Causation in long DUST DISEASE

[pdf-embedder url=”/wp-content/uploads/2020/07/Precedent-April-edition-causation-in-long-tail-dust-disease-claims-extract.pdf”]

The common compensable conditions include asbestosis, lung cancer and mesothelioma. The main issues regarding causation with respect to these conditions are discussed below.


Asbestosis is interstitial lung disease caused by past asbestos exposure.2 It is a condition which typically develops over prolonged periods of asbestos exposure. Classic exposure histories include those who worked in asbestos mines or asbestos factories.3
The typical way in which a diagnosis of asbestosis is established is by reference to clinical and radiological grounds, based on the following criteria:

  • a history of moderate to heavy asbestos exposure that is typically, but not always, occupational and often protracted for many years;
  • clinical signs of interstitial fibrosis in the form of end inspiratory crackles on auscultation of the lung fields, especially in the lower zones;
  • detection of reticular-linear diffuse opacities in the lower zones of the lung fields on radiologic examination;
  • classically, restrictive impairment of lung function; and
  • usually, but not always, associated parietal pleural fibrous plaques and/or diffuse pleural fibrosis.4

Despite the longstanding body of evidence linking asbestos exposure with asbestosis, the diagnosis can sometimes be challenged. There are various reasons for this. For example, radiological appearances of asbestosis can mimic other forms of fibrotic lung disease, which are unrelated to asbestos exposure.

In Lo Presti v Ford Motor Co of Australia Ltd (No 2),5 the plaintiff worked as a motor mechanic for two Ford dealerships from 1970 to 1987. The plaintiff alleged that he developed asbestosis as a result of working with asbestos- based friction materials during this employment. The defendant argued that the plaintiff did not suffer from asbestosis but another form of pulmonary fibrosis. The Court noted that some fibrotic lung conditions exhibit many of the same characteristics as asbestosis. The Court referred to conditions such as idiopathic pulmonary fibrosis and non-specific interstitial pneumonia. Both parties called epidemiological evidence. The defendant argued that there is a particular threshold level of exposure below which asbestosis will not occur. Ultimately, the Court found that it is the medical evidence which will dictate whether there can be a diagnosis of asbestosis. In this case, no biopsy had been done. Interestingly, the Court found that the plaintiff ’s cumulative exposure was less than 25 fibre/ml years. Historically, this has been seen as a benchmark level of exposure below which asbestosis will not occur, but the judge did not accept that proposition and Prof Robinson’s evidence was accepted. Prof Robinson identified pleural plaques
and pulmonary fibrosis which he diagnosed as asbestosis in circumstances where he described the exposure level as moderate or low.

In Reilly v Malabar Electric Pty Limited & Ors,6 the plaintiff alleged that he was exposed to asbestos dustand fibre while employed by the first defendant, Malabar Electric Pty Ltd, as an apprentice and electrician from 1960 to 1980. During this period, the plaintiff worked at Housing Commission sites and state government sites for the Department of Public Works. The plaintiff also endured asbestos exposure while employed by the fourth defendant, John Goss Projects Pty Ltd, in 1987. The plaintiff alleged that his history of asbestos exposure led to the development of asbestosis. The case settled against the fourth defendant by the time of trial, and of the remaining three defendants only Malabar Electric disputed the diagnosis. The resolution of the issue of diagnosis turned on whether the plaintiff suffered from asbestosis or some other form of interstitial pulmonary fibrosis. In contrast to Lo Presti, the Tribunal accepted that the plaintiff ’s cumulative exposure to asbestos was in excess of 25 fibre/ml years.7 However, it was clearly stated that the exposure level is not a conclusive determinant. A process of exclusion was undertaken and rheumatoid arthritis, drugs, aspiration of gastric contents, wood dust and radiation exposure were excluded as possible causes. Reference was made to the radiological evidence, and a detailed analysis was undertaken regarding clinical findings including finger clubbing, crackles and median survival rate. Based on a detailed consideration of all relevant factors, the asbestosis diagnosis was not established.

In Amaca Pty Ltd v Tullipan,8 the plaintiff worked as a carpenter and he was exposed to asbestos containing building products for over 20 years. The Court of Appeal was asked to determine whether the decision of the Dust Diseases Tribunal of New South Wales (the Tribunal) which held that the plaintiff ’s terminal condition, allegedly caused by the inhalation of asbestos dust, was asbestosis rather than idiopathic pulmonary fibrosis, should be upheld. The asbestos exposure level was considered to be sufficient to induce asbestosis. No biopsy evidence was available. Major weight was placed on the longevity of the disease. It was held that asbestosis typically progresses slowly as compared to idiopathic pulmonary fibrosis; the plaintiff had suffered the disease for over 12 years. After considering all relevant criteria, the Court of Appeal upheld the decision of the Tribunal.

There are other reasons, such as the presence of active co-morbidities, which can complicate a diagnosis. While uncommon, lung tissue can be examined for the purposes of performing a fibre count.9

Lung cancer

Asbestos is a recognised carcinogen.10 It has been established that it can cause lung cancer but it is a dose-dependent disease.11 Accordingly, it is essential to establish sufficient asbestos exposure, particularly in the presence of a competing risk factor.

Case authorities often refer to the Helsinki criteria.12 A summary of the criteria is as follows:

  • the presence of asbestosis (although in this scheme, asbestosis has significance mainly as a surrogate for cumulative exposures comparable to the exposure indices set out below); or
  • a sufficient count of asbestos bodies (although occupational histories are probably a better indicator of lung cancer risk than fibre burden analysis); or
  • estimated cumulative exposure to asbestos of 25 fibre/ml years or more; or
  • an occupational history, the only means whereby latency can be evaluated, of one year of heavy exposure to asbestos (for example, manufacture of asbestos products, asbestos spraying, insulation work with asbestos materials, demolition of old buildings) or five to ten
  • ars of moderate exposure (for example, construction
  • shipbuilding). A two-fold risk of lung cancer can be reached with exposures of less than one year in duration if the exposure is of extremely high intensity (for example, spraying of asbestos insulation materials); and
  • a minimum lag-time of ten years.

In McDonald v State Rail Authority (NSW) & Others,13 the plaintiff died from lung cancer at 47 years of age shortly after his hearing began. The proceedings were continued by his widow for the benefit of his estate. The plaintiff alleged that he was exposed to asbestos when he was employed by the New South Wales Government Railways (as an apprentice fitter) between 1960 and 1965; by Queensland Alumina Ltd from 1967 to 1968; and by Comalco Products Pty Ltd between 1969 and 1977. The plaintiff stopped smoking approximately three years before his death. It was accepted that the plaintiff ’s smoking history was between 25 and 30 pack-years,14 and that a history of 25 pack-years of smoking is sufficient to cause lung cancer. The Tribunal accepted the fibre burden hypothesis – that lung cancer may be triggered by asbestos exposure in the absence of asbestosis where the exposure was sufficient to have caused asbestosis. However, there was significant difficulty in establishing the extent of the plaintiff ’s asbestos exposure. Evidence that was taken from the plaintiff in the hours before he passed away was considered unreliable. The Tribunal concluded that the asbestos exposure could only be determined by inference. Numerous expert witnesses gave evidence, and it was determined that an exposure history of at least 25 fibre/ ml years is required before asbestosis can develop. It was held that the plaintiff ’s exposure history was too light and consequently insufficient to cause asbestosis.

In Judd v Amaca Pty Ltd,15 the plaintiff was 63 years old and had contracted lung cancer. He argued that although he had been a heavy smoker for over 42 years, the asbestos dust and fibre that he inhaled while he worked as a carpenter materially contributed to the development of his lung cancer. The plaintiff did not suffer from clinically detectable asbestosis. The Tribunal noted that if causation was to be proven by an increase in risk, a doubling of the risk would need to be established – unless other circumstances could be relied upon to weigh the probabilities in favour of the plaintiff. Taking a common sense approach, the Tribunal noted that the risk from smoking was much greater than from asbestos exposure. The plaintiff sought to rely on the following passage in McDonald under s25B of the Dust Diseases Tribunal Act 1989 (NSW) (reliance on general issues already determined in other Tribunal proceeding):

‘the issue resolved in the plaintiff ’s favour specifically stated is: carcinoma of the lung may be attributed to asbestos exposure in the absence of asbestosis where the exposure was sufficient to have caused asbestosis’.16

The Tribunal ultimately found that the plaintiff did not reach the 25 fibre/ml year threshold. Curiously, the Tribunal found that upon the present state of medical knowledge the relative risk for development of lung cancer inherent in asbestos cement building materials is doubled, at 50 fibre/ml years. The interaction between smoking and asbestos exposure was also considered. The Tribunal was not persuaded that on balance the plaintiff would not have contracted cancer in the absence of his asbestos exposure. Further, even if there was some acceleration of the lung cancer as a result of asbestos exposure, the Tribunal was not persuaded that the acceleration ‘was more probably than not substantial rather than de minimis’.17 The plaintiff ’s case failed.

In Amaca Pty Ltd v Ellis,18 proceedings were brought on behalf of Mr Cotton’s estate by his widow. Mr Cotton had been exposed to respirable asbestos fibres in the course of
his employment with the Engineering and Water Supply Department (SA) between 1975 and 1978, and Millennium Inorganic Chemicals Ltd between 1990 and his death in 2002. Mr Cotton had smoked on average between 15 and 20 cigarettes per day for about 26 years. The High Court observed that there is no scientific or medical examination that can say with certainty what caused Mr Cotton’s lung cancer, or what the cause of lung cancer is in any particular case.19 The plaintiff ’s case on causation depended on inference. Epidemiological evidence was adduced from witnesses who provided an opinion of relative risk from smoking exposure and asbestos exposure. The relative risk of smoking heavily outweighed that of exposure to asbestos. Ultimately, the evidence did not establish facts which positively suggested that it was more probable than not that the negligence of any defendant was a cause of Mr Cotton’s cancer. It was only established that his exposure to asbestos was a possible but not a probable cause of his cancer. Ellis highlights the risks of relying on an inference that is based on an increase in risk in circumstances where there is a competing risk factor.

In Allianz Australia Ltd v Sim; WorkCover Authority (NSW) v Sim; Wallaby Grip (BAE) Pty Ltd (In liq) v Sim,20 proceedings were brought on behalf of Mr Sim’s estate by his widow. The plaintiff alleged that Mr Sim’s occupational exposure to asbestos spray caused his lung cancer over four periods of employment, from around 1964 to 1979. Mr Sim was diagnosed with diffuse pleural thickening and asbestosis,21 and had stopped smoking 30 years before he died. Every medical expert who was called in the plaintiff ’s case dismissed smoking as a cause of Mr Sim’s lung cancer. As the defendants called no expert medical opinion on the issue of causation, the Tribunal was entitled to draw an adverse inference.22 Accordingly, it was not necessary to make an election between two competing causes of Mr Sim’s condition. The Court of Appeal held that satisfaction of the ‘but for’ test is not an essential requirement when determining causation. The Court approached causation on the basis of the ‘material contribution’ test. It held that an increase in risk of developing lung cancer is not to be equated with factual causation. In circumstances where the negligence of each defendant was insufficient to affect the damage, but the combined force of two defendants was sufficient, each should be held liable. In other words, each period of alleged asbestos exposure materially contributed to the cause of Mr Sim’s lung cancer.


The only known cause of mesothelioma is asbestos exposure. Unlike some of the heavy dose diseases mentioned above, such as asbestosis, there is no safe level below which mesothelioma does not develop.23

In Amaca Pty Ltd v Booth,24 the High Court affirmed the application of the ‘cumulative effect theory’ to establishing causation in mesothelioma cases. Mr Booth endured asbestos exposure in a domestic and occupational environment. His occupational exposure arose from around 1953 to 1983 while he worked with asbestos containing friction products as a motor mechanic. The appellants argued that the evidence of the medical witnesses focused on risk rather than cause and the medical evidence did not support a finding that exposure had been a cause of Mr Booth’s mesothelioma, on the basis of the Court’s decision in Ellis. Chief Justice French distinguished Ellis on the basis that there was a competing cause, whereas in the present case there was not. This judgment confirms that all material exposures to asbestos (above de minimis) may be deemed to be a cause of mesothelioma.

While issues of causation in mesothelioma cases are now settled, it is always important to ensure that sufficient exposure evidence is called. In King v Amaca Pty Ltd,25 the plaintiff alleged that his mesothelioma developed due to being exposed to asbestos dust while visiting one of the defendant’s factories in Perth to repair a machine in 1972. The plaintiff attended the factory over the course of two hours on three separate days. There was a combined asbestos exposure period of six hours. The court held that there was sufficient evidence of causation to support a verdict in favour of the plaintiff and this was upheld on appeal.26 However, relying on an inference in the causation of mesothelioma can be risky and some cases have failed on this basis.27


A range of factors come into play in establishing causation of asbestos disease, including the type of asbestos a plaintiff was exposed to, the duration and intensity of exposure, the latency of the disease and medical findings and opinion.

The most common asbestos disease which will be the subject of future litigation is mesothelioma. While the issues of causation with regards to mesothelioma are now settled, there will be new challenges to face when acting on behalf of third wave victims. Issues regarding the ‘low-dose’ cases have been highlighted above. Obtaining detailed instructions in relation to the extent of asbestos exposure at an early stage is vital.

Notes: 1 See Werfel v Amaca v The State of South Australia [2019] SAET 159, [2]. 2 BT Mossman and A Churg, ‘Mechanisms in the pathogenesis of asbestosis and silicosis’, American Journal of Respiratory and Critical Care Medicine, Vol. 157(5), 1998, 1666–80. 3 Banton v Amaca Pty Ltd [2007] NSWDDT 29. Mr Banton was diagnosed with asbestosis and later mesothelioma. 4 VL Roggli et al, ‘Pathology of asbestosis: An update of the diagnostic criteria’, Archives of Pathology & Laboratory Medicine, Vol. 134(3), 2010, 462–80. 5 [2008] WASC 12. 6 [2011] NSWDDT 9. 7 Ibid, [73]. 8 [2014] NSWCA 269. 9 James v Seltsam Pty Ltd & Ors [2017] VSC 506. 10 This has been recognised by the International Agency for Research on Cancer:
. 11 FJH Brims et al, ‘Pleural plaques and the risk of lung cancer in asbestos- exposed subjects’, American Journal of Respiratory and Critical Care Medicine, Vol. 201(1), 2019, 57–62. 12 DW Henderson et al, ‘After Helsinki: A multidisciplinary review of the relationship between asbestos exposure and lung cancer, with emphasis on studies published during 1997–2004’, Pathology, Vol. 36(6), 2004, 517–50. 13 [1998] NSWDDT 4. 14 ‘Pack-years’ is a clinically-assigned numerical value of lifetime tobacco exposure. 15 [2003] NSWDDT 12. 16 [1998] NSWDDT 4, [72]. 17 [2003] NSWDDT 12, [119]. 18 [2010] HCA 5. 19 Ibid, [2], [70]. 20 [2012] NSWCA 68. 21 The Helsinki criteria states that diffuse pleural thickening, due to its threshold dose being moderate to heavy exposure, is assigned similar significance to asbestosis regarding attribution of disease. 22 Jones v Dunkel (1959) 101 CLR 298. 23 Amaca Pty Ltd v Booth [2011] HCA 53. 24 Ibid. 25 [2011] VSC 433. 26 Amaca Pty Ltd v King [2011] VSCA 447. 27 See eg, King v Caltex Petroleum Pty Ltd [2013] NSWDDT 4.

Date Posted: July 15, 2020