White and Military Rehabilitation and Compensation Commission (Compensation)
[2017] AATA 1555
•27 September 2017
White and Military Rehabilitation and Compensation Commission (Compensation) [2017] AATA 1555 (27 September 2017)
Division:VETERANS' APPEALS DIVISION
File Number: 2016/6309
Re:Graham White
APPLICANT
AndMilitary Rehabilitation and Compensation Commission
RESPONDENT
DECISION
Tribunal:Senior Member J Sosso
Date:27 September 2017
Place:Brisbane
The decision under review is set aside and in lieu thereof the Applicant is entitled to the payment of compensation pursuant to the Safety, Rehabilitation and Compensation Act 1988 for the claimed condition, namely adenoid cystic carcinoma of the external auditory canal.
.........................[Sgd]...............................................
Senior Member J Sosso
CATCHWORDS
COMPENSATION – Naval service – where Applicant has a rare cancer – where Applicant was exposed to chromate dust during Naval service – whether Applicant’s cancer an injury – whether there is a causal link between service and Applicant’s cancer – Forst principles – where medical evidence uncertain – Applicant’s cancer is a disease – decision under review set aside and substituted
LEGISLATION
Safety, Rehabilitation and Compensation Act 1988 ss 4, 5A, 5B, 14
Safety, Rehabilitation and Compensation and Other Legislation Amendment Act 2007CASES
Adelaide Stevedoring Company Limited v Forst (1940) 64 CLR 538
Amaca Pty Ltd v Ellis & Ors (2010) 240 CLR 111
Commissioner of Police v Rea [2008] NSWCA 199
EMI (Australia) v Bes (1970) 44 WCR 114
Kennedy Cleaning Services Pty Ltd v Petkoska (2000) 200 CLR 286
Military Rehabilitation and Compensation Commission v May (2016) 257 CLR 468
Tabet v Gett (2010) 240 CLR 537
Telstra Corp Ltd v Mahon (2004) 39 AAR 484REASONS FOR DECISION
Senior Member J Sosso
27 September 2017
INTRODUCTION
On 15 July 2016 Mr Graham Thomas Robert White (the Applicant) lodged a claim for compensation for adenoid cystic carcinoma (ACC) of the external auditory canal – Exhibit 1 T4 pp. 24-29.
The Applicant was born in 1971 and enlisted in the Royal Australian Navy (RAN) on
13 February 1995 when he was 23 years of age. He served in the RAN until his discharge on 3 April 1999 holding the rank of Able Seaman – Exhibit 1 T13 p. 54. The Applicant was a very fit man prior to enlisting, working as both a personal trainer and as a martial arts coach. After his discharge in 1999 he worked as a commercial diver on offshore oilrigs – Exhibit 3 p. 2.
Amongst the Applicant’s various postings while enlisted, he was posted to HMAS Hobart from 1 April 1996 until March 1997 – Exhibit 1 T14 p. 56. HMAS Hobart was a guided missile destroyer built in the United States for the RAN. It was commissioned in December 1965 and decommissioned in May 2000. Prior to the 1980s it was the usual practice to use strontium chromate as an undercoat on naval ships constructed in the United Stated (US) – Exhibit 3 p. 6.
In 2008 the Applicant was diagnosed ACC of the external auditory canal and underwent surgery. In a report dated 20 August 2008 Professor David Sidransky, Director of the Head and Neck Cancer Research Centre at Johns Hopkins Medicine made the following observations – Exhibit 1 T5 p. 35:
“Mr Graham White was found to have an adenoid cystic carcinoma (ACC) involving the external auditory canal which was excised and found to have involved margins at histology. He is currently experiencing pain at the site of the tumor 4 months after surgery. His probable prognosis without radiation treatment includes a near 100% chance of recurrence and more probably than not recurrence within 2 years. The chance of local recurrence with timely radiation therapy is close to 50%. The chance of developing distant metastases and/or dying from this disease with extensive local extension in either case within 5 years is also about 50%.”
The material before the Tribunal suggests that despite surgery the full tumour was not removed, and the Applicant was advised to undergo radical surgery for removal of his right ear and mastoid bone. Due to domestic troubles, he did not have the radical surgery, nor did he have any chemotherapy or radiotherapy – Exhibit 3 p. 3.
The Applicant’s health has progressively deteriorated. He lives alone, cannot work or drive and has lost significant weight. He has developed deafness, and symptoms of vertigo and nausea. The Applicant is in constant pain, particularly on the right side of his face and body – Exhibit 3 pp. 3-4. The Applicant’s state of health, in short, is extremely poor.
The Applicant contends that during his RAN service he was exposed to carcinogenic substances, and that the issue to be determined by the Tribunal is whether the Applicant’s ACC was contributed to, to a significant degree, by his employment in the RAN – Exhibit 6 paras 1-2.
The Tribunal was provided with a Statement of the Applicant (Exhibit 2) which outlines the background to his claim (paras 5- 16):
“5. During my service with the RAN, I believe that I was exposed to strontium chromate and aqueous film foaming as well as a number of other possibly dangerous chemicals which I do not know the names of. I also recall being exposed to asbestos during my postings to HMAS Watson, Hobart and Kuttabul.
6. On 1 April 1996, I was posted to HMAS Hobart as a Combat Systems Operator.
7. During my posting to HMAS Hobart, my duties as a Combat Systems Operator involved use of the fire control system 1 operator.
8. Additionally, when I was initially posted to HMAS Hobart there was a shipside refit. As the refit went for a while, it started with the ship in dry dock before it was moved to the pier at Garden Island. The ship was docked at the pier for a while.
9. As part of my duties during the refit, I was given the task of removing the paint from the ship’s hull and sides before we re-painted the ship’s hull and sides.
10. I was asked to remove the old paint from the ship’s hull and sides by chipping and grinding the old paint off the ship until it was bare metal. The chipping and grinding caused a lot of dust, which was predominately yellow and grey in colour. I believe that this dust included strontium chromate in dust form. This is because I was told by the people supervising me in the refit that the yellow dust was dangerous and a carcinogenic.
11. I recall doing this every day during the refit. I recall this was my main duty during this time. I recall that the refit went for months and lasted the majority of my deployment to HMAS Hobart. I do recall being deployed to HMAS Hobart after the refit had finished. However, I do not recall this being for a long period of time.
12. For the purposes of the refit, I was provided with personal protection equipment which included paper contamination suits. The paper contamination suit covered me from my shoes to my head. It left only my face and hands exposed. My mouth and nose were covered by a paper dust mask. I also was given compressible ear plugs. However, I was often required to remove these ear plugs so that I could speak to and hear orders from my commanding officers. As the dust would often coat the outside of the earplugs, the dust would be deposited into my ear wax when I removed and replaced the ear plugs.
13. Additionally, during my posting on the HMAS Hobart, I was the dive yeoman and the ship’s diver. My duties associated with this role include searches and maintenance of the ship’s hull as well as sea bed searches. I recall seeing at least three feet of accumulated yellow and grey paint flakes, which I believe to be the dust from the paint from the ship on the sea beds at Garden Island whilst conducting these searches.
14. I also recall that I was often required to enter the water while paint was being removed from the side of the ship. This meant that there was a dust film caused by the paint on the surface of the water as I was entering the water. I was only required to do this sporadically but do recall doing so a few times. These dives would usually take about an hour.
15. I also recall that the ship’s hull was coated with antifouling paint. As a diver I was required to swim along the bottom of the ship’s hull, rubbing my hands along the surface feeling for mines. These dives would usually take about an hour but I only recall doing them sporadically. As this work was done using scuba equipment, my head was always exposed to the water as well as anything in it. My head would always get wet during these dives.
16. I do not know the exact nature of the antifouling paint used on the hull of the ship. However, I am aware that a number of antifouling paints can have quite harmful effects when they come into contact with skin or are ingested.”
The Applicant also (paras 17 – 19) claimed that he was exposed to asbestos dust during the refit of HMAS Hobart and during his posting to HMAS Watson (October 1995 to March 1996). However, research conducted by Mr Denis Hilder, Research Officer with the Department of Defence (dated 22 August 2016) concluded that any exposure of the Applicant to asbestos fibres in one form or another would have been “minimal at best” – Exhibit 1 T25 p. 84. In any event, the alleged exposure of the Applicant to asbestos fibres is not the basis of the matter before the Tribunal.
On 9 September 2016 Ms Tanya Barber, Delegate of the Military Rehabilitation and Compensation Commission (the Respondent), denied liability to pay compensation for the Applicant’s claimed ACC of the ear condition. Her reasons for denying liability were as follows – Exhibit 1 T31 p. 109:
“After considering all available evidence, I am not reasonably satisfied that your adenoid cystic carcinoma of the external auditory canal can be attributed to your defence service.
Defence has confirmed that exposed to strontium chromate, asbestos and other substances during service is possible, however independent medical evidence concludes that no relationship between exposure to these substances and the claimed condition exists.
Independent medical evidence obtained from Professor Richard Fox found there are currently no reports providing a causal relationship between exposure to strontium chromate or asbestos, and the development of an adenoid cystic carcinoma of the external auditory canal.
Based on all the available evidence, Professor Fox found that your defence service, specifically your exposure to strontium chromate and asbestos, contributed 0% to the causation of your claimed condition.”
This decision was subsequently reconsidered by a Reconsiderations Officer who, on
11 November 2016, affirmed the decision of Ms Barber – Exhibit 1 T38 pp. 124 – 126.
The Applicant’s contentions are as follows (Applicant’s Outline of Submissions (AOS) paras 2 – 3):
(a)the Applicant was exposed to a carcinogenic substance (strontium chromate dust) whilst posted to HMAS Hobart;
(b)the exposure included dust getting into his ear via repeated insertion and removal of earplugs;
(c)the Applicant subsequently developed cancer at the site of his right ear canal (adenoid cystic carcinoma) which was diagnosed in 2008;
(d)the Applicant’s exposure to strontium chromate was a likely cause of his cancer;
(e)the Applicant’s cancer is an “injury” within the ”disease” limb of s 5A(1)(a) of the Safety, Rehabilitation and Compensation Act 1988 (the Act);
(f)the cancer is an ailment that was contributed to, to a significant degree, by the Applicant’s employment by the Commonwealth.
The Respondent contends (Exhibit 8 – p. 7 para 1) that the date of the Applicant’s injury for the purposes of the Act post-dates 13 April 2007, with the ACC first diagnosed in 2008. The Safety, Rehabilitation and Compensation and Other Legislation Amendment Act 2007 moved, with effect from 13 April 2007, the definition of “injury” into s 5A. This is not contested by the Applicant.
The Respondent makes the following concessions (Exhibit 8 p. 8 paras 4 – 5):
(a)the Respondent accepts that the evidence supports a finding that it is possible that the Applicant came into contact with asbestos materials during his naval service; and
(b)the Respondent accepts that the evidence supports a finding of the possibility that the Applicant may have been exposed to strontium and zinc chromate dust or other yellow primers through sanding, grinding and cutting whilst working on HMAS Hobart.
Consequently, it is accepted that the Applicant suffers from ACC of the external auditory canal and that the date of the ”injury” for the purposes of the Act is after 13 April 2007, with an accepted date of diagnosis of 2008.
The key issue in dispute is whether the Applicant’s ACC of the external auditory canal has been contributed to, to a significant degree, by his service with the RAN such that liability should be accepted pursuant to ss 5A and 14 of the Act.
As will be outlined below, the resolution of this matter involves making findings in the context of conflicting medical evidence as to whether there is a link between exposure to strontium chromate and the development of ACC.
THE LAW
The term “injury” is defined by s 5A of the Act to mean:
“(a) a disease suffered by an employee; or
(b) an injury (other than a disease) suffered by an employee, that is physical or mental injury arising out of, or in the course of, the employee’s employment; or
(c) the aggravation of a physical or mental injury (other than a disease) suffered by an employee (whether or not that injury arose out of, or in the course of, the employee’s employment), that is an aggravation that arose out of, or in the course of, that employment;
but does not include a disease, injury or aggravation suffered as a result of reasonable administrative action taken in a reasonable manner in respect of the employee’s employment."
This definition replaced an earlier formulation which was located in s 4(1). For present purposes the differences between the two are not material. The definition contained in
s 4(1) and the task required of the Tribunal was explained by French CJ, Kiefel, Nettle and Gordon JJ in Military Rehabilitation and Compensation Commission v May (2016) 257 CLR 468 (May) as follows (at pp. 479-482):
“[42] The set of conditions answering the definition of “injury” in the Act relevantly comprises two sub-sets, “disease” and “injury (other than a disease)”, the latter sometimes referred to, not necessarily helpfully, as injury simpliciter. They comprise separate but related bases of liability. Each has a different meaning in the statutory scheme.
[43] As appears from the definition of “disease”, a “disease” for the purposes of the Act must be an ailment or an aggravation of an ailment. That is not sufficient to establish the existence of a disease. The ailment or aggravation thereof has to have been contributed to in a material degree by the employee’s employment by the Commonwealth.
[44] An “injury (other than a disease)” covers the other sub-set of ”injury”. Various aspects of this limb of the definition of “injury” should be observed. First, the phrase “other than a disease” means that if an employee establishes that they have a “disease” within para (a) of the definition of “injury”, there is no need to consider para (b)…
[49] It is against that background that the Act requires the tribunal of fact to give consideration to the “precise evidence, on a fact by fact basis, … accepted at trial” and then to ask certain questions in order to determine whether an employee is suffering a “disease” or an ”injury (other than a disease)”.
[50] First, does the evidence amount, relevantly to something that can be described as an “ailment”, being a physical or mental ailment, disorder, defector morbid condition? Second, if so, was that state contributed to in a material degree by the employee’s employment by the Commonwealth?
[51] If the answer to both questions is “Yes”, then there is a disease within para (a) of the definition of “injury”. Of course, in some cases, the answer to those questions may be admitted. That is, the employee may admit that the answer to the first question, or both the first and the second questions, is “No”.
[52] If there is not a “disease” within para (a) of the definition of “injury”, the tribunal of fact next inquires whether there is an ”injury (other than a disease)” within para (b). The third question is – does the evidence demonstrate the existence of a physical or mental “injury” (in the primary sense of that word)? Generally, that will be determined by asking whether the employee has suffered something that can be described as a sudden and ascertainable or dramatic physiological change or disturbance of the normal physiological state. However, that judicial language is not to be construed or applied as if it were the words of a statute defining a necessary condition for the existence of an ”injury (other than a disease)”…”
(Footnotes omitted)
Applying the above methodology to this matter, the initial questions to be answered are whether the evidence before the Tribunal satisfies it that the Applicant suffers from an ailment, and, if so, whether that ailment was contributed to, to a significant degree by his defence service.
“Disease” is defined by s 5B of the Act. Subsection 5B(1) defines disease as an ailment suffered by an employee, or an aggravation of an ailment, that was contributed “to a significant degree” by the employee’s employment.
The requirement that the ailment was contributed to, to a significant degree applies to diseases where an employee first sought treatment or which first resulted in incapacity or impairment, whichever is first. This test came into operation on 13 April 2007, and replaced the previous test, that the ailment was contributed to “in a material degree” by the person’s employment. The Applicant first sought medical assistance for ACC in 2008. Accordingly, the test to be applied is “significant degree” and not “material degree”.
Subsection 5B(2) outlines a non-exhaustive list of matters that may be taken into account in determining if an ailment was contributed to, to a significant degree, by an employee’s employment.
MEDICAL EVIDENCE
Evidence of Professor Fox
The Respondent relies on the evidence of Professor Richard Fox, consultant oncologist. Professor Fox is an Honorary Consultant, Department of Clinical Haematology and Medical Oncology at the Royal Melbourne Hospital. Professor Fox prepared a report dated 14 April 2017. The relevant parts of that report are set out below – Exhibit 7 pp. 2- 3:
“Adenoid Cystic Carcinoma
Adenoid cystic carcinoma involves the skin as well as many organs such as salivary glands, palate, sub-maxillary gland. Other more uncommon locations are the skin, external auditory canal, nasopharynx, lacrimal gland, bronchial tubes, uterine cervix and breast.
The tumour source appears to be the eccrine glands or apocrine glands in the skin & other organs..
As an adnexal skin tumour it would have evolved from sweat glands or hair follicles.
Chromate (VI) Toxicity
I note supplied is chapter from the IARC (International Agency on Research in Cancer Monograph 100C regarding carcinogenicity of Chromium (VI).
It causes the causation potential of chromates for lung cancer and possibly nasal sinus.
It notes that estimates of the numbers of workers potentially exposed to Chromium (VI) compounds, has been developed by CAREX (carcinogen exposure) in Europe.
Based on occupational exposure to known and suspected carcinogens collected during 1990 to 1993, the CAREX database estimates that 785,692 workers were exposed to hexavalent Chromium compounds in the European Union.
58% of workers employed in the following four industries; manufacture of fabricated metal products, manufacture of machinery except electrical, manufacture and household service and transport. CAREX Canadian estimates that 83,000 Canadians are occupational exposed to Chromium (IV) compounds.
There is no mention of the development of skin cancer following these occupational exposures. Nor is there a mention of Adenoid Cystic carcinoma.
Based on the report of Dr David Douglas and the mechanism of induction of adenoid cystic carcinoma described by him, one would have expected logically that carcinoma of the skin would be produced by Chromium (IV) compounds acting locally on the skin to which obviously many thousands of people would have been exposed.
Skin irritation by chromates is noted and often leading to potentially benign skin ulcers. But skin cancers do not develop.
If Dr Douglas’s concept was correct regarding Mr Graham White, he would have developed a skin irritation in the external auditory canal.
I note the document from OSHA (Occupational Safety and Health Administration of US Department of Labour) mentions health effects of hexavalent Chromium.
It notes that industrial sources of hexavalent Chromium are chromium pigments in dyes, paints, inks and plastics, anticorrosive agents to paints and primers, chrome painting by depositing Chromium metal on surfaces and other sources.
It notes how hexavalent Chromium can harm employees by causing lung cancer in workers who breathe airborne hexavalent Chromium, it notes irritation or damage to the nose, throat and lung if hexavalent Chromium is breathed at high levels. It notes irritation or damage to the skin and eyes if hexavalent Chromium contacts these organs in high concentrations.
There is no mention of skin cancer.
There is no mention of the causation of adenoid cystic carcinoma.
In fact, the entire literature based of adenoid cystic carcinoma indicates there is no known cause whatsoever.
There is speculation that HPV viruses may be involved and there is some evidence for that. Therefore, in my opinion Dr Douglas hypothesis re Mr White, though appearing logical is not in accord with epidemiological data & is fanciful...”.
Professor Fox had prepared an earlier report dated 5 September 2016. The conclusions he reached in the earlier report were re-iterated in his April 2017 report. Relevant extracts from the earlier report are set out below – Exhibit 1 T11 p. 45:
“In terms of relationship to his potential exposure to strontium chloride, I carried out a computer search of the United States National Institute of Health Database as well as a general computer search.
There is an IARC monograph (Vol100c, on chromate salts). It notes that studies indicate there is an excess risk of lung cancer among workers exposed to chromium 6, particularly in chromate production, chromate pigment production and chromium electro-plating.
There are some case reports, cohort studies and case control studies that suggest a possible excess of cancer of the nose and nasal sinus among workers exposed to chromium 6.
It notes however this latter evidence is susceptible to publication and reporting, because many of the cohort studies do not report on nasal cancers and it is not clear how to evaluate the significance of the case reports.
There is little evidence that exposure to chromium 6 causes stomach or other cancers. There was no mention of relationship to adenoid cystic carcinoma.
Adenoid cystic carcinoma is a rare carcinoma that typically arises in salivary glands but can occur at other sites including skin. It can also involve the external ear canal as well as many other sites.
It is a locally aggressive tumour characterised by local recurrence and late metastases. There is virtually nothing known about its aetiology or cause.
There are no reports of it in relationship to chromate exposure.
There are certainly no reports regarding asbestos or other chemicals exposure as potentially causative.
My opinion is therefore that there is no known relationship to his service.”
Professor Fox gave evidence during the hearing and referred to an article published in the American Journal of Industrial Medicine (2015, Volume 58 pp. 905 – 913) by Gibb, Lees, Wang and O’Leary entitled “Extended Followup of a Cohort of Chromium Production Workers” – Exhibit 10.
The study evaluated the mortality of 2,354 workers first employed at a Baltimore chromate production plant between 1950 and 1974.
The study followed two earlier research projects which focused on workers at a chromate production plant in Baltimore who were newly employed between 1 January 1945 and 31 December 1974. Only males who were employed more than 90 days were included in the study. The focus of the studies was the increased lung cancer risk among workers in the chromate-production industry.
The conclusion reached was that cumulative chromium exposure was a risk factor for lung cancer death, but that cancer deaths, other than lung cancer, were not significantly elevated. Of the 1,613 chromium workers who subsequently died, 460 died of cancer related causes and of that number only nine had skin related cancers – Exhibit 10 p. 908.
Professor Fox’s oral evidence was entirely consistent with his written reports. He re-iterated that in his opinion there was no link between chromium exposure and the cancer suffered by the Applicant. He again referred to the research conduct by the IARC and said that there was a proven link between exposure to chromium and lung cancer but no evidence of it causing skin cancer.
He testified that ACC was a rare cancer, with relatively little research on its cause. However, there was no research that indicated a link between ACC and chromium exposure, and in support of that proposition referred at some length to the findings in Exhibit 10.
Professor Fox, under cross-examination, while accepting that ACC was rare and the research about its causes relatively scant, opined that to suggest that there was link to it and chromium exposure would take one into an area of speculation.
In short, the evidence of Professor Fox was clear and unequivocal, namely that there is no medical basis to conclude that there is a causal link between chromium exposure and ACC.
Evidence of Dr David Douglas
The Applicant relies on the evidence of Dr David Douglas, Consultant Occupational Physician. Dr Douglas has particular expertise in occupational and environmental toxicology, risk assessment and related research. From 1973 to 1979 Dr Douglas held appointments at the University of London and then as Head of Scientific Policy at the UK Health and Safety Executive. On returning to Australia he worked in occupational health and safety areas with the South Australian Health Commission, CSR and the NSW State Pollution Control Commission. He was also, between 1989 and 2000, expert consultant to the International Labour Organisation in Geneva – Exhibit 5. He is the author of many articles and chapters in learned professional publications on the subject of the health and safety implications of workplace conditions, including occupational cancer – Exhibit 9.
Dr Douglas was of the very firm opinion that there was a link between the Applicant’s exposure to strontium chromate and the development of his ACC. Dr Douglas opined as follows – Exhibit 3 pp. 8 – 10:
“It is my opinion that, on the balance of probabilities, Mr White’s adenoid cystic carcinoma of the right external auditory canal, now with local invasive cancer, is directly attributable to his service in the Australian Navy. In particular, it is due to service in 1996 when he carried out maintenance work on HMAS Hobart. During that work he was frequently exposed to heavy concentrations of dust containing strontium chromate used as a constituent of paint used in the undercoat when painting HMAS Hobart.
Even before considering the scientific literature it is intuitively obvious that the contamination of the right ear canal with dusts on an earplug could lead to skin problems either immediately or subsequently. I compare this intuitive opinion with that of a rash on the skin in the exact distribution of a previously applied sticking plaster – it would be inconceivable to consider the rash unrelated to the plaster.
Similarly, it is inconceivable to consider that there was no direct link between the exposure of dust on an earplug and the subsequent development of the tumour at the site of the earplug.
However, the scientific literature contains significant data which provide a biologically plausible explanation as to why the dust, containing strontium chromate, when deposited in the right external auditory canal, subsequently led to the development of the rare skin tumour namely adenoid cystic carcinoma.
In his submission to DVA dated 5 September 2016, Professor Richard Fox rejected Mr White’s claim for a causal link between his exposure and his cancer, largely based of his reading of Volume 100C of the IARC Monographs on the Evaluation of Carcinogenic Risks to Humans concerning Chromium (VI) Compounds. A copy of the relevant pages from Monograph 100c is enclosed. But Professor Fox did not consider fully the implications of that publication.
One important omission is the fact that a rare exposure as experienced by Mr White, and development of a very rare tumour (which had not been accurately described in pathological terms until about the 1970s), is impossible to link causally using the broad epidemiological approach used in the research which found chromate-6 compounds caused lung cancer and possibly sinonasal cancer. Instead, in such exposures and outcomes as in the case of Mr White, it is important to consider toxicological mechanisms in seeking causal associations.
At page 156 of the IARC Monograph Volume 100c, it is stated that chromium-6 compounds, including strontium chromate, have been tested for carcinogenicity by several routes in several species and strains of experimental animals:
Calcium chromate induced lung tumours in mice when given by inhalation, and local tumours when given by intramuscular administration. In rats, it caused lung tumours when given by intratracheal or intrabronchial administration, bronchial tumours by intrabronchial administration, and local tumours when treated by intrapleural or intramuscular administration.
Lead chromate (and its derived pigments) administered by subcutaneous or intramuscular injection caused malignant tumours at the site of injection and renal tumours in rats. Subcutaneous administration of basic lead chromate caused local sarcomas in rats.
In rats, zinc chromates caused bronchial carcinomas when administered by intrabronchial implantation, and local tumours when given intrapleurally, subcutaneously, or intramusculary.
Strontium chromate caused bronchial carcinomas (intrabronchial implantation administration), and local sarcomas (intrapleural and intramuscular administration) in rats.
The importance of these data is the fact that cancers arose not only in the lung where human cancers have been attributed causally to chormate-6 compounds, but also at the site of the application of various chromate-6 compounds, including strontium chromate.
This is analogous to Mr White’s exposure where strontium chromate was locally applied in an abrasive dust on an ear plug which, from its insertion, would cause microtrauma to the lining of the right external auditory canal and therefore have the potential to provide a local dose of strontium chromate to the abraded skin. The subsequent development of cancer is a multistage process and would have taken several years. It is consistent with the known mechanism of cancer induction, that Mr White’s exposure in 1996 was consistent with his subsequent diagnosis of the adenoid cystic carcinoma in 2008. The cancer would have been developing, without Mr White’s awareness, during the years 1996 to 2008.”
(Emphasis in the original)
Dr Douglas was provided a copy of Professor Fox’s supplementary report of 14 April 2017, and provided, inter alia, these comments – Exhibit 4 p. 2:
“Additionally, Professor Fox draws great strength from the fact that skin cancers of any type have not been reported in the mortality studies of a wide range of chromate workers both in the United States and in Europe. This is understandable as skin cancers do not feature in mortality studies because, by and large, skin cancers are not fatal conditions as compared with lung cancer for which chromate is well recognised as a causative factor.
In his final paragraph Professor Fox has stated “Dr Douglas’ hypothesis re Mr White, though appearing logical, is not in accord with epidemiological data and is fanciful”. I would remind Professor Fox that the first report of a link between chromate exposure and cancer appeared in the Glasgow Medical Journal published in 1890. It concerned a case of adenocarcinoma of the left inferior turbinate body and perforation of the nasal septum in the person of a worker in chrome pigments”. If the editor of that journal had considered the association of exposure and outcome to be fanciful, then it probably would not have been published and the risk of chromates raised in the wider community. Professor Fox should be well aware that all medical conditions do not have clear-cut causal factors and it is only by applying logical and lateral thinking that a greater understanding is obtained.”
Dr Douglas was vigorously cross-examined by Mr Clark. Dr Douglas denied Mr Clark’s assertions that he was an advocate for the Applicant and that he was influenced by an irrelevancy.
Dr Douglas re-iterated that ACC was not the subject of extensive medical research, and only since the 1970s has it been specifically recognised and been the subject of scientific papers. He also stressed the importance of research on animals and stressed the direct relevance of that research to the question of the causal relationship between ACC and exposure to chromates.
CONSIDERATION
Introduction
The issue to be determined by the Tribunal is relatively narrow, but extremely vexed.
It is not contested that chromate-based paint is listed as a category 1 carcinogen – Exhibit 7 p.1.
It is not contested that strontium chromate was used as a primer paint on metals – Exhibit 7 p.1.
It is not contested that the United States used strontium chromate on their ships prior to the 1980s, and that, consequently, RAN ships built in the United States prior to circa 1980 (including HMAS Hobart) would have had it used as an undercoat – Exhibit 8 para 12 p. 3.
It is not contested that the Applicant was exposed to chromate dust in the course of his duties on HMAS Hobart – Exhibit 8 para 5 p. 8.
The Tribunal finds, on the evidence presented, that the Applicant’s right ear canal was directly and repeatedly exposed to strontium chromate dust whilst he was performing duties on HMAS Hobart.
It is also not contested that the Applicant was diagnosed with ACC in circa 2008 – Exhibit 8 para 1 p.7.
It is not contested that there is a causation potential of exposure to chromates and the development of lung cancer, and possibly nasal sinus cancer – Exhibit 7 p. 2.
The issue in dispute is whether there is a causal relationship between the Applicant’s exposure to strontium chromate and the development of ACC. Or, more particularly, whether the Applicant’s ACC condition was contributed to, to a significant degree, by his naval service such that liability should be accepted pursuant to ss 5B and 14 of the Act.
The medical evidence could not be more divergent. The medical evidence adduced by the Applicant strongly suggests such a link, whereas that adduced by the Respondent denies absolutely the possibility any such link.
Mr Clark submitted that the Applicant was, in effect, asking the Tribunal to engage in an exercise of speculation. He submitted that there was nothing in the medico-scientific literature to support the proposition that there is a causal connection between the exposure to chromates and the development of ACC. In the absence of a sound scientific basis for the argument that there is a causal link, the Applicant’s case could only be characterised as speculative. Mr Clark said that in order for the Tribunal to find liability there had to be a link, on the balance of probabilities, between the Applicant’s exposure to chromates and his ACC, but here the evidence disclosed no link. Finally, Mr Clark submitted that Dr Douglas’ evidence did not stand up to scrutiny because it lacked a sound and proven medical/scientific basis.
Mr Black submitted that the link between the Applicant’s exposure to chromates and the development of ACC could be characterised as “unlikely”. He said that this was so as ACC is a relatively rare condition and that the number of times individuals may have developed ACC after chromate exposure was extremely low. However, he submitted, the fact that it is unlikely or rare does not mean that it is impossible, and Dr Douglas’ evidence highlighted that there was a medico-scientific basis for concluding that, on the balance of probabilities, there was a causal link between the Applicant’s exposure to chromates and his ACC.
The Applicant initially raised the exposure of the Applicant to asbestos in dust form both during his posting on HMAS Hobart and also during his posting on HMAS Watson – Exhibit 6 paras 3-4. However, in later submissions (AOS) and during the course of the hearing, the sole focus of the Applicant’s case was the contended link between exposure to strontium chromate and the development of ACC. Accordingly, the Tribunal’s decision is based solely on the question whether chromate exposure was, on the balance, the cause of the Applicant’s ACC.
The Forst Principles
Mr Black drew the Tribunal’s attention to Adelaide Stevedoring Company Limited v Forst (1940) 64 CLR 538 (Forst). That case concerned a waterside worker who was powerful and vigorous and in apparent good health, albeit of advancing age. After performing two tasks involving muscular exertion he collapsed and died. There was a conflict of medical evidence. The worker’s death was due to coronary thrombosis, but this was generally not related to physical exertion. A majority of the Court found in favour of the worker’s widow.
Rich ACJ said (at pp. 563-564):
“I am greatly impressed by the sequence of events. The deceased, who had arrived at an age when arterio-sclerosis and atheroma afflict mankind, was a stevedore’s labourer. On the day of his death he climbed up the jib of the crane and lay prone on the crane with his arms outstretched, trying to replace a wire which had come off the gin. He failed to do so, returned to the deck and for some time, with his arms in a position raised over his head, helped in holding up a wire rope. Immediately after performing this task he collapsed. What weighs so much with me is the fact that he was brought to a standstill, as an ordinary observer would think, by the exertion he had undergone: Cf. Partridge Jones and John Paton Ltd. v. James. I do not see why a court should not begin its investigation, i.e., before hearing any medical testimony, from the standpoint of the presumptive inference which this sequence of events would naturally inspire in the mind of any common-sense person uninstructed in pathology. When he finds that a workman of the not-so-young standing attempts in a posture calculated by reason of the pressure on the stomach to disturb or arrest the rhythm of the heart a very strenuous task not forming part of his ordinary work and then collapses almost immediately and dies from a heart condition, why should not a court say that there is strong ground for a preliminary presumption of fact in favour of the view that the work materially contributed to the cause of death? From this standpoint the investigation of physiological and pathological opinion shows no more than the current medical views find insufficient reason for connecting coronary thrombosis with effort. Be it so. That to my mind is not enough to overturn or rebut the presumption which flows from the observed sequence of events. If medical knowledge develops strong positive reasons for saying that the lay common-sense presumption is wrong, the courts, no doubt, would gladly give effect to this affirmative information. But, while science presents us with no more than a blank negation, we can only await its positive results and in the meantime act on our own intuitive inferences.”
(Footnotes omitted)
The Tribunal’s attention was also drawn to the decision of the New South Wales Court of Appeal in Commissioner of Police v Rea [2008] NSWCA 199 (Rea), where Handley AJA said (at para [8]): “…it is now well established that the Forst principles are not limited to cases where there is an immediate temporal connection between the alleged cause and the injury.”
During the course of the hearing, Mr Clark drew the Tribunal’s attention to paragraph 22 of the decision of the High Court in May. In that paragraph their Honours outlined that the Tribunal decision found there was a temporal relationship between the incident in question (vaccinations) and the onset of symptoms.
If there is an immediate temporal connection between the alleged cause and the injury (disease), then as Forst highlights, the intuitive process explained by Rich ACJ is made that much more obvious. However, as explained in Rea, the absence of such a temporal connection is neither fatal to the application of the Forst principles, nor more generally to the finding of liability under the Act.
Handley AJA in Rea also quoted with approval a passage from EMI (Australia) v Bes (1970) 44 WCR 114 (Bes) at p. 119, where Herron CJ said:
“…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 the 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.”
The Forst principles have been referred to, and applied, not only by various Members of this Tribunal and by the Federal Court on appeal (e.g. Telstra Corp Ltd v Mahon (2004) 39 AAR 484), but by all levels of the judiciary in every jurisdiction of the Commonwealth. It will suffice to note that in the recent High Court decision of May French CJ, Kiefel, Nettle and Gordon JJ said (at para [62]/p. 484):
“…The evidence to be adduced, of course, will vary from case to case and, where appropriate, may take into account common-sense inferences drawn from a sequence of events.”
Their Honours cited in approval of that proposition Forst and, in particular, the passage of Rich ACJ outlined above and also Dixon J at pp. 569 – 570. Dixon J made, inter alia, this observation (at p. 570):
“Tempting as it always is, particularly in matters of bodily health, to argue from a sequence of external events, such reasoning is justified only when positive knowledge or common experience supplies some adequate ground for believing that the events are naturally associated.”
Is there a causal link?
Care must always be taken when drawing inferences in the context of an evidentiary matrix which is subject to widely divergent and contradictory expert opinion. It is trite, but critical, to bear in mind that inferences can only be drawn from proven facts. Opinion or assertion is an illusory base from which inferences can be drawn.
Causation has always been a vexed and difficult concept. A recent example which illustrates this difficulty is Amaca Pty Ltd v Ellis & Ors (2010) 240 CLR 111 (Ellis).
In that case a heavy smoker who was exposed to respirable asbestos fibres in the course of his employment died of lung cancer. He commenced legal proceedings before his death (at the age of 45) against, inter alia, two of his employers where he had been exposed to respirable asbestos fibres.
The medical evidence was that both tobacco smoke and asbestos inhalation were capable of producing the cancer. No medical examination could ascertain why the worker developed lung cancer. Experts gave epidemiological evidence which drew conclusions from studies of large groups. One Professor estimated that the probability of the worker’s lung cancer being caused by smoking alone was 67% and asbestos only at 3%. Another Professor’s estimation was 92% and 0.1% respectively. The expert evidence was consistent and pointed, overwhelmingly, towards tobacco smoking being the most likely cause of lung cancer – Ellis at [24] – [28]/125-126.
The High Court unanimously held that causation had not been established. The evidence established no more than that exposure to asbestos might have been a cause of the lung cancer, but it did not establish that it was more probable than not that asbestos was a cause.
It is clear from Ellis that to establish causation in the absence of settled and established medical science, the proven facts must be sufficiently strong and consistent to support a definite inference of causation.
Mr Black did not advance his case by submitting that it was open to the Tribunal to draw Forst inferences even though the causal link was “unlikely”. If the factual matrix presented to the Tribunal was so scant and fragile that there was no “adequate ground for believing” that the Applicant’s condition is “naturally associated” with his service, then the Tribunal would agree with Mr Clark that this amounts to an invitation to draw inferences from speculation, and itself would be an exercise in speculation. Based upon the Tribunal’s reading of either the reasoning of Rich ACJ or (more particularly) Dixon J in Forst, without such a ground, the Applicant’s case would fail.
It is also not the case that medical science conclusively says that there is no link between exposure to chromates and the development of ACC. If that were the case, then, as explained by Herron CJ in Bes, there would be no scope to apply the Forst principles.
Further, it is not the case that medical science conclusively says that the link between exposure to chromates and the development of ACC is miniscule or extremely unlikely, compared with other much more likely pathological scenarios, as was the case in Ellis. Again, if the evidence before the Tribunal disclosed that state of affairs, the causal link could not be established.
The Forst principles were enunciated in a case where a presumptive inference flowed from the observed sequence of events and where the state of medical science was inconclusive and presented only a “blank negation”.
The evidence presented in this case fits squarely within the evidentiary scenario painted by Rich ACJ in Forst. Unlike Ellis, the medical science in this case is relatively embryonic, unsettled and disputed.
It is the case that chromium is carcinogenic, and that studies published since 1890 have concluded that it may cause cancer. However, those studies are, from the material presented to the Tribunal, not extensive, and the focus of medical science has been on determining if there are links between chromate exposure and the development of lung cancer, and, to a lesser degree, nasal cancer. Further, it would appear that the link between chromate exposure and lung cancer has been accepted by a number of medical researchers.
It is also the case that ACC is a rare disease, and, fortunately, afflicts relatively few people. As a consequence, the Tribunal was informed that it has not been the subject of the extensive medical research that many other forms of cancer have.
Professor Fox is an eminent and well known medical professional. He is very experienced in his recognised fields of endeavour, and, for example, was referred to in the Ellis decision (at para [18]/124). Mr Clark submitted that Professor Fox’s clear and unequivocal written and oral evidence that there is no medical research to support a causal link between chromate exposure and ACC should be accepted. If the Tribunal accepted that invitation then there would be no scope to apply the Forst principles. The observed sequence of events would in this case be overturned by medical knowledge that says “that the lay common-sense presumption is wrong”.
However, the Tribunal was also presented with the clear and unequivocal evidence of Dr Douglas, who was equally adamant that the medical research on mice and rats which proved that there was a direct link between chromate exposure and skin cancers.
In this case, the Tribunal has not engaged in an exercise of independently attempting to peruse whatever extant medical research exists on chromate exposure and its links to the development of cancer. The Tribunal has proceeded on the basis of the material presented, the oral evidence and the submissions of counsel.
The scientific evidence before the Tribunal neither supports the proposition that exposure to chromates can cause ACC, nor conclusively rules it out as a possibility. `Extensive workplace tests do indicate that chromate exposure can lead to the development of lung cancer. However, the medical evidence of chromate exposure on animals discloses that there may be a link between chromate exposure and skin cancers.
If medical evidence were to actively disprove a link between the results of experimentation on animals and human reactions to carcinogens, then the evidence Dr Douglas pointed to about the effects of chromate exposure on mice and rats would have no weight. However, there is no evidence before the Tribunal which would suggest that the experimentation on animals is irrelevant to assessing the link between chromate exposure and skin cancers in humans. Nor was the Tribunal presented with any accepted scientific evidence that would suggest that the research of chromate exposure in animals can be distinguished for some pathological or other reason.
In short, the Tribunal is presented with a confused medico/scientific state of affairs, where professionals of great experience and learning are at loggerheads.
It is not even the case, as in Forst, where the state of medical research had only reached the stage of a “blank negation”. Here the research is ostensibly divergent. It is for this reason that the Tribunal characterises the research, or at least so much of it as was drawn to the Tribunal’s attention, as “embryonic”.
Accordingly, the Tribunal accepts the Applicant’s contention that the known facts of his exposure to a carcinogenic substance in the course of his employment directly on the site of his subsequent ACC gives rise to a presumptive inference of a causal link. The Tribunal accepts that the evidence presented does not meet a medical standard of certainty, but that is not required. The evidence is sufficient to reach a conclusion on the balance of probabilities – Tabet v Gett (2010) 240 CLR 537 at p. 578 per Kiefel J.
Conclusion
The task required of the Tribunal, as explained by the High Court in Kennedy Cleaning Services Pty Ltd v Petkoska (2000) 200 CLR 286 at p. 300 is to give consideration to “the precise evidence, on a fact by fact basis …”
In this matter there are relatively few contested facts. The evidence is straightforward. The Applicant, while serving in the RAN was exposed to strontium chromate dust and approximately 12 years later was diagnosed with ACC. He was 25 years of age when he was exposed to strontium chromate dust and 37 when he was diagnosed with cancer. The Applicant is now approximately 46 years of age and is terminally ill.
The stark sequence of events outlined previously leads to, or strongly suggests, a presumptive inference that his exposure to chromate dust and the development of ACC are linked. Certainly, no other plausible explanations were ventilated during the proceedings. The fact that the Applicant was inserting into his right ear canal on a relatively frequent basis over an extended period of time, ear plugs that were exposed to strontium chromate dust and he subsequently developed cancer of the right ear, leads to the drawing of a common-sense inference.
The real issue, though, is whether the medical evidence presented displaces this inference, drawn as it is, from a sequence of events by persons “uninstructed in pathology”.
Care must be taken in drawing inferences from supposed sequences of external events. As Dixon J warned in Forst (at p. 570) there must be “adequate” grounds for believing that the events are “naturally associated”.
Further, where medical science is settled and casts doubt on the correctness of the presumptive inference, the inference gives way to the weight of medical science. In short, if a sequence of events leads to a conclusion that medical science says is impossible, unlikely or improbable, then no presumptive inference can be drawn. Ellis clearly illustrates that where medical science suggests that the development of a particular form of cancer is very unlikely from the particular facts, then the Forst inference is displaced.
Here, the medical science is not secure and settled. There are clearly significant differences of opinion between the medical experts. Perhaps if more detailed scientific evidence was presented, a clearer picture might emerge, such that a more secure conclusion could be formed by the tribunal of fact. However, that is speculation. All that this tribunal of fact can do is to work with the evidence that was presented and proceed to reach a conclusion therefrom.
The starkly divergent medical evidence and the relatively meagre state of medical science on the links between chromate dust exposure and the development of ACC, do not provide a basis for displacing the clear and undisputed sequence of external events outlined. Should there be medical science which securely disproves that there is a causal link between chromate dust exposure and the development of ACC, then, to quote Rich ACJ in Forst (at p. 564) “we can only await its positive results and in the meantime act on our own intuitive inferences”.
Accordingly, I find that the Applicant’s military employment contributed, to a significant degree, to the development of his claimed condition and that the Applicant’s ACC is a compensable injury under the Act.
DECISION
The decision under review is set aside and in lieu thereof the Applicant is entitled to the payment of compensation pursuant to the Safety, Rehabilitation and Compensation Act 1988 for the claimed condition, namely adenoid cystic carcinoma of the external auditory canal.
I certify that the preceding 90 (ninety) paragraphs are a true copy of the reasons for the decision herein of Senior Member J Sosso
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Associate
Dated: 27 September 2017
Date of hearing: 2 August 2017 Counsel for the Applicant: Matt Black Solicitors for the Applicant: Maurice Blackburn Lawyers Counsel for the Respondent: Charles Clark Solicitors for the Respondent: Moray and Agnew