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Asbestosis is the form of pneumoconiosis induced by exposure to asbestos dust with the term being coined by Thomas Oliver in 1925 and established in the literature within a couple of years when a series of cases was described[1][2].

Despite being first described as a sickness of the lungs in the slaves that wove asbestos into cloth by Strabo (Greek (63/4 BC - c. AD 24) and Pliny the Elder(Roman 23–79), the issue did not result in formal regulation until 1931, when the widespread use of asbestos allowed the pathology and specific association to be defined. Indeed, this association was the one that initially drove asbestos into the occupational health limelight, not the later demonstration of an association with malignancy (mesothelioma and carcinoma). An isolated death from the disease, subject to post mortem (unlike the 9 coworkers who pre-deceased him), had been well described in 1900, emphasising the occupational association, but most patients were thought to have tuberculosis and, of course, many did develop this, sometimes as well (31% in one series[3]).

In 1924, William E Cooke published a case report, enlarged in 1927 to a formal paper, on asbestos-related disease in the context that, by then, others had shown similar pathology, able to be separated from usual silicosis, and had cases in life where TB could not be proven despite reasonable investigation. So by 1927, the characteristic presence of asbestos fibres in the lungs at post mortem allowed accurate retrospective diagnosis[4]. In 1930, Edward Merewether further confirmed that inhalation of asbestos dust can cause a fatal disease. Moves to stop the use of asbestos, at least in the UK, was relatively swift thereafter. The 1931 UK Asbestos Industry Regulations negotiated by Dr Thomas Legge, suppressed industrial asbestos dust by 1933. However, considerable later exposure took place in the demolition and salvage industries right into the 1960s. Other sources of significant exposure were war-time shipbuilding and bomb sites, with significant pulmonary disease being manifest sometimes 40 or 50 years later.

In 1935 Kenneth Lynch and W Atmar Smith identified a "possible relationship" between pulmonary asbestosis and carcinoma of the lung,[5] which is now accepted as causative.


If a proven occupational history is present and high resolution CT concurs, not all cases require a tissue diagnosis.


  1. Diffuse interstitial fibrosis
  2. Presence of asbestos bodies (see below)


The fibres by themselves are extremely thin and can be hard to see by light microscopy. However, they often become coated by iron and calcium, the former can be stained with Perls' staining to bring out the fibres, as in this photomicrograph.

By light microscopy, there should be more than 2 asbestos bodies per square centimetre of tissue. Light microscopy is a good, but imperfect, surrogate measure for fibre burden as compared to formal quantification of asbestos fibres in tissue digests.[6][7] Formal fibre counts involve taking ~2cm3 blocks of fixed or fresh lung tissue from 3 different parts of the lung, avoiding tumour and thickened pleura. These are then chemically treated to digest the organic tissue, leaving only the non-organic fibres. These are quantified most accurately by electron microscopy, although conventional microscopy with phase-contrast or dark ground illumination can also be used. As most individuals will have had some degree of asbestos exposure, these results have to be interpreted in the context of a reference range of appropriate controls.

Because some asbestos types elicit a stronger biological reaction than others, light microscopy counts may underestimate the fibre burden (e.g. ~25% of amosite fibres can be seen in contrast with ~5% of crocidolite fibres). EM fibre counts are therefore superior, but are performed only specialised centres (Llandough Hospital in the UK).


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