeneity among studies (12 = 0.00%m P=0.682). Being male, exposure to chrysotile or mixed asbestos, working at (sic) textile industry, long study follow-up (220 years), Asia, Europe and America cohorts with larger cohort size (>500), and high-exposure group all contribute to significantly higher SMR". [43] Dr Monigatti noted the studies cited by Dr McBride show that: If a causative association between asbestos and oesophageal cancer does exist it is likely to be dose dependent, with the risk elevated for only those who were heavily exposed for long periods. [44] In response to the question whether medical science recognises a possible relationship between asbestos exposure and oesophageal cancer, Dr McBride commented: There are many cases in which we cannot establish a causal relationship and in which epidemiology may help. The principles for doing so were first laid down by Sir Austin Bradford Hill in 1965. 1. Strength of the association size of the risk, but do not dismiss if small. The risks shown in these studies in high risk workers were in the order of two-fold, which is consistent with a 'more likely than not' hypothesis. 2. Consistency repeatedly observed in person, place and time with different situations and techniques Several occupational cohort studies have observed elevated OS rates after asbestos exposure, and have suggested that risk might be dose-dependent. 3. Specificity limited to specific workers, types and sites of disease. The evidence seems to be, at present, that the risk is greater for asbestos exposed workers, the histological ty type being oesophageal adenocarcinoma of the oesophagus. 4. Temporality cause before effect, especially when remote in time. The effect has been seen in cohort studies 5. Biological gradient there is a dose response curve, rising risk with rising exposure, preferably linear. The effect is seen in those with the highest levels of exposure, which is consistent with a dose response relationship. 6 . Plausibility biologically plausible, depends on the technology of the day. The strongest association for the carcinogenicity of asbestos is with the amphiboles, crocidolite and amosite, and the risk of mesothelioma. This has recently been shown to have a linear dose response relationship. 7 . Coherence should not conflict with known facts about the disease. Coherence is, in my opinion, present. 8. Experiment does mitigation of cause reduce the risk. Not applicable. 9. Analogy does another exposure cause a similar effect, if so accept a lesser risk. Tobacco smoke is also a risk factor. [45] Dr Monigatti responded: Dr McBride offers an opinion to the contrary, based on his application of the Bradford Hill criteria for causation. These criteria are well recognised and universally accepted. I do not agree that when they are applied to oesophageal cancer and asbestos a causative association emerges as being more likely than not. If that were so, the IARC would have acknowledged it by inclusion in Group I (i.e. probably carcinogenic to humans). Dr Mcbride cites a number of references to support this view by referenced only two. However, I managed to locate the others. Submissions of the parties [46] Ms Woodhouse submitted this case involves science that is evolving and the fact the relevant science may be unsettled is no reason to prevent the Court from drawing an inference on causation. Ms Woodhouse cited the following statement of Spigelman CJ in Seltsam: [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 enquiry 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 for 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. [47] Ms Woodhouse submitted on the first issue: (a) Therefore in summary: i. Dr Mcbride has noted that this is an evolving area in science, which involves a rare tumour, however this does not disenable the Court from finding of an association if. The epidemiological studies available do support causation in terms of an HR over 2.0; iii. Dr Monigatti has noted that the development in the oesophageal cancer is biomechanically plausible. (b) Taken together, it is submitted that the evidence supports a relationship between high exposure to asbestos and the development adenocarcinoma of the oesophagus. Accordingly, the first question posed is answered in the affirmative. 48] Mr Bisley submitted asbestos is one of the noxious substances listed in Schedule 2 of the Act in respect to lung cancer and mesothelioma. Cancer of the oesophagus is not listed because there is no medical consensus that asbestos can cause this type of cancer. [49] Mr Bisley submitted the medical experts conclude that research in this area is under investigation, and a causative relationship cannot be ruled in or out. The strength and quality of the studies must be assessed as undertaken by Dr Monigatti. The evidence is sparse and any effect will only be at high doses. [50] Mr Bisley submitted that Seltsam does not replace the principles governing causation in Ambros'. Mr Bisley submitted although a court may find causation where only a possible connection is allowed by medical science, that will invariably require stronger evidence in other respects, for example, an absence of other possible causes. Discussion 51] The question for determination is whether medical science acknowledges a possible connection between asbestos exposure and oesophageal cancer. If there is no possible link, that is a bar to further consideration. If there is a possible link then the inquiry is directed to the question whether a causative link is established on the whole of the evidence as held in Attapatu-Weerasinghe10. [52] The discussion of Spigelman CJ in Seltsam is cited with approval in Ambros, the controlling decision in respect of causation: 68] Spigelman CJ in Seltsam said that the only time that a Judge is not able to draw a robust inference of causation are cases where medical science says that there is no possible connection between the events and the injury or death - see at 275. If the facts stand outside an area in which common experience can be the touchstone, then the Judge cannot act as if there were a connection. However, if medical science is prepared to say that there is a possible connection, a Judge may, after examining all the evidence, decide that causation is probable. He referred in this regard to the comments of Herron CJ in EMI (Australia) Limited v BES at 242. In the case at hand Spigelman J, reversing the trial judge's findings, did not consider the evidence sufficient to infer causation. He was joined in that view by Davies A-JA. Stein JA dissented. [69] We agree that the question of causation is one for the courts to decide and that it could in some cases be decided in favour of a plaintiff even where the medical evidence is only prepared to acknowledge a possible connection. We refer to Dais v Accident Compensation Corporation DC WN 178/2002 5 August 2003, Smith v State Insurance Ltd at 959 and Estate of Albert Francis McQueen v Accident Compensation Corporation DC HM 190/2005 28 June 2005. . Accident Compensation Corporation v Ambros [2008] 1 NZLR 340 (CA). 10 Attapatu-Weerasinghe v Accident Compensation Corporation [2017]NZHC 142. [53] I accept the submission of Ms Woodhouse that a Court is able to draw an inference on causation, even if the relevant science is unsettled. However, a valid inference as to causation can only be drawn on the basis of facts supported by evidence, and not on the basis of supposition or conjecture. In Ambros the Court cautioned "there must be sufficient material pointing to proof of causation on the balance of probabilities for a Court to draw even a robust inference on causation. Risk of causation does not suffice." [54] Ms Woodhouse submitted Dr Monigatti and Dr McBride appear to agree there is a possible connection between asbestos exposure and oesophageal cancer at a high level. [55] I did not have the actual research documents before me. Drs Monigatti and McBride commented on them in their respective reports as set out in the background section to this issue. I turn to consider their comments, particularly as to the indications for causation generally. [56] In the 2014 Offermans' study Dr Monigatti noted 'the authors concluded that their findings supported the notion that asbestos entails an increased risk of oesophageal adenocarcinoma but only at prolonged, high-exposure levels'. He noted the strengths of the study as including the large sample size, prospective design, long follow up and adjustment for confounding factors such as alcohol and smoking. Dr Monigatti explained the meaning of Hazard Ratio (HR) noting HR for results by histology of oesophageal cancer as 2.52. He explained that a HR of 2.0 is the generally accepted threshold for causation on the balance of probabilities. Dr Monigatti also noted the duration of high exposure had a continuous variable per 10 years. [57] Dr McBride noted in Offermans a total of 187 cases of oesophageal cancer, with 61 of these being of squamous cell cancer and 126 cases of oesophageal adenocarcinoma. For the group with HR 2.52, Dr McBride noted: For OAC [oesophageal adenocarcinoma] this was also observed for the other asbestos exposure variables, including duration, cumulative probability x intensity and duration of high exposure. The authors comment that 'As such, the analyses reported here provide some further support for an association with (OAC) but not squamous cell carcinoma. [58] Dr Monigatti referred to the strengths and weaknesses of the 2015 study by Boulanger. The participants had worked in a French asbestos reprocessing plant. The strengths were prospective design and measurements of exposure and weaknesses included small sample size and failure to adjust for confounding factors. Dr Monigatti's referral to the conclusions by the authors of the study. Dr Monigatti noted the authors' view of a causal link which suggested rather than established a causal relationship between asbestos exposure and cancer of the oesophagus in men. [59] In respect to the Offermans and Boulanger studies, Dr McBride stated 'neither of these studies indicate causation'. What he does say about these two studies is that 'the risks shown in the studies in high risk workers were in the order of two-fold which is consistent with a more likely than not hypothesis'. Again, consistent does not mean an established causal relationship. Dr McBride then refers to the studies again in his later report and opines there is a risk for high risk workers. In his final report, Dr McBride reviews the studies cited in his earlier report and concludes these studies indicate an association between asbestos exposure and cancer risk' which is accepted in relation to other cancer types. However, Dr McBride does conclude "the evidence for an association with oesophageal cancer is now much stronger". [60] In the 1985 study by Morgan et al, Dr Monigatti explained this study included three occupational groups: asbestos factory workers, insulators and ship yard workers and asbestos miners. The authors summarised the standardised mortality ratio (SMR), that is the sum of the observed deaths divided by the sum of the expected deaths x 100. The authors found a significantly elevated SMR of 214 for oesophageal cancer based on the data from four studies and acknowledged the numbers were small (only 21 cases) and the confidence interval of 95% was wide. Dr Monigatti noted the wider the confidence level, the more likely it is that explanations other than asbestos exposure would account for the association shown. Dr McBride described the cohort drawn from the occupational groups in this study as a high exposure cohort. [61] The Fortunato study of 2014 relates only to stomach cancer and has no relevance to this case. [62] The Institute of Medicine research is significant for noting the risk factors. Two studies of American insulation workers and asbestos factory workers showed strong evidence of increased risk between oesophageal adenocarcinoma and 'any' asbestos exposure. Whilst this factor is significant, the meta-analysis failed to show causal association. Further, three case-control studies reviewed failed to show consistent results. Dr McBride particularly noted the Committee's conclusion that the evidence is inadequate to infer the presence or absence of a causal relationship between asbestos exposure and oesophageal cancer. In other words, it could not be ruled in or out. [63] The 2016 Li study represents the most recent meta-analysis reporting occupational exposure to asbestos was associated with an excess risk of 1.24, that is slightly above the base line of 1. However, Dr Mcbride does not explain the meaning of excess risk or relevance to oesophageal cancer. The size of the study is not explained, relevance to levels of exposure, or the weight to be given to it. However, I do observe the heavy exposure period in the study recorded 20 years. [64] In response to the question whether medical science recognises a possible relationship between asbestos and oesophageal cancer, Dr McBride referred to the Bradford Hill principles. He said they do not apply to the individual but do provide a framework. These principles were referred to by the Court in Ambros as follows: [76] We consider that statistical evidence may be of use in the assessment of causation but the limitations of such evidence must be clearly borne in mind. There is always a risk that statistical evidence gives an illusion of precision that is lacking. Statistics as to what has happened to other patients in similar situations are also not necessarily a guide to what might have happened in the case at hand - see at [72]. Such evidence can, however, as pointed out by Spigelman CJ, provide evidence of possibility which might translate into the requisite degree of probability, depending on the strength of that statistical evidence and any other relevant evidence pointing to causation. We did not hear argument on the Hill factors but it might be that they deserve further consideration to see if they might provide a possible framework for assessing the weight to be applied to certain statistical evidence in some cases. [65] Dr Monigatti stated that if the Bradford Hill criteria were satisfied then the IARC would acknowledge there was a causal relationship. There is no doubt the IARC conclusions reported by the experts here are significant because no causal link between asbestos and oesophageal cancer is found. I take into account the IARC conclusions rely not only on epidemiological evidence but also on animal studies of biological activity. However, the utility of the Bradford Hill criteria is as a framework when considering the studies and a causation. [66] The Court of Appeal's caution about the use of statistics is instructive when considering any single ratio. That said, Drs Monigatti and McBride agree as to the strength of the Offermans study. [67] However, Dr Monigatti stated the weakness of the studies as a whole were clearly recognised by the IARC. Dr Monigatti acknowledged that at best the studies showed if a causative association between asbestos and oesophageal cancer does exist it is likely to be dose dependant with the risk elevated only in those who were heavily exposed for long periods. He referred to examples from the studies of the occupational groups in which heavy exposure might occur such as asbestos workers sanding, cutting or grinding material with asbestos. [68] Dr McBride noted oesophageal adenocarcinoma is a rare tumour and he is candid that epidemiology cannot establish causation: Because it is a rare tumour causation cannot be established but must be inferred from the epidemiology. The diagnosis of OA in cohort studies was previously not good, but with better diagnostic methods studies are now showing a strong association between those with high levels of exposure and OA. Conclusion [69] In my opinion the experts in this case have considerable experience and qualifications in occupational medicine. I take into account Dr McBride's significant qualifications in research and his epidemiology training. Dr Monigatti is the chief occupational medical specialist adviser to the Corporation. [70] I take into account their helpful analysis of the studies. Taken together, I conclude their comments on the epidemiological evidence acknowledge that a causal link may exist but only where heavy and prolonged asbestos exposure occurs. [71] Adopting the approach of Judge Powell (as he then was) in LS", the question here is whether generally medical science says there can be no possible connection between asbestos exposure and oesophageal cancer. I conclude the epidemiological studies do admit a possible causal connection may exist where there is heavy and prolonged exposure. This issue is answered in the affirmative. [72] Having determined that a possible causal connection exists, I turn to consider whether there is an actual causal link. Issue two: Was Mr Gilchrist's asbestos exposure causative? [73] Whilst the first issue addressed the epidemiological evidence as a matter of general causation, the second issue is often referred to as specific causation. [74] In Bird and Hastings" the Court noted that actual evidence of realistic or significant exposure is required, rather than mere speculation. Potential exposure is not a basis for cover. Background [75] Mrs Gilchrist described the work tasks of her husband: 13 3. My husband worked as an orderly at Oamaru Hospital for 21 years until 2000. During this period, he worked in the boiler room and as a general handyman. In 2000 the Hospital closed and we both lived on site as caretakers. In 2004, the site was sold to Worthwhile Industries, and demolition was ordered. My husband was involved in the demolition and "cleaning up" of this process. This involved clearing the debris after Rimu panelling was removed from the interiors. In 2008, he did similar work in the old laundry and in the building as a hammer hand. I am now of the firm opinion (given the evidence that has come to light) that Rodney would have been exposed to asbestos during this time. 1 LS v Accident Compensation Corporation [2013] NZACC 385. 2 Bird v Accident Compensation Corporation [2011] NZACC 26 and Hastings v Accident Compensation Corporation [2018] NZACC 68. 13 Affidavit of Lois Gilchrist sworn on 24 October 2018. 5. Before demolition work started, we were under the understanding that asbestos had been removed. It hadn't, this was a false sense of security. The demolition crew never realised that there was still asbestos left in the building, or how much, until the OSH reports were released. The workers never knew that the demolition should have been done by specialists. The demolition was completed essentially with hammers and nails - which is obviously not adequate in terms of protective gear. 6. OSH shut down the site for a day. It reopened, and we were told it was fine. My husband was given white overalls and paper masks to work with. OSH did not come back to recheck the site. . During the demolition stage, a lot of overseas workers were employed. I am not sure of their whereabouts now. Therefore I cannot check to see how they are doing or if they have similar issues. [76] Other affidavit evidence was provided from Frances Rangi" and Christine Miller.15 Ms Woodhouse submitted this evidence establishes there was asbestos exposure to a degree that caused cancer in other workers. [77] Dr McBride took Mr Gilchrist's occupational history from Mrs Gilchrist. Dr Mcbride noted possible exposure, intensity and duration of exposure and biological evidence of exposure as follows: Possible exposure It is very difficult to say how much asbestos exposure Rodney might have experienced, however the death of a boilerman from lung cancer suggests that exposure had been going on for 25 years prior to the closure of the hospital. It is clear that asbestos abatement also took place after the closure of the hospital and prior to 2005. The nature of the contamination and the condition of the asbestos material make it almost certain that this was not carried out under the supervision of an approved person. The presence of amosite on plant associated with the boiler house means that exposure during cleaning duties, boiler maintenance or especially removal of the boilers and associated equipment would have been high. . . . Intensity and duration of exposure One must take into account the possible asbestos exposure experienced by Mr Gilchrist over the years. He started work there in 1979, with boiler room duties including 'cleaning up', well known to give rise to high exposures. The most worrying aspect was that the insulation in the boiler room probably contained amosite or 'brown' asbestos, a potential lung carcinogen. This has 14 Affidavit sworn on 15 October 2018. 5 Affidavit sworn on 13 November 2018. been shown, for mesothelioma, to carry extraordinary risk when individuals are exposed at a young age as electricians, carpenters or joiners. His role as general handyman would also have exposed him to asbestos in the hospital, once again with high risk amphiboles such as crocidolite present. From the OSH reports, asbestos was prevalent as a building material and carried the high risk forms. Again, and of greatest concern, was the uncontrolled demolition which went on between 2000 and 2005, which almost certainly gave a very high to extreme risk of asbestos exposure. Rodney was involved in cleaning up, which in my experience gives rise to intense levels of exposure. Emphasis added] 78] A report dated 18 August 2005 from Mr Purdie-Smith, Health and Safety Inspector, Department of Labour to Worthwhile (Oamaru) Limited noted: As you are aware, myself, Clive Doubleday (OSH Health and Safety Inspector) and Murray Flint (Plumbing Inspector, Waitaki District Council), visited this property on 2 August 2005, to determine the location and condition of asbestos products that had been used in the construction of the old hospital buildings. We viewed various buildings accompanied by the site caretaker Mr Rodney Gilchrist. Asbestos was identified in several locations in these buildings and, in some instance, in a deteriorated condition. It is likely that asbestos products will be found in areas other than those identified below. It was also noted that several buildings had asbestos based roof cladding. If not already in place, a register will need to be compiled to record the known locations of asbestos and, any other locations where asbestos is located in the future. Any persons entering the areas where asbestos has been identified will have to be advised of the presence of the asbestos in that area and, what precaution they will need to take to ensure their own safety and to prevent damage to the asbestos product. [79] In his report dated 20 July 2017, Dr Monigatti observed that the presence of asbestos at the hospital is true of most, if not all, industrial buildings in New Zealand constructed before 1970. The Department of Labour's report does not of itself provide sufficient information to assess Mr Gilchrist's level of exposure to asbestos. [80] Dr Monigatti explained: There is no evidence that this background level of exposure is enough to cause even the cancers well recognised to be asbestos-related, such as pleural mesothelioma. .. To constitute a significant above-background load there has to be active disturbance of asbestos containing materials that results in the release of large numbers of inspirable fibers. The vast majority of asbestos-related pleural and mesothelioma cancers develop in workers who generated dust from cutting, grinding, or sanding asbestos materials with machine tools or who worked next to others doing so.... It is quite likely that Mr Gilchrist came into contact with asbestos during his tasks as an orderly at Oamaru Hospital when on boiler house duties and when cleaning up during demolition of old buildings. He commenced there in 1979, and it was not until the 1980s that the hazards of asbestos became widely known and the precautions to protect workers from hazardous exposure came into effect. Even so, given that Mr Gilchrist was employed primarily as an orderly and not as a boiler attendant or demolition worker it is difficult to envisage how he could have had sufficient above-background exposure to put him at risk of developing asbestos-related disease of any sort. [Emphasis added] [81] On the asbestos present at the hospital, Dr McBride commented on the Department of Labour letter and noted: An inspection was carried out by OSH at the Devon Terrace site in 2005. The most worrisome aspects of this were that crocidolite was attached to some of the floors in the nursing home, which had been disturbed and was lying on the floor. In the boiler house, residual asbestos remained in the form of gaskets and rope product, along with asbestos on the floor that had probably been removed from the boiler. Calcium calcite (silicate?) insulation was also found on plant adjacent to the boiler house. Mike Purdie-Smith, the inspector, believed that this normally contained amosite. Other buildings had pipe insulation and cladding containing asbestos. Also of concern was super 6 roofing, which contained both chrysotile and amphiboles, including amosite. There are comments on the file about demolition being carried out with inadequate respiratory protection. OSH recommended that access should be restricted and further work involving asbestos removal be classified as 'restricted' The case for the appellant [82] Ms Woodhouse submitted Mr Gilchrist was exposed to a high level of asbestos during the time he worked at the Oamaru hospital that caused or contributed to the cause of his cancer because Mr Gilchrist worked in an asbestos laden environment for 29 years, the building was known to have dangerous amounts of asbestos present evidenced by the Health and Safety notices of prohibition; There was at least one significant period of time, when cleaning up following the demolition work, where Mr Gilchrist was exposed to disturbed asbestos fibres for a prolonged period of time; Mr Gilchrist's duties were of a nature that put him in direct proximity with airborne asbestos; The length of Mr Gilchrist's tenure was such that additional exposures during more minor undocumented renovations and repairs is highly likely given the extensive presence of asbestos. Discussion [83] I have already determined that the epidemiological evidence suggests a possible causal connection where there is heavy and prolonged exposure. I must now assess the whole of the evidence whether that possible causal link can be treated as an actual causal link. [84] Ms Woodhouse submitted there are considerable evidential difficulties in the case given Mr Gilchrist's passing. I agree. 85] The area of dispute between the parties concerns Mr Gilchrist's level of exposure to asbestos. Dr Monigatti opined Mr Gilchrist's exposure was not much above the background or community level of exposure and unlikely to be harmful. Dr McBride countered Mr Gilchrist sustained high level exposure particularly during the period he described as uncontrolled demolition between 2000 and 2005. This is not explained and appears in error. The evidence is demolition began in 2004 with OSH involved in 2005 and demolition completed in 2006. The agreed facts note the demolition began in 2004. Ms Woodhouse submitted the exposure period was 29 years. However, she accepted the higher exposure occurred in the demolition period. [86] Against the background of evidential difficulties, I must determine whether the various strands are strong enough to support a conclusion that heavy exposure caused or contributed to the cause of oesophageal adenocarcinoma. [87] In reviewing the evidence of Mr Gilchrist's exposure, I turn to consider factors including the medical records, work history, the presence of asbestos products at the hospital, the demolition work and other risk factors for oesophageal adenocarcinoma. Medical records [88] There is no evidence in the medical records of the expected signs of exposure to asbestos. It appears an x-ray was first taken according to Mrs Gilchrist's evidence at review. However neither she nor Dr McBride had a copy of the x-ray report. Dr McBride first opined minor fibrous scarring on the CT scan. He stated in his May 2017 report that: Biological evidence of exposure The CT scan was reported as showing fine linear scaring consistent with asbestosis. If this scarring was indeed due to asbestos exposure this confirms that the levels of exposure were high, with, most likely, a high proportion of amphibole fibres. [89] Dr McBride stated the earliest signs of asbestosis are "fine linear opacities visible on a high contrast (high voltage) film" and the films taken should be reviewed "as that will be evidence of asbestos exposure". [90] Dr Milne reviewed the CT scan undertaken in 2010 by Dr Letts of Mr Gilchrist's lungs and chest and reported the imaging represented "a high-quality examination of the lungs using a High-Resolution CT protocol". Dr Milne found "no pleural plaques were demonstrated." [91] In his October 2018 report, Dr McBride received the results of the CT scan and agreed there were no pleural plaques "these being one of the common radiological signs of asbestos exposure". [92] This is an important finding because Dr McBride's conclusion of high or intense exposure is derived in part from his earlier interpretation of the radiology. Dr Monigatti stated the absence of pleural plaques in the radiology militates against Mr Gilchrist's exposure to asbestos having been much above the background level. I conclude the evidence on the radiology, particularly from Dr Milne is compelling that there was no evidence of signs of exposure to asbestos. Work history [93] The evidence of Mr Gilchrist's work history is provided by Mrs Gilchrist's evidence. This evidence is found in the deceased client cover questionnaire (the questionnaire) completed by Mrs Gilchrist, in Dr Mcbride's reports (informed by Mrs Gilchrist), in her evidence at review and in her affidavit filed in this appeal. [94] Mr Gilchrist worked as an orderly between 1979 and 2000. Mrs Gilchrist says his duties as an orderly included cleaning in the 'boil house building' at the hospital. But the detail of what cleaning up entailed in the boiler house is lacking. Whilst Mrs Gilchrist stated Mr Gilchrist was involved in disposing body parts in an incinerator in the boiler house, there is no explanation as to what the cleaning work entailed in the boiler house. Dr McBride suggested tasks of cleaning duties, boiler maintenance and boiler removal would amount to exposure at a high level. There is no evidence Mr Gilchrist undertook the maintenance and removal work. It is accepted Mr Gilchrist undertook cleaning work as part of his role as an orderly and this occurred in the boiler house. [95] In the questionnaire, Mrs Gilchrist recorded that all the boil house workers who worked with Mr Gilchrist died of asbestos related cancers. I take into account the evidence of Mrs Rangi and Mrs Miller. I observe their husbands were boilermen. Mrs Miller records her husband worked at a number of places where he was exposed to asbestos and Oamaru Hospital is listed as only one of them. Mr Miller and Mr Rangi both suffered diseases listed in schedule 2 of the Act. [96] In 2000 the hospital buildings were sold and both she and Mr Gilchrest lived on site as caretakers. In the questionnaire Mrs Gilchrist recorded Mr Gilchrist working as a supervisor undertaking cleaning work tasks between 2001 and 2002. This is not explained in the additional information attached to the questionnaire or in Mrs Gilchrist's affidavit. Dr McBride records Mr Gilchrist cleaned up after damage and 'clean up gives rise to high levels of exposure.' However, this statement is unexplained. [97] Between 2002 and 2004, the questionnaire records Mr Gilchrist worked as a foreman at an orchard in Roxburgh. [98] From 2004 to 2010 the questionnaire records Mr Gilchrist was employed at the Oamaru hospital site as caretaker and undertaking building and construction tasks. Mrs Gilchrist mentioned her husband's general handy man skills. Mrs Gilchrist stated in the additional information sheet attached to the questionnaire that: In 2004 Rodney started working back at the old Oamaru hospital site, he was employed by the Goodland Group they had bought the buildings to redevelop. He assisted with developing the old hospital to motels etc. He assisted in demolishing a wing of the hospital and working alongside Chinese workers from Auckland. There was asbestos in the walls and roof of the building. They did supply some masks but there was no certified asbestos professional on site. [99] Mrs Gilchrist's affidavit explains Mr Gilchrist cleared the debris after rimu panelling was removed from the interiors. In her affidavit, Mrs Gilchrist states that Mr Gilchrist was involved in cleaning up in the demolition. Dr McBride recorded demolition lasted two years with Mr Gilchrist cleaning up alongside the demolition work, in other buildings on the hospital site. [100] There is no doubt Mr Gilchrist had a role cleaning up in the demolition period in his role as caretaker. Asbestos at the Oamaru hospital [101] There is no doubt there was asbestos at the Oamaru hospital. The type of asbestos product and the location of the materials and their disturbance are discerned from Department of Labour information released to Mrs Gilchrist under the Official Information Act 1982. [102] The Department of Labour appears to have been actively concerned about the site since January 2005 because of visas issues relating to the overseas workers engaged at the site. [103] In August 2005 Mr Gilchrist accompanied the OSH Health and Safety Inspector, the Plumbing Inspector and the Project Manager for the demolition contractors to identify both the location and condition of asbestos used in the construction of the hospital buildings. The Department of Labour report to the Project Manager for the site identifies the buildings containing asbestos and noted that some of it had been damaged. Three areas were particularly identified where asbestos had been disturbed. Disturbances are referred to as "asbestos fibres entering the air" which appear to be caused by demolition which began in 2004 and ceased in 2005 following the Department of Labour report. The report specifically identifies the areas of disturbance. [104] First, that crocidolite (blue asbestos) has been disturbed on the ground floor of the nursing home. Secondly, calcite insulation containing amosite (brown asbestos) in an area adjacent to the boiler house. Thirdly, the type of asbestos product was not identified but noted as asbestos pipe lagging lying on subfloor areas in the maternity building. It was noted "this ground now has a level of contamination that needs to be determined". The report also noted but was unsure about the asbestos asbestos in the rope product and gaskets in the boiler house. The residue was noted as likely to be asbestos. [105] OSH closed the site. From 2005 the demolition continued with safety precautions noted in the notices in evidence. Respiratory protection appears to have been provided. Mrs Gilchrist's evidence is the protection given to her husband was a pair of white overalls and a paper mask. Mrs Gilchrist says the site was closed for a day and there was no ongoing supervision from OSH. I observe the Department of Labour notices record 'proactive visit to site' by OSH from August 2005 to January 2006. Whilst there are prohibition notices in the OSH documents, I cannot discern the length of the closure. [106] Given the large number of demolition workers employed by Worthwhile onsite, the nature of Mr Gilchrist's work tasks apart from cleaning is unclear. Whilst he was involved in the demolition, he was not a demolition worker. When he accompanied the OSH inspectors in August 2005 he was recorded as the caretaker. There is no doubt, he was the caretaker, and he was involved in cleaning. I form the impression from Mrs Gilchrist that he may have been using his general handyman skills. But there is no detail. Mrs Gilchrist stated both she and her husband understood the asbestos had been removed before demolition, but it had not. This suggests that when demolition began it became apparent in 2004. Since Mr Gilchrist accompanied the OSH inspection in 2005 he would then have had direct knowledge of the areas of disturbed asbestos at the site. [107] It is difficult to draw an inference that he was working along-side the workers as might occur in an asbestos factory, as a worker who is cutting, grinding and sanding being the work tasks the subject of high-level exposure discussed in the studies. However, it is accepted he was undertaking cleaning work and may have used his handyman skills. Whilst Dr McBride says the handyman duties would have placed him in an area of high exposure, there is insufficient evidence. [108] Ms Woodhouse submitted the demolition aside, Mr Gilchrist had general cleaning duties prior to the demolition which placed him in direct proximity with airborne asbestos, and he would have come in contact with the asbestos in the course of his general duties. There is insufficient evidence of Mr Gilchrist working in airborne asbestos prior to demolition as Ms Woodhouse submits. Dr Monigatti accepted that cleaning up as an orderly and as a caretaker did not place him at a level of risk beyond background exposure to asbestos. [109] I find that it is a long bow to draw on the evidence before me that Mr Gilchrist was heavily exposed to asbestos in his work tasks in comparison to those workers referred to in the studies, working in an asbestos factory. Dr Monigatti opined: To constitute a significant above background load there has to be active disturbance of asbestos-containing materials that results in the relevance of large numbers of insufficient figures. The vast majority of asbestos related pleural and peritoneal cancers develop in workers who generated dust from cutting, grinding or sanding ... [110] There is no doubt Mr Gilchrist's work history exposed him to asbestos. However, there is insufficient evidence for me to infer that the level of exposure of Mr Gilchrist was above background exposure. I take this into account as a strand in the evidence, but the evidence is unclear that Mr Gilchrist was exposed to high levels of asbestos in his work tasks as an orderly and caretaker. Risk factors [1 1 1] I take into account the evidence of predisposition. There are three factors that clearly disposed Mr Gilchrist towards the adenocarcinoma. He was a heavy smoker, smoking 20 cigarettes a day according to his GP. The IARC noted that tobacco is a risk factor in the list of matters that cause oesophageal cancer. Obesity is also a major risk factor together with the fact that Mr Gilchrist suffered from reflux, another risk factor. Ms Woodhouse made enquiries of the GP and omeprazole was prescribed latterly in Mr Gilchrist's life. This risk factor is not important following the enquiry with the GP. The final two risk factors are that Mr Gilchrist was male with men suffering from this form of cancer more frequently than women, and that he was at the highest risk age. [1 12] Ultimately, as counsel agreed, I must determine which evidence of the two experts is to be preferred. [113] I accept Ms Woodhouse's submission, given Dr McBride took Mr Gilchrist's work history from Mrs Gilchrist, he was more sensitive to the work undertaken. Notwithstanding his recording of the occupational history, I find it difficult to accord it more weight because when all is said and done, his opinion on exposure is uncertain. On the one hand, Dr McBride opines 'it is very difficult to say how much asbestos exposure Rodney might have experienced", yet on the other, he engages in a speculative assessment in which he claims a high degree of certainty, using language that exposure was "high" or "intense". I take into account Dr McBride's conclusion is reached in part, from the radiology. [114] I accept it is inevitable that a degree of speculation will be required in circumstances where a claimant is not able to give evidence. However, I accept Mr Bisley's submission that Dr Mcbride's analysis reaches a level of risk of causation that the Court of Appeal in Ambros warned cannot establish causation. I find difficulties with Dr McBride's analysis for the following reasons: [i] He relies on the 2010 CT imaging to support a view of high asbestos exposure. This view is at odds with the expert opinion, particularly of Dr Milne and Dr Letts, the 2010 who agree the imaging shows no evidence of asbestosis. Rather, the 2010 imaging suggests that any exposure was not intense enough to be harmful. [ii] He has not explained which of the work tasks he considers would have disturbed (or involved exposure to disturb) asbestos materials so as to create or involve inhalable dust. There is no evidence to support his suggestion that Mr Gilchrist was involved in joining and plumbing tasks or that he removed boilers and was exposed to asbestos in that way. [iii] He has not explained why he suggests cleaning up duties would lead to high levels of exposure. In considering Mr Gilchrist cleaned up disturbed material, there is no evidence of how this was done, or how often this happened. Dr McBride's comment here is at odds with Dr Monigatti's view that the tasks of an Orderly do not ordinarily involve above background asbestos exposure. [iv] Dr McBride's description of brown asbestos in the hospital boiler house is at odds with the 2005 OSH report which describes an area adjacent to the boiler house believed to contain the type of insulation which normally contained brown asbestos. Dr McBride did however acknowledge that none of the asbestos material was actually tested. [v] There are some factual errors in Dr McBride's report, including: Insulation in the boiler room contained amosite, which is in fact only in the adjacent area; Demolition was from 2000 onwards, when in fact it began in 2004; Mr Gilchrist undertook joinery and plumbing and removal of boilers. There is no evidence of these tasks. Mr McBride draws a speculative link between Mr Gilchrist's condition and the evidence on behalf of another hospital worker, the late Mr Rangi. The link is speculative because Mr Gilchrist did not work as a boilerman whereas Mr Rangi did. Further, Mr Rangi died of a different cancer to Mr Gilchrist. The medical and employment history of the co-workers is not known. [vi] Whilst Dr McBride mentions tobacco smoking as a risk factor, he has not engaged with Mr Gilchrist's other relevant risk factors which have an established causative link with oesophageal cancer. [115] Ms Woodhouse submitted that in reliance on Dr Monigatti's report, the Corporation's position has shifted in this case. She said that the initial position was that asbestos exposure was not disputed. The Corporation had asserted only that this type of cancer was not caused by asbestos. [116] At hearing, Mr Bisley submitted that the Corporation's position on exposure had not changed. It was accepted there was asbestos exposure. There was need to consider the science and understand what it means which necessarily involves careful review of the evidence as to the level of exposure experienced by Mr Gilchrist. [117] Ms Woodhouse submitted the Corporation was firm in its view that exposure was not an issue at review. It is the case that issues can change from a review to an appeal. However, looking at the review decision, I observe that the Reviewer notes the Corporation's case, that Mr Gilchrist was likely exposed to asbestos in the course of his work. That is not at odds with the position submitted by Mr Bisley for the Corporation. [118] When I consider Dr Monigatti's evidence, it is that background exposure to asbestos is common and does not cause any sort of asbestos-related cancer. What is required to cause such cancer is heavy and prolonged exposure to disturbed asbestos containing material. [119] I find that Dr Monigatti's evidence consistent and therefore compelling. He explains what causes asbestos related cancers in occupational terms. Secondly, he considers the work tasks of Mr Gilchrist as an orderly, general handyman, and as a caretaker involved in general cleaning duties and does not speculate what the tasks may or may not have involved. Thirdly, if there is doubt as to any causal link between asbestos exposure and oesophageal cancer, it is consistent with the IARC view. To the extent that a causal link may exist, where heavy and prolonged asbestos exposure occurs, it explains what would ordinarily bring about such a level of exposure and why Mr Gilchrist does not fall into that category. Finally, Dr Monigatti considers the risk factors for Mr Gilchrist and how these increased his chances of developing oesophageal cancer are explained. Unlike asbestos exposure, these are factors with an unequivocal causal link to oesophageal cancer. [120] Finally, Ms Woodhouse submitted, relying on s 30(2)(b) of the Act, the Court needs only to find contribution to cause. Whilst contribution does suffice, I cannot ignore the self-standing alternate theory of causation engaging two of the three major risks factors for oesophageal cancer which does not require any contribution when there is evidence only of potential cause of the oesophageal cancer and in circumstances where there is little evidence beyond conjecture as to the extent of the exposure. [121] The fundamental problem is the evidence concerning asbestos exposure reaches only a level of risk of causation because of the speculation about the extent of the exposure. Conclusion [122] Having carefully reviewed the evidence, what does it all amount to? I have determined the epidemiology evidence supports a possible causal connection may exist where there is heavy and prolonged exposure. [123] I cannot make out an actual causal link on the evidence before me. In the event I am persuaded by Dr Monigatti's reasoning. I conclude there is insufficient evidence of heavy or prolonged exposure which falls short of the requirement for a valid inference of causation based on facts supported by the evidence. There is no medical evidence in Mr Gilchrist's records, that is the radiology before me, of the signs of asbestos exposure. Whilst there is evidence of asbestos exposure, there is insufficient evidence to conclude Mr Gilchrist's work tasks resulted in heavy exposure to asbestos, that is there is no evidence of either prolonged work tasks disturbing asbestos materials or of prolonged work with disturbed materials. Finally, there is the credible explanation for this type of cancer which does not require any input at all from asbestos. Mr Gilchrist was predisposed to certain risk factors for this type of cancer. [124] For all these reasons, I conclude that the strands of the rope taken together do not support a finding on the balance of probabilities that Mr Gilchrist's asbestos exposure rises to the level that it was heavy or prolonged and therefore causative of the adenocarcinoma of the oesophagus. This issue cannot be answered in the affirmative. Issue three: Was there a higher risk for Mr Gilchrist's workplace? [125] I conclude there is insufficient evidence on the balance of probabilities that persons who experience heavy and prolonged exposure to asbestos (whether through work tasks or through work environment) are at significantly greater risk of suffering oesophageal cancer than those who are not so exposed. [126] Accordingly, this limb of the test is not satisfied. Decision [127] Reviewing the requirements under s 30 of the Act, I am satisfied: [i] Mr Gilchrist was not employed in an environment that has a relevant particular property or characteristic. The relevant property or characteristic is heavy exposure to asbestos, as opposed to background exposure. There is insufficient evidence to prove that heavy exposure occurred in this case. S 30(2)(a)(i) requirement is not met. [ii] Mr Gilchrist's employment tasks did not have a relevant particular property or characteristic. That is because there is insufficient evidence to conclude that any of Mr Gilchrist's work tasks resulted in heavy exposure to asbestos, that is there is no evidence of either prolonged work tasks disturbing asbestos material or of prolonged work with disturbed materials. S 30(2)(a)(ii) requirement is not met. [ifi] Although there is a possible link between heavy exposure to asbestos and adenocarcinoma of the oesophagus, there is insufficient evidence of heavy exposure. For this reason, I cannot conclude that heavy exposure caused or contributed to the development of this type of cancer. Accepting the evidence of Dr Monigatti, background exposure is not enough to cause harm. S 30(2)(b) requirement is not met. [128] Since s 30(2)(a) and (b) requirements have not been met, it is not necessary to consider s 30(2)(c). However, for the sake of completeness, there is insufficient evidence to conclude on the balance of probabilities, that persons who experience heavy and prolonged exposure to asbestos, whether through work tasks or through work environment, are at significantly greater risk of suffering adenocarcinoma of the oesophagus than those who are not so exposed. S 30(2)(c) requirement is not met. [129] Accordingly, the Corporation was correct to decline cover for a work-related gradual process injury. Result [130] The appeal is dismissed. [131] There is no issue as to costs. Genese I Have Judge Denese Henare District Court Judge Solicitors: John Miller Law, Wellington for the appellant Buddle Findlay, Wellington for the respondent ACR 160-16-Estate of Gilchrist