Rogalski, Martin --- "Causation in latent onset disease claims" [2023] PrecedentAULA 18; (2023) 175 Precedent 24

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CAUSATION IN LATENT ONSET DISEASE CLAIMS

SELECT CASES

By Martin Rogalski

In latent onset disease cases, it is sometimes difficult to precisely determine whether exposure to a specific substance has caused or materially contributed to the development of a medical condition. This can occur for a variety of reasons including when there is exposure to multiple toxic agents, limited scientific evidence or an idiosyncratic response following exposure to a toxic agent.

‘The common sense approach to causation at common law is quite different from a scientist’s approach to causation ... An inference of causation for the purposes of the tort of negligence may well be drawn when a scientist, including an epidemiologist, would not draw such an inference.’^[1]

This article provides an overview of latent onset disease cases with discussion of recent developments.

SILICA

Silica is a ‘mineral that exists in various forms, including sand, quartz, and flint’.^[2] Products that contain silica include paint, paper, rubber, plastic, pharmaceuticals, food, cement, plaster, cat litter, potting soil, plaster board, and miscellaneous construction materials.^[3]

There has been a relatively recent spike in incidences of silica-induced disease. Stonemasonry, in particular, has been in the media spotlight. One major issue causing this spike has been the absence of (or at least ineffective) personal protective equipment issued to workers. The other major issue has been the substantial increase in dry cutting during manufacture and installation of artificial stone, which can contain substantially more silica when compared to natural stone.^[4] The rate of disease development in relatively short latency periods has been alarming. Latency periods of less than five years have been reported.^[5].

Exposure to silica dust gives rise to the risk of developing various conditions including silicosis, lung cancer, silico-tuberculosis and immune-mediated diseases.^[6]

It has been estimated that that approximately 10,390 of predicted future lung cancer registrations could arise among all workers who were exposed to silica dust at work in 2016, and approximately 83,090 silicosis cases will arise in the future as a result of current occupational exposure to silica dust.^[7]

Many cases have been pursued in respect of more common silica-induced conditions such as silicosis and lung cancer. The Dust Diseases Tribunal case of Badenoch v Granite Transformations Pty Ltd^[8] explored the less common condition of lymphadenopathy (swelling of the lymph nodes) where the plaintiff alleged that the condition was caused by exposure to silica dust. The Tribunal was asked to determine whether it had jurisdiction to determine the plaintiff’s claim in circumstances where the first defendant alleged that hilar lymphadenopathy was not a ‘dust-related condition’.^[9] The plaintiff adduced medical evidence from two eminent experts, Dr Richard Slaughter and Dr Robert Edwards, who agreed that the hilar lymphadenopathy was (radiologically and clinically) silica-related.

ASBESTOS

Asbestos is ‘a fibrous mineral that is incombustible and does not conduct heat’.^[10] It has been used in thousands of products,^[11] including joint compound, vinyl floor tiles, sheeting, adhesives, roofing tiles, felts, siding, acoustic ceilings, gloves, brake pads, brake shoes, fire blankets, fire doors, thermal pipe insulation, water pipes and filters.

A large body of medical literature confirms that asbestos exposure can lead to the development of various medical conditions, including asbestos related pleural plaques, asbestosis, lung cancer, mesothelioma and benign pleural effusions.^[12]

Some asbestos diseases can develop in different areas of the body. For example, mesothelioma usually develops in the pleura, although in rare cases it can present in the peritoneum, pericardium or tunica vaginalis testis.

In Werfel v Amaca Pty Ltd^[13] the plaintiff claimed damages for mesothelioma of the tunica vaginalis testis (MTVT). He alleged that he was exposed to asbestos dust and fibre emanating from asbestos cement sheeting manufactured by the defendant in several periods spanning from about 1994 to about 2005 while he undertook handyman work in Adelaide.

The defendant put virtually every possible issue in dispute. In terms of causation, however, the defendant argued that there was insufficient proof that inhaling asbestos dust can cause MTVT because:

1. MTVT is such a rare form of mesothelioma that there is insufficient epidemiological and other data demonstrating a connection; and

2. the prominent form of asbestos that the plaintiff was exposed to is less carcinogenic than other types of asbestos and, according to expert evidence, could not cause mesothelioma.

The South Australian Employment Tribunal rejected the defendant’s arguments, preferring and accepting the plaintiff’s evidence, which included expert medical opinion from eminent pathologist, Professor Sonja Klebe. The judgment refers to pertinent parts of Professor Klebe’s evidence, which included extensive discussion of pathological findings and biological plausibility of MTVT despite its extremely rare incidence. It established that the role of asbestos in the pathogenesis of mesothelioma has been established (including peritoneal mesothelioma) and the same causal effects contributing to causation of mesothelioma in the peritoneum applies to MTVT.^[14] Once the Tribunal made those findings, causation was established in favour of the plaintiff.

In King v Caltex Petroleum Pty Ltd,^[15] the plaintiff, who started proceedings before he died, alleged that exposure to asbestos dust during his work for Caltex from 1969 to about the 1980s caused his condition of mesothelioma.

Much of the plaintiff’s work was clerical, administrative and managerial rather than hands on. He visited numerous sites and buildings that were constructed of asbestos materials. When describing his work, the plaintiff referred to those buildings and where they were, but he did not suggest any specific exposure to asbestos. The plaintiff did not suggest ‘that his duties involved anything in relation to those buildings other than his mere presence’.^[16]

The judge held that for the plaintiff to succeed in establishing the case, it would need to be proven that first, the late plaintiff had the opportunity to be exposed to asbestos and second, that he was, in fact, exposed. The judge was satisfied as to the former but not the latter, which he held to be ‘entirely circumstantial’.^[17] Expert evidence from a respiratory specialist was unable to assist the plaintiff. A verdict was entered for the defendant.

Seltsam Pty Ltd v McGuiness^[18] was an appeal regarding a judgment in favour of the plaintiff, which determined that he suffered from an asbestos-induced renal cell carcinoma. On appeal, the principal issue raised was the application of epidemiological evidence to prove causation.

Chief Justice Spigelman emphasised that:

‘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 relationship. 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?’^[19]

The NSW Court of Appeal found that in order to succeed in establishing causation, the evidence needs to rise above the mere level of possibility or increased risk. Rather one must establish that on the balance of probabilities the relevant exposure did create or increase the risk of injury and that risk had eventuated.^[20] The Court discussed the process of inference from circumstantial evidence that combines primary facts like ‘the strands in the cable’ which ‘must be capable of bearing the weight of the ultimate inference’.^[21] Ultimately, it was held that the epidemiological studies and expert epidemiological opinion evidence on general causation went no further than establishing a possibility and did not justify an inference of causation in the present case. The appeal was successful.

FERTILISER

In Cowen v Bunnings Group Limited,^[22] the plaintiff alleged that as an employee at Bunnings in Mt Isa she swept up spilled fertiliser for over two hours and inhaled significant amounts of the fertiliser dust. The plaintiff alleged that she developed various symptoms during the course of her work and later that day. She went to work the next day with symptoms. She had limited recollection of that day other than serving a customer. Her next memory was waking from a coma.

The plaintiff alleged that her inhalation of fertiliser dust caused her to develop pneumococcal meningitis, encephalitis and septicaemia. The plaintiff did not wear any personal protective equipment during the course of her work.

The respondent alleged that the plaintiff had a pre-existing respiratory illness that was equally likely to have caused the conditions she developed. The defendant put causation as the sole issue in dispute.

Four eminent medical specialists gave evidence. Two specialists thought there was a causal connection on the balance of probabilities. The other specialists agreed it was ‘certainly not implausible’ but did not go further.^[23]

An attempt was made to recreate the plaintiff’s work environment and a scientific report commissioned by the defendant provided strong corroboration of the plaintiff’s evidence regarding her dust exposure.

Dr McCormack was the first of the experts to advance a theory regarding the development of the plaintiff’s illness. Two of the experts were initially reluctant to adopt this theory on the basis that there was an absence of medical and scientific literature recording the relationship between irritation of the nasopharynx by dust and invasive pneumococcal disease. Ultimately, these experts conceded that their reasoning on the issue was unjustified and they could not maintain an opinion of the relationship being implausible.

The defendant argued there were five other possible causes for the plaintiff’s injury. However, two of these five factors were not pleaded. The other factors (that the plaintiff had a different or novel serotype of the pneumococcal bacterium, that it was the chronic exposure to sulphur dioxide in the Mt Isa atmosphere and that the plaintiff was suffering a cold prior to the day in question) were not accepted.

In determining causation, the Supreme Court of Queensland gave significant weight to the ‘compelling features’:

‘The compelling features pointing to a causal connection are, firstly, the strong relationship in time between one event, and the other. The second is the nature of the material to which the plaintiff was exposed and the duration of exposure which, on any view, was serious and unpleasant and, in particular, caused immediate and prolonged upper respiratory tract symptoms.’^[24]

The Court adopted a common sense approach and held that, while the event was unusual, in consideration of the temporal connection and expert medical opinion, the plaintiff must succeed.

PERFLUOROALKYL AND POLYFLUOROALKYL SUBSTANCES

Perfluoroalkyl and polyfluoroalkyl substances (PFAS) are a group of over 4,700 heterogeneous compounds with amphipathic properties and exceptional stability to chemical and thermal degradation.^[25] PFAS have been used in many industrial and commercial applications.

Currently, it seems that there is insufficient statistical evidence of whether PFAS pose a significant risk to human health. Statistically significant outcomes linking adverse effects of PFAS exposure seem to be limited to animal-based studies.^[26] However, there are thousands of medical journal articles on the topic of impacts of PAFS on human health. Review articles show that there are possible associations between PFAS exposure and adverse human health outcomes, including immune and thyroid dysfunction, liver disease, lipid and insulin dysregulation, kidney disease, adverse reproductive and developmental outcomes, and cancer.^[27] However, confident conclusions are unable to be drawn at this stage. One of the major limitations in improving understanding of the issue is that there are so many PFAS compounds to investigate. Other barriers that limit a deeper understanding of PFAS’ impact on human health include varying conditions of exposure and characteristics associated with the exposed target^[28]. It does not seem as though there are any reported cases for personal injury arising from PFAS exposure in Australia and this is perhaps not surprising considering findings from published literature.

Having said the above, there have been successful claims that alleged loss and damage due to PFAS property contamination from the use of firefighting foam by the Royal Australian Air Force (RAAF) bases of Williamtown, Oakey and Katherine. Three class actions were brought for nuisance, negligence and for contraventions of the Environment Protection and Biodiversity Conservation Act 1999 (Cth) on behalf of land and business owners.^[29]

Contracts of sale have also been avoided on the basis of breaches of disclosure obligations regarding the presence of PFAS on relevant properties.^[30]

OTHER TOXIC SUBSTANCES

Legislation has been introduced in different jurisdictions to recognise increased risks of certain occupations and improve access to compensation entitlements for those who work in these roles. For example, presumptive legislation for firefighters.^[31] Broader presumptive provisions are available for Commonwealth employees.^[32]

Various other toxic substances exist that have given rise to compensation claims for latent onset disease, including pyrolysed oil in aircraft cabins,^[33] flour mill dust,^[34] bagasse, agricultural chemicals such as Roundup, lead, coal dust, polycyclic aromatic hydrocarbons, formaldehyde, diesel fumes, isocyanates and many others, which are too numerous to mention in the confines of this article.

CONCLUSION

While some harmful products (such as asbestos) become banned, new products seem to continually emerge and enter the market. PFAS compounds are one such example. It is important to keep abreast of such developments so as to ensure client entitlements are adequately protected. And it is critical to record prompt and comprehensive histories of client exposure to toxic substances in cases involving latent onset disease. The full extent of exposure must be recognised to properly frame allegations respecting each cause of action and pursue the case in the most effective manner.

Martin Rogalski is a lawyer at Rogalski Lawyers. PHONE [phone] EMAIL [e-mail].

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^[1] Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262, 286, [143] (Spigelman CJ).

^[2] ‘[S]ilica’, Cambridge Dictionary <https://dictionary.cambridge.org/dictionary/english/silica>.

^[3] JM Elzea, ‘The regulation of crystalline silica: an industry perspective’, Journal of exposure analysis and environmental epidemiology. Vol. 7, No. 3, 1997, 377–84.

^[4] DC Glass, C Dimitriadis, J Hansen, RF Hoy, F Hore-Lacy, MR Sim, ‘Silica exposure estimates in artificial stone benchtop fabrication and adverse respiratory outcomes’, Annals of Work Exposures and Health, Vol. 7, No. 66(1), 2022, 5–13.

^[5] J Nowak-Pasternak, A Lipińska-Ojrzanowska, and B Świątkowska, ‘Silicosis after short-term exposure’, Occupational Medicine (22 October 2022) <https://doi.org/10.1093/occmed/kqac113>.

^[6] M Ding, F Chen, X Shi, B Yucesoy B, B Mossman, and V Vallyathan, ‘Diseases caused by silica: mechanisms of injury and disease development’, International Immunopharmacology, Vol. 2, No. 2–3, 2002, 173–82.

^[7] Curtin University, The Future Burden of Lung Cancer and Silicosis from Occupational Silica Exposure in Australia: A Preliminary Analysis (Report, 2022).

^[8] [2022] NSWDDT 1.

^[9] Ibid, [9]. Section 3 of the Dust Diseases Tribunal Act 1989 defines ‘dust-related condition’ as ‘(a) a disease specified in Schedule 1, or (b) any other pathological condition of the lungs, pleura or peritoneum that is attributable to dust.’

^[10] ‘[A]sbestos’, Oxford Reference (2023) <https://www.oxfordreference.com/display/10.1093/oi/authority.20110803095427620;jsessionid=73997BB886152C9BEDDC5118520CA7C6>.

^[11] G Reid G, S Klebe, N van Zandwijk and AM George, ‘Asbestos and zeolites: from A to Z via a common ion’, Chemical Research in Toxicology, Vol. 34, No. 4, 2021, 936–951.

^[12] AW Musk, N de Klerk, A Reid, J Hui, P Franklin, F Brims, ‘Asbestos-related diseases’, The International Journal of Tuberculosis and Lung Disease, Vol. 24, No. 6, 2020, 562–567.

^[13] [2019] SAET 159.

^[14] Amaca Pty Ltd v Booth [2011] HCA 53 dealt with the causation of mesothelioma and discussed what is known as the ‘cumulative effect theory’ in some detail.

^[15] [2013] NSWDDT 4.

^[16] Ibid, [10].

^[17] Ibid, [29] (Kearns J).

^[18] [2000] NSWCA 29.

^[19] Ibid, [60].

^[20] Ibid, [107].

^[21] Ibid, [137].

^[22] [2014] QSC 301.

^[23] Ibid, [14].

^[24] Ibid, [39] (Alan Wilson J).

^[25] E Panieri, K Baralic, D Djukic-Cosic, A Buha Djordjevic, L Saso, ‘PFAS Molecules: A Major Concern for the Human Health and the Environment’, Toxics, Vol. 10, No. 2, 44.

^[26] Australian Government, ‘How might PFAS affect us’? <https://www.pfas.gov.au/about-pfas/affects>.

^[27] SE Fenton, A Ducatman, A Boobis, JC DeWitt, C Lau, C Ng, JS Smith and SM Roberts, ‘Per- and polyfluoroalkyl substance toxicity and human health review: Current state of knowledge and strategies for informing future research’, Environmental Toxicology and Chemistry, Vol. 40, No. 3, 2021, 606–630.

^[28] Ibid.

^[29] The settlement of the claims was approved in Smith v Commonwealth of Australia (No 2) [2020] FCA 837.

^[30] Cheshire v Jennings (No 2) [2021] SASCFC 11.

^[31] See, for example The Workers Compensation Act 1987 (NSW), s19A and sch 4; Firefighters’ Presumptive Rights Compensation and Fire Services Legislation Amendment (Reform) Act 2019 (Vic); Workers’ Compensation and Rehabilitation Act 2003 (Qld), ss36B-36E; , div 4A and sch 4A; Return to Work Act 2014 (SA), sch 3; Workers Rehabilitation and Compensation Act 1988 (Tas), s27 and s28 and sch 5; Return to Work Act 1986 (NT), s50A and the Return to Work Regulations 1986 (NT), cl 5B and 5C.

^[32] Safety, Rehabilitation and Compensation Act 1988 (Cth), s7(8).

^[33] Turner v Eastwest Airlines Ltd [2009] NSWDDT 10.

^[34] Manildra Flour Mills (MFG) Pty Ltd v Britt [2007] NSWCA 48.