Background

Idiopathic Pulmonary Fibrosis (IPF) is a condition in which the lungs become scarred and breathing becomes increasingly difficult.

IPF is commonly identified by a diagnosis of exclusion; essentially a diagnosis of lung fibrosis of unknown cause.

The incidence of IPF is much higher than the incidence of asbestosis, and has risen steadily in the UK in recent decades. Current annual death rates of 6,000 are seen. IPF can affect people of all ages, but around 85% of diagnoses are made in patients over 70 years of age.

Claimants who have been unable to establish an asbestosis diagnosis (for example because they cannot establish an exposure history which exceeds the conventional threshold of 25 fibre ml years) are often re-categorised as suffering from IPF which, as a condition of unknown cause, is self evidentially non-compensatable.

However assumptions in this area have been called into question in a paper prepared by members of the Health and Safety Laboratory in Buxton (UK Asbestos Imports and Mortality due to Idiopathic Pulmonary Fibrosis)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757753/

The authors sought to compare mortality data as a result of mesothelioma, asbestosis and IPF, with asbestos imports.

The paper made the following conclusions:

  1. A rising IPF mortality rate has been seen, without any apparent explanation;
  2. A linear relationship between mortality for mesothelioma and IPF (and a less strong relationship for asbestosis mortality) and historic UK asbestos import statistics.
  3. A strength of association between IPF and historical imports similar to that in mesothelioma.
  4. Accepting that previous studies failed to establish any risk factors from IPF, the strength of relationship between IPF mortality and historical asbestos imports raises a question of whether a proportion of IPF mortality is due to unrecognised asbestos exposures.

Discussion

Asbestos claimants are often elderly and provide poor exposure histories. Possible explanations for this include the time elapsed since the exposure occurred, indirect exposure as a bystander, and handling materials that at the time were not identified as containing asbestos.

Where an exposure assessment concludes that the generally accepted asbestosis threshold of 25 fibre ml years (lifetime exposure) is not met, a diagnosis of IPF is preferred to one of asbestosis.

The authors inevitably question whether a 25 fibre ml year threshold is realistic in view of their own findings and also those of previous studies. They cite as an example the Dutch practice of accepting an asbestosis diagnosis with a history above a 5 fibre ml threshold.

They raise the questions of whether there is a need for a more accurate method of assessing lifetime occupational asbestos exposure and whether existing diagnosed cases of IPF should be re-categorised as asbestosis cases.

In a later article (http://eprints.whiterose.ac.uk/107085/1/Ann%20Occup%20Hyg-2016-Barber-649-50.pdf) the authors advocate the formulation of an occupation based risk matrix as a potential solution to overcoming difficulties of establishing causation.

The British Lung Foundation estimates in excess of 30,000 people in the UK currently suffer from IPF and it is estimated that 6,000 new cases will be diagnosed annually. In British Lung Foundation data, the incidence rate increases dramatically with age and it is therefore unsurprising that the death rate (based on entries in death certificates) is also so high.

In contrast, the incidence rate for asbestosis (assessed for IIDB purposes) was 1,175 in 2015, reflecting a long term upward trend. The established causes of IPF are varied with fibrosis being created in response to damage of the lung arising from smoking, acid reflux, viruses, family history and also environmental factors (including dust/spore inhalation, including asbestos).

IPF therefore shares several of the demographic risk factors of asbestosis mortality, yet epidemiological studies of IPF have not identified links with previous asbestos exposure. Certain occupations have however been linked with an increased risk of IPF in Britain, particularly workers exposed to metal and wood dusts.

What this means for insurers

The authors of this paper acknowledge that the linear relationship between asbestos imports and the incidence of IPF, whilst statistically significant, fall short of confirmatory of medical causation in individual cases. Nevertheless the fact that the relationship is similar to that seen from mesothelioma mortality will undoubtedly serve to encourage further research in this area. Cases need close scrutiny because it is sometimes possible to challenge causation on the basis of radiology and clinical signs and symptoms (see footnote).

Accordingly it will also be likely to encourage claimants and their medical experts in challenging the applicability of the threshold on the basis of the emerging evidence based to the effect that an absolute threshold requirement does not take account of individual susceptibility to fibrosis.

Claimants, without alternative explanations, will undoubtedly be encouraged down this route and there is therefore the prospect of significant increases in asbestosis claim numbers if current and future epidemiology supports an asbestosis diagnosis. A risk based matrix would undoubtedly assist claimants seeking to establish an asbestos cause for IPF, particularly where individual case evidence is deficient.

Equally, claimant experts may wish to challenge existing IPF diagnosis even in cases of lower lifetime exposures where other known causes of IPF do not apply. Insurers have seen reducing asbestosis claim numbers in recent years, but this study provides an example of why optimism in this area may be misplaced.

Footnote

  • A study using HRCT scans found there was a significant difference between IPF and asbestosis in pleural changes. In addition, there were significant differences between IPF and asbestosis in several parenchymal abnormalities on CT, especially in the less advanced stage of both diseases. On multivariate analysis, HRCT features that distinguished asbestosis from IPF were sub-pleural lines at a distance of less than 5 mm from the inner chest wall, sub-pleural dots and parenchymal bands. In conclusion it was found there are significant differences between IPF and asbestosis in the parenchymal and pleural abnormalities on CT. (https://www.researchgate.net/publication/295688646_The_comparison_of_high-resolution_computed_tomography_findings_in_asbestosis_and_idiopathic_pulmonary_fibrosis)
  • UIP pattern fibrosis is rarely observed in asbestos-exposed subjects, and shows no dose–response correlation with asbestos fibres on mineral analysis; this points to an alternative disease, such as IPF. The results indicate that UIP pattern fibrosis should not be regarded as genuine asbestosis, irrespective of the status of asbestos biomarkers, and this impacts upon the post-mortem handling of asbestos-related deaths. (http://onlinelibrary.wiley.com/doi/10.1111/his.12951/full)