Could evolving medical science challenge the approach to causation in asbestos related disease claims?
Two recently published articles suggest scientific research is making progress in finding genetic signatures/markers to identify exposure to asbestos in asbestos induced lung cancer and mesothelioma.
Summary
A review, Lung Cancer caused by asbestos: What a reporting pathologist needs to know, by Klebe et al, published in the Lung Cancer journal in 2024 concluded that while there is no molecular signature available to identify asbestos induced lung cancer at present, work in this area may hold promise for one to be found in the future.
Another study, From asbestos exposure to carcinogenesis: Transcriptomic signatures in malignant pleural mesothelioma, by Rosati et al published in the Experimental and Molecular Pathology Journal in May 2025 concluded that its findings deepen the understanding of the molecular landscape underlying asbestos induced pathology in malignant pleural mesothelioma which lays the foundation for future investigations including the development of biomarkers.
If markers are identified, whether in asbestos induced lung cancer or mesothelioma, this will assist in claims where exposure history may not be known and will be particularly beneficial in asbestos induced lung cancer cases which are multi factorial in origin.
Background
The review by Klebe considered the current use of the Helsinki criteria for attributing lung cancer to previous asbestos exposure, and the potential for an asbestos-induced lung cancer signature to be identified in the future. Whilst attributing a patient’s lung cancer to asbestos exposure has no bearing on treatment, it does have important medico-legal implications.
Simultaneous exposure to other carcinogens such as tobacco smoke and silica adds complexity to the issue of causation in asbestos induced lung cancer. The morphology of an asbestos induced lung cancer is identical to a lung cancer induced by one of many other causes, including smoking which remains the most dominant causative factor for lung cancer and complicates any contribution or cause from asbestos or any other inhalational carcinogens.
The risk of lung cancer is doubled when a person is exposed to 25 f/ml years. A histological diagnosis of asbestosis under the Helsinki criteria requires the identification of diffuse interstitial fibrosis in technically sound lung samples plus the presence of 2 or more asbestos bodies per section area of 1cm2 or a count of uncoated asbestos fibres (by electron microscopy) that falls in the range recorded for asbestosis by the same laboratory. However, many lung cancer diagnoses today are made on the basis of core or endobronchial biopsies in which there is insufficient non-neoplastic lung tissue present to reliably comment on the presence or absence of asbestosis. Further, fibre counts are variable throughout the lungs, with higher counts found in the lower lobes. Significant numbers of asbestos bodies can occasionally be seen in tissue sections from patients without interstitial fibrosis, and the presence of one or even a few asbestos bodies does not equal a histological diagnosis of asbestosis. A pathologist may not have been given any information about an individual’s exposure to asbestos. A routine histopathology report may state no asbestos bodies are identified which may be given inappropriate significance in determining the cause of lung cancer and affect the individual’s ability to pursue a claim.
This leads to the question of whether other histopathological features or markers could diagnose asbestos induced lung cancer. The review found that a particular histological type neither establishes nor excludes asbestos induced lung cancer regardless of smoking status, and the anatomical location of the tumours does not determine causation. Asbestosis is used as a surrogate for asbestos exposure but has limitations and the absence of fibrosis does not exclude significant exposure to asbestos. Whilst histologists should comment on the presence or absence of fibrosis, asbestos bodies, plaques and rounded atelectasis, these assessments have limitations when assigning or dismissing a causative effect in lung cancer.
As there are multiple causal factors for lung cancer, it may be difficult or even impossible to find a unique molecular marker for one typical carcinogen such as asbestos. A molecular marker would be an ideal tool to link an individual’s lung cancer to asbestos exposure. A mutational signature consisting of a particular combination of mutations which are identifiable has emerged for a range of cancer types where the pattern of mutations reflect a particular mutagen to the extent that it is valid to deduce that exposure to the mutagen must have occurred at some stage in the patient’s past. For example, a mutational signature has been identified associated with smoking due to mutagens in tobacco. This “smoking signature” has been identified in most of the common lung cancer histological subtypes. It would be of great benefit to identify a similar asbestos exposure signature.
The study by Rosati et al, which aimed to identify gene expression profiles specific to malignant pleural mesothelioma patients with a history of asbestos exposure was published in May 2025, and concluded that the study has further deepened the understanding of the molecular landscape that underlies asbestos induced carcinogenesis in malignant pleural mesothelioma. The identification of specific differentially expressed genes and enriched gene ontology terms related to biological processes lays the foundation for future investigations including the development of biomarkers with potential implications for the diagnosis and prognostic assessment of malignant pleural mesothelioma. In contrast to lung cancer, asbestos exposure is recognised as the primary cause for malignant pleural mesothelioma.
The findings of the Rosati study identified several genes that are differentially expressed in malignant pleural mesothelioma patients with documented asbestos exposure leading to the characterisation of a distinct gene expression profile. This offers a foundation for future investigations. There are acknowledged limitations in this study including limited sample size and experimental validation of the transcriptomic results.
Genetic mutations play a crucial role in the pathogenesis of malignant pleural mesothelioma with frequent alterations in tumour suppressor genes. Biomarkers therefore offer a promising route for improving early diagnosis and prognosis.
What this means for Defendants and Insurers
The presence of other non-asbestos carcinogens complicates the causation issues in asbestos induced lung cancer claims. Attributing lung cancer to a patient’s exposure to asbestos therefore has important causation implications.
The decision in the case of Heneghan v Manchester Dry Docks Ltd was a significant judgment for asbestos related lung cancer claims as the Court approved a new approach to causation in finding that damages should be apportioned in accordance with an individual defendant’s proportionate share of exposure to asbestos. As noted in Heneghan there are 2 aspects to proving causation – what caused it and who caused it. Identification of markers in the future may determine the first of those questions.
The more recent decision in Holmes v Poeton Holdings Ltd [2023] EWCA Civ 1377 held that the material contribution test for causation applies to indivisible (mesothelioma) as well as divisible (asbestos induced lung cancer) conditions. In practice, the application of material contribution to indivisible conditions such as occupational cancers is difficult to prove because the causal mechanisms are often unknown or speculative. The claimant must prove “generic causation”, ie that the insult caused by the breach was capable of causing the injury, and “individual causation”- that it has in fact made a contribution to the injury which is more than minimal. In cancers where there may be other potential causes, it will be beneficial to know whether asbestos exposure is certain based on biomarkers. Scientific developments in biomarkers will assist in identifying and linking the cause of asbestos related cancers.
In relation to mesothelioma, as Lord Rodger in the case of Sienkiewicz observed “The Fairchild exception was created only because of the present state of medical knowledge. If the day ever comes when medical science can identify which fibre or fibres led to the malignant mutation and the source from which that fibre or those fibres came, then the problem which gave rise to the exception will have ceased to exist.”
If future identification of markers could confirm the cause or the contribution made by mutagens to causing disease, there is the potential for science to play a part in determining causation in asbestos related claims. Given it is not unusual to see claimants with mesothelioma who have de minimis or no easily identifiable source of asbestos exposure, it is possible to see how these biomarkers could assist in defending claims and demonstrating, for example, an idiopathic cause. Whilst there remain no identifiable markers at present, the prospect of identifying them seems to be getting closer and developments in this area should be watched with interest by those dealing with asbestos related claims.
Clyde & Co are specialists in dealing with disease claims, and we closely monitor developments around asbestos diagnoses. For more on this subject, you can read all of our previous articles here, and if you have any questions about this topic you can contact Barbara Goddard or any of our Occupational Disease and Legacy Claims team.