Stress and cancer – how might an Australian experience be replicated in the UK?

  • Étude de marché 15 juillet 2024 15 juillet 2024
  • Royaume-Uni et Europe

  • People challenges

Culhana v State of New South Wales (NSW Police Force) & Others [2024] NSWPIC 257 is a recent Australian case which, although a workers compensation decision rather than a court judgment, merits discussion on the approach to causation taken by the Personal Injury Commission.

How might such a case play out in the UK courts, and could we see attempts here to develop stress or other mental health claims, relying on stress-related illness as a gateway to other significant conditions such as cancers?  

The facts

Mr Craig Stockwell (the deceased worker) was employed as a police officer by the State of New South Wales (NSW Police Force) (the first respondent). In the course of his employment with the first respondent, the deceased worker sustained a psychological injury, liability for which was accepted by the first respondent’s insurer.

The deceased worker was subsequently diagnosed with Barrett's oesophagus and adenocarcinoma, liability for which was disputed.

The deceased worker died on 27 November 2022 as a result of metastatic gastroesophageal functional carcinoma. His de facto partner (the applicant) made a claim for compensation in respect of the death.

The question for the Commission

Regarding the entitlement to compensation, the question for the Commission was whether the worker’s Barrett’s oesophagus, adenocarcinoma and subsequent death resulted from the post-traumatic stress disorder (PTSD) caused by his work as a police officer. In answering this question, the Commission was mindful that causation is often not direct and immediate and “what is required is a commonsense evaluation of the causal chain.”

The Commission’s findings

The Commission heard from a number of medical experts who all agreed that the deceased worker experienced reflux of acid into the oesophagus and the subsequent development of Gastro-oesophageal reflux disease (GORD), leading to Barrett’s oesophagus and eventually adenocarcinoma. The Commission noted that the medical evidence also consistently indicated that the development of those conditions was multifactorial.

Relying on Bonnington Castings v Wardlaw [1956] AC 613, the Commission observed that it was not necessary for the applicant to establish that the injury (in this case, PTSD) was the “primary” or “predominant” cause of the conditions resulting in death, only that it was sufficient that the injury materially contributed to the death.  

The Commission accepted that a number of factors potentially contributed to the deceased worker’s adenocarcinoma, several of which were unrelated to the injury. Nevertheless, they noted, even if they accepted these non-work factors as the main or predominant contributing factors, all of the medical experts agreed that stress, smoking and possibly alcohol were also contributing factors, through their effect on gastric secretions and, in the case of smoking, the separate carcinogenic effect.

The Commission was satisfied that the evidence on which the applicant relied was capable of satisfying the relevant test of causation because it demonstrated a causal relationship between the deceased worker’s PTSD and increased acid secretions in his stomach leading to GORD and consequently Barrett’s oesophagus and adenocarcinoma. On the balance of probabilities, it was found that the contribution of the deceased worker’s PTSD to the adenocarcinoma and his subsequent death was material.

How might a UK jurisdiction court approach this question following Holmes v Poeton Holdings Limited [2023] EWCA Civ 1377?

Edward Sainsbury and I commented on Holmes in an insights article published in November. 

In Holmes, the Court of Appeal confirmed that the material contribution test applied to indivisible conditions, such as occupational cancers, as well as divisible conditions. One of our conclusions was that the requirement to evidence a causal contribution places significant limits on the effect of the Court’s ruling in practice. Is the reasoning in Culhana sufficiently consistent with Holmes such that a similar outcome might be reached in work-stress/cancer claims in UK jurisdictions, or does it relax those parameters too far? 

The claimant in Holmes submitted that he had been exposed to unsafe levels of an organic solvent (TCE) whilst working for the defendant, and this made a material contribution to Parkinson’s Disease, which he was diagnosed with in 2014. The Court of Appeal addressed causation in two stages; firstly, generic causation, specifically whether TCE could cause or materially contribute to Parkinson’s Disease, and secondly, individual causation, and whether the claimant could demonstrate that his negligent exposure to TCE had caused his condition. 

Generic causation was not made out, on the basis that epidemiological and medical studies (based on animal studies alone) only went as far as establishing that TCE exposure was a risk factor for Parkinson’s Disease and a plausible mechanism. Applying this reasoning to a case such as Culhana, it is important to point out that no recognised epidemiological or medical studies have verified a causal mechanism between stress and cancer. The medical experts in Culhana did however cite various research publications dating back to the 1990s which showed a relationship between stress and GORD. Professor Richard Fox, an oncologist for the applicant, went on to say that Barrett’s oesophagus was a condition which developed as a consequence of chronic GORD and predisposed patients to the development of adenocarcinoma of the oesophagus. Other risk factors included central abdominal obesity and smoking, although there was no clear-cut relationship between alcohol ingestion and the condition. In support, he relied on Epidemiology of Barrett's Oesophagus and Oesophageal Adenocarcinoma (TM Runge et al, 2015). The respondent’s oncologist disagreed and considered that the development of reflux and later Barrett’s oesophagus was related to the anatomy of the gastro-oesophageal junction, which far outweighed other contributing factors. Crucially, he did not cite any relevant literature to support this view.

As to individual causation, the Court of Appeal in Holmes cited Wilsher v Essex Health Authority [1988] AC 1074, finding there were a number of possible causes and insufficient evidence that the claimant’s exposure to TCE had caused his condition. Applying this second stage to a case such as Culhana, a court would need to assess whether there were any non-work related factors which would have caused increased stomach acidity leading to the development of Barrett’s oesophagus, and the subsequent adenocarcinoma (or indeed whether there were other direct cancer risk factors at play). If so, the court would then need to decide whether the work stress mechanism did make some causal contribution in fact, which was more than de minimis, to the outcome, or whether any of the factors could be a cause and did in fact make a causal contribution/were the cause. A key battleground for such questions in disease cases is the extent of epidemiological support for relevant associations and what the courts can take from that in reaching conclusions as to causation in principle and in fact.  In cases reliant on stress and psychological trauma as the initiating factor, there is the added dimension that stress can itself be multi-factorial, and in work-stress cases there is often much difficult analysis of the causal relevance of concurrent stress factors external to work.  

In Culhana, the deceased worker had a history of obesity, which the medical experts considered was a contributing factor, but the Commission paid little regard to this. Such a broad-brush approach to causation would not be replicated in the UK courts and, in a case where there may be many other potential causes, a claimant is likely to find it impossible to prove individual causation unless they can prove mechanism of the disease, potentially at cellular level.

The Commission concluded that there was a series of events set in motion by the psychological injury, which started an unbroken chain of causation resulting in the deceased worker’s death from cancer.  The causative chain, viewed as uninterrupted by the Commission in Culhana, appeared to treat the deceased worker’s increased smoking and drinking as part and parcel of his PTSD, but this was fact-specific and borne out by witness testimony which aligned with the medical history. Would smoking and drinking be treated as separate bio-mechanical factors by a UK court, and therefore distinct from the psychological injury?  

Cancer Research UK specifically states that stress does not directly cause cancer, although it does concede that stress can lead to unhealthy changes in behaviour which can impact a person’s cancer risk. The National Cancer Institute in the USA advises that a link between chronic stress and cancer remains unclear, and points to studies conducted to date that have had varying results. The most persuasive is a 2019 meta-analysis of nine observational studies in Europe and North America which found an association between work stress and the risk of lung, colorectal and oesophageal cancers1. It is therefore submitted that, in cancer cases at least, by reference to the current state of the science, stress would be afforded even less weight than that which was given to TCE exposure by the Court of Appeal in Holmes, and deemed a risk factor at best. 

Potential for development in UK jurisdictions

Culhana is of interest because (on its facts) it accepted a link sufficient to support a damages claim between psychological trauma and cancer.  The courts in UK jurisdictions have accepted links between stress and some other conditions; stress and heart attacks in Hardman v The Pub Estate [2005] EWCA Civ 553 and, in Corr v IBC Vehicles [2008] UKHL 13, a causal link between stress or psychological trauma and a deceased’s own actions in the form of suicide.

The current HSE statistics on work-related ill health and injury suggest that of 1.8 million cases, 875,000 are attributable to work-related stress, depression or anxiety (higher than pre-pandemic levels). Statistically, some of these workers will go on to develop cancers. Stress claims will be potentially attractive to the claimant market in the new world of extended fixed recoverable costs (FRC) because they may fall outside the FRC regime due to value, or attract higher FRC figures due to the potential for arguments around complexity and vulnerability. A case involving cancer or other similar diagnosis on the back of work-related stress would likely be above and beyond the FRC regime altogether, and an attempt to bring a claim similar to Culhana in the UK courts remains to be seen. 


1Yang T, Qiao Y, Xiang S, et al. Work stress and the risk of cancer: A meta-analysis of observational studies. International Journal of Cancer 2019; 144(10):2390–2400.

Fin

Auteurs supplémentaires:

Blanche Richards, Knowledge Lawyer

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