The demographics of Mesothelioma in the UK are changing. The HSE’s “Mesothelioma mortality by occupation statistics for 2025” document that the proportional rate of Mesothelioma mortality for carpenters and joiners is now roughly 5X the average of all occupation-related fatalities.  That’s a statistically significant increase from roughly 4X the average in 2005, and the continuing upward trajectory is worrying.  More broadly, Mesothelioma mortality continues to rise significantly amongst skilled male construction and building-related workers, while amongst female workers, Mesothelioma mortality rates have risen significantly in secretarial and related occupations and in teachers and educators (1). The numbers for these specific working cohorts stand in contrast with the significant declines in Mesothelioma proportional mortality rates observed in many job categories linked to heavy industry, and they suggest a different pattern of exposure, specifically, to the continuing presence of asbestos in UK workplaces built before the 1999 ban on new use of asbestos-containing building materials.

The vast majority of asbestos imported into the UK between 1950 and 1999 was Chrysotile, aka white or serpentine asbestos.  Epidemiological data consistently show that people exposed to Chrysotile are at lower risk – but not zero risk – of developing Mesothelioma, when compared to workers exposed to Amphiboles, such as Amosite (brown asbestos) or Crocidolite (blue asbestos). Indeed, Chrysotile continued to be imported into the UK long after use of Amphiboles was phased out (2).  The list of building materials containing Chrysotile prior to 1999 is extensive (3) and Chrysotile constitutes a large proportion of the ongoing occupational, and likely domestic, exposure to asbestos in buildings constructed or refurbished with such materials prior to 1999.  The key question is how dangerous is Chrysotile?  With seed funding from Action on Asbestos, my research team have started to investigate this very question.

My lab specialises in the use of genetically modified mice to investigate how cancers develop in the lung and chest cavity.  Intrapleural injection of 25 micrograms (a microgram is one millionth of a gram) of Amosite asbestos into genetically unmodified mice was previously shown to give rise to pleural Mesothelioma in approximately 20% of mice by 18 months post injection (4). A separate research group generated genetically complex mice enabling experimentally controlled inactivation of up to 3 genes that are frequently mutated in human Mesothelioma, and showed that inactivation of both copies of the right combination of 3 genes (Bap1, Cdkn2a and Nf2) sufficed to result in pleural Mesothelioma in the absence of any asbestos exposure (5).   We combined these protocols to determine if intrapleural injection of asbestos would make any difference in mice that had already acquired enough mutations to drive Mesothelioma, initially using Amosite asbestos as our high-risk fibre most likely to have an effect.  A single intrapleural injection of 25 micrograms of Amosite shortened the humane lifespan of such mice by as much as 40% (6).  More recently, we have repeated this experiment using 25 micrograms of Chrysotile asbestos and got roughly the same result.  We are currently performing a side-by side analysis in littermate mice to confirm the initial findings.  To date, our data indicate that Chrysotile asbestos, if it gets into the chest cavity, does as much harm as Amosite.

How do we reconcile these data with the human epidemiology?  Our direct intrapleural injection protocol obviously by-passes the lungs, and all forms of asbestos have to pass through the lungs to reach the chest cavity of exposed individuals.  Does asbestos not cause similar harm to the lungs as it does when it reaches the pleura?  Indeed – all forms of asbestos are acknowledged as risk factors for lung cancer (7).  A recent meta-analysis found that Chrysotile asbestos poses a particularly high risk for Lung cancer, with as many as 9 Lung cancer fatalities for every Mesothelioma fatality linked to Chrysotile exposure (8).  Is there any evidence of this happening in the UK?

Mesothelioma is not uniformly distributed across the UK – it occurs in hotspots, historically in places associated with heavy industries such as ship building.  As such, we reasoned that local Mesothelioma rates could be used as a rough surrogate for asbestos exposure.  In collaboration with Prof. Peter Hall, Uni Edinburgh, we used data accessible through Public Health Scotland (9) to examine European age standardised rates (EASRs) for Mesothelioma across 17 Scottish health boards and asked if there is any geographic correlation with those for Lung cancer.  We applied the same approach to investigate any possible relationship with cancers of the Pancreas (similarly poor prognosis as Mesothelioma) or Prostate (given the male predominance of Mesothelioma).  Averaged over years 1998-2022, we found a shockingly strong positive correlation between the EASRs for Mesothelioma and Lung cancer across the Scottish health boards (Pearson R > 0.84), but no correlation with Pancreatic cancer (Pearson R < 0.21) and a mild negative correlation with Prostate cancer (Pearson R < -0.45).  The co-incident geographic distribution suggests that a sizeable proportion of Lung cancer in Scotland may share a common cause with Mesothelioma.  Importantly, the DNA mutation signatures that arise from cigarette smoking are almost entirely absent from Mesothelioma (10, 11) – smoking thus fails to account for the observed correlation with rates of Lung cancer.  That leaves asbestos exposure as the next most likely culprit.

What about experimental evidence?  We turned again to our genetically modified mice, this time using mice that are genetically predisposed to Lung Adenocarcinoma.  After sporadic activation of cancer-predisposing mutations (in this instance, KRas^G12D and mild overexpression of cMYC) in the lungs of adult mice, we dosed mice once per week with intratracheal (i.e. oral) delivery of 10 micrograms of Chrysotile asbestos, for 5 weeks, to model repeated low-dose exposure.  As we saw in our Mesothelioma mouse models, dosing with Chrysotile accelerated tumour development and significantly reduced the humane lifespan in our Lung cancer mouse model.

Where does that leave us?  The 1999 legislation banning new use of asbestos didn’t make it all magically disappear.  As cases linked to direct use of asbestos decline a growing proportion of cases will be linked to building maintenance and long-term building occupancy, domestic and occupational.  Lung cancers linked to asbestos exposure may be a far greater problem than previously considered, and the medical community need to be alert to this issue, especially in areas with high incidence of Mesothelioma.  We need higher resolution geographic and demographic data to identify persons still at risk, and a mandatory – not voluntary – registration of all buildings that still contain asbestos of any type.  I firmly believe that we need a nationwide asbestos eradication policy, similar to that in place in the province of Victoria, Australia.

Returning to the nurse drawing my blood.  The needle is out (finally!) but I’m still talking.  I tell her of my concerns about asbestos in buildings. “There was a workman in the other day,” she said, “suited up and wearing respiratory protection.  He was doing what looked like fairly routine repairs in the room just down the hall.  I asked him why he was wearing so much PPE.  He told me there was asbestos in the area he was working on.  He was protected, but none of the hospital staff [working in the area] were.  Have I been exposed?”

How would you answer?

References

1. UK Health & Safety Executive. Mesothelioma mortality by occupation statistics in Great Britain, 2025. https://www.hse.gov.uk/statistics/assets/docs/mesothelioma-mortality-by-occupation.pdf
2. Gilham C, Rake C, Burdett G, Nicholson AG, Davison L, Franchini A, et al. Pleural mesothelioma and lung cancer risks in relation to occupational history and asbestos lung burden. Occup Environ Med. 2016;73(5):290-9.
3. UKATA. https://www.ukata.org.uk/library/about-asbestos/
4. Chernova T, Murphy FA, Galavotti S, Sun XM, Powley IR, Grosso S, et al. Long-Fiber Carbon Nanotubes Replicate Asbestos-Induced Mesothelioma with Disruption of the Tumor Suppressor Gene Cdkn2a (Ink4a/Arf). Curr Biol. 2017;27(21):3302-14 e6.
5. Badhai J, Pandey GK, Song JY, Krijgsman O, Bhaskaran R, Chandrasekaran G, et al. Combined deletion of Bap1, Nf2, and Cdkn2ab causes rapid onset of malignant mesothelioma in mice. J Exp Med. 2020;217(6).
6. Farahmand P, Gyuraszova K, Rooney C, Raffo-Iraolagoitia XL, Jayasekera G, Hedley A, et al. Asbestos accelerates disease onset in a genetic model of malignant pleural mesothelioma. Front Toxicol. 2023;5:1200650.
7. Wolff H, Vehmas T, Oksa P, Rantanen J, Vainio H. Asbestos, asbestosis, and cancer, the Helsinki criteria for diagnosis and attribution 2014: recommendations. Scand J Work Environ Health. 2015;41(1):5-15.
8. Darnton L. Quantitative assessment of mesothelioma and lung cancer risk based on Phase Contrast Microscopy (PCM) estimates of fibre exposure: an update of 2000 asbestos cohort data. Environ Res. 2023;230:114753.
9. Public Health Scotland. https://publichealthscotland.scot/publications/cancer-incidence-in-scotland/cancer-incidence-in-scotland-to-december-2023/
10. Bueno R, Stawiski EW, Goldstein LD, Durinck S, De Rienzo A, Modrusan Z, et al. Comprehensive genomic analysis of malignant pleural mesothelioma identifies recurrent mutations, gene fusions and splicing alterations. Nat Genet. 2016;48(4):407-16.
11. Mangiante L, Alcala N, Sexton-Oates A, Di Genova A, Gonzalez-Perez A, Khandekar A, et al. Multiomic analysis of malignant pleural mesothelioma identifies molecular axes and specialized tumor profiles driving intertumor heterogeneity. Nat Genet. 2023;55(4):607-18.

Footnote. 

Except where noted, this article refers to several experimental studies that are unpublished at the time of writing and findings should therefore be considered preliminary.

Daniel J. Murphy is Professor of Lung Cancer & Mesothelioma at the School of Cancer Sciences, University of Glasgow and the CRUK Scotland Institute.