Asbestosis J61

Author: Dr. med. S. Leah Schröder-Bergmann

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Last updated on: 06.01.2023

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Asbestos dust lung disease

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It is unclear where the asbestosis first appeared. It was first observed in 1900 in England by Montague Murray, then in 1912 by Wedler in Canada and in 1914 in Germany by Fahr and Feigl.

The first writings about asbestosis in England were written by Cooke in 1924 (Heine 1960).

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Asbestosis is one of the pneumoconioses.

In asbestosis, a deposit of asbestos fibres in the lungs occurs. The macrophages are able to phagocytise fibres of < 10 µm. Longer fibres are also able to penetrate the alveolar epithelium, but when phagocytosis is attempted they cannot be broken down by the macrophages. By releasing mediators and stimulating fibroblasts, these deposits lead to an increase in the connective tissue fibres between the alveoli, the so-called diffuse fibrosis of the alveolar septa.

The asbestos needles in turn pass through the wall of the alveoli to the pleura. There they cause the changes typical of asbestosis such as pleural plaques, calcifications, etc. The changes in the lung or pleura in the form of pleural plaques are always bilateral and are therefore an indicator of asbestos exposure (Kirchner 2018).

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Asbestosis is classified into four degrees of severity according to a proposal by the National Institute for Occupational Safety and Health and the American Pneumoconiosis Committee (Heine 1960):

  • Grade 1
  • Grade one is also known as "minimal asbestosis".
  • Light microscopy reveals minimal asbestosis in which the fibrosis involves at least one bronchiolus respiratorius.
  • Grade 2
  • In grade two asbestosis, two or more layers of adjacent alveoli or the alveolar ducts are already involved in fibrosis.
  • Grade 3
  • A grade three asbestosis already shows a confluence of fibroses.
  • Grade four
  • Only in fourth-degree asbestosis are there thick-walled, honeycombed cavities.

Since 1929 asbestosis has been part of the Ordinance on Occupational Diseases (BKV), and the Moers Convention in the 1970s stipulated that silicosis can only be considered to be a disease for which compensation is due if there is at least a radiological spread of category 2/3. Since then, non-threshold silicoses of the scattering grades 1/1, ½, 2/1 and 2/2 have mostly not been compensated (Baur 2005).

After critical discussion of the Moers Convention, this was then replaced by an S2 guideline for the assessment of silicosis (Baur 2008).

It was not until 1980 that the ILO (International Labour Office), whose aim is to improve working and living conditions, drew up an international finding scheme for the changes in X-ray images caused by asbestos exposure, the so-called ILO Classification of Pneumoconiosis 1980. The coding is based on numbers and letters. For more details see Bücheler 1998 Table 4.13. These criteria were later changed by the ILO in 2000 (Dörfler 2008).

If small, roundish shadows of the type p, q, r or s, t, u with a scattering degree of 1/1 and higher are detectable in conventional chest radiographs, an occupational disease according to No. 4101 of the BKV is present. Since 2008, it has been possible in Germany to recognise the existing functional restrictions in the sense of chronic obstructive bronchitis and/or pulmonary emphysema as an occupational disease in those affected with a degree of variance of 1/1 and above and to report this as a case of reduced earning capacity in accordance with No. 4101 of the BKV, which is then compensated accordingly by the accident insurance institution (Kotschy-Lang 2011).

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Exposed occupational groups for asbestosis are:

  • miners in asbestos mining (Canada, South Africa, Russia)
  • Manufacturers and users of asbestos products (eternit, building materials, insulation for power and heat lines, brake pads, fireproof blankets and clothing, etc.)
  • Electrician
  • Painter
  • Family members of the occupational groups concerned (e.g. washing of work clothes)

According to information from the GVS (Central Office for Workers at Risk of Asbestos), there are currently around 500,000 people registered there. The number of undetected cases is estimated to be just as high.

In Germany, asbestos-induced malignancies are the most common occupational cancer. Due to the long latency period (15 - 50 years), a peak of the diseases is expected around 2020 (Herold 2018).

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The cause of asbestosis is inhaled asbestos dust from various silicates such as amosite, anthophyllite, chrysotile, crocidolite, etc., which have a fibre width of less than 3 µg in diameter and a length of more than 10 µg. It is only at these proportions that the fibres are able to penetrate the alveoli on the one hand, and on the other hand that their removal by macrophages is significantly more difficult (Piper 2007).

Clinical features
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  • Cough
  • sporadic slightly bloody sputum
  • dyspnea
  • reduced performance
  • night sweats

The pleura reacts to chronic irritation by asbestos fibers in different ways (Müller 1996):

A so-called asbestos pleurisy may develop, which progresses to hyalinosis complicata with often bilateral diffuse pleural fibrosis localized predominantly in the middle and lower fields and in the pleura pulmonalis. Hyaline or calcified pleural plaques in the area of the chest wall or diaphragm often also occur. At this stage, pulmonary asbestosis is not necessarily also present.

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Sonography: Sonography often shows signs of pleural effusions (signs of asbestos pleuritis; the effusion is usually nonspecific, without signs of inflammation and rich in fibrin).

Computed tomography: Frequently, computed tomography reveals pleural (often calcified) plaques of the parietal pleura, less frequently of the visceral pleura, often bilaterally; sometimes these plaques are also found in the region of the cardiac contour. In advanced stages, reticular to coarse striated changes of the subfields up to honeycomb form are found. Furthermore, ball atelectasis as well as compensatory emphysema of the upper fields (Piper 2007).

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Histologically there is a non-specific chronic inflammatory foreign body reaction.

Microscopic detection of so-called "asbestos corpuscles" both in the sputum and in the bronchial lavage. Asbestos corpuscles can be distinguished from pseudoasbestos corpuscles by polarisation-optical means; pseudoasbestos corpuscles are fibrous particles which are often also surrounded by an iron-containing sheath; however, in the case of asbestos corpuscles, an optically transparent, weakly birefringent central fibre can always be seen which has plane-parallel edges in the longitudinal axis (Heine 1960).

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In the case of asbestosis in particular, a detailed occupational history should be taken.

The fibrotic changes are almost exclusively bilateral, often with a preference for the middle and lower subpleural sections. However, clinical and radiological evidence of fibrosis is only found in a late stage of asbestosis at severity grades three and four (Heine 1960).

Auscultation: During the auscultation endinspiratory fine bubble rales are found

Lung function: Lung function can change as follows:

  • restrictive ventilation disorder
  • Decrease in compliance with reduction of vital capacity (VC) and total lung capacity (TLC)
  • Reduction of the diffusion capacity (DLCO)

Bronchoscopy / Thoracoscopy: Biopsies taken during bronchoscopy or thoracoscopy should be histologically examined for the detection of asbestos corpuscles.

Differential diagnosis
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  • interstitially fibrosing lung diseases of other genesis
  • Pulmonary asbestoses almost always show pleural changes. The most sensitive detection is the HRCT. Therefore, in pulmonary fibrosis without pleural changes, a different etiology should always be considered (Herold 2018).

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Pleural fibrosis: There is a dose-response relationship for the development of pleural fibrosis, but this is not true for the carcinogenic effects of asbestos.

Bronchial carcinoma: After 16 - 18 years of prolonged exposure, 12% - 17% develop bronchial carcinoma. The risk is further increased if the individual smokes. In this case, the risk is greater than the sum of both risk factors (so-called multicative or superadditive effect). To better estimate the tumor risk, the term "fiber years" is used. 1 fiber year corresponds to 1 x106 fibers per m³ x 1 year. The risk of developing lung cancer, for example, doubles at 25 fiber years (Herold 2018).

Note: For lung carcinoma to be recognized as an asbestos-related occupational disease, the so-called "bridge symptoms" must be present. Bridge symptoms include:

  • the presence of asbestosis (minimal asbestosis is also sufficient)
  • the presence of pleural changes due to asbestosis (pleural plaques)
  • the detection of at least 25 fiber years

Laryngeal carcinoma: Laryngeal carcinoma also occurs more frequently after exposure to asbestos and is also considered a risk factor in addition to the main risk factors of smoking and alcohol.

Mesothelioma: Another malignant disease induced by asbestos is mesothelioma. They most commonly develop in the pleural region, occasionally in the peritoneal region, and very rarely in the pericardial region. Mesotheliomas are up to 90% due to asbestos exposure (Craighead 2011). They represent the so-called "asbestos-related signal tumor" for exposure to asbestos fibers that has taken place. Mesotheliomas can occur after even brief exposure to asbestos, even without the presence of minimal asbestosis (Herold 2018). Because these tumors are extremely rare in the general population without asbestos exposure, any mesothelioma is considered asbestos-induced until proven otherwise. With regard to insurance claims, there must be a history of occupational asbestos exposure.

Respiratory insufficiency: In addition to malignant diseases, respiratory insufficiency and cor pulmonale - with the corresponding symptomatology - frequently occur in the context of asbestosis.

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If mesothelioma develops, the prognosis is very unfavourable. A curative therapy is rarely possible. The mean survival time is about 1 year (Herold 2018).

If a bronchial carcinoma develops, the prognosis depends on the histological type, the tumor stage, the general condition of the patient and the immunological status. The mean 5-year survival rate is between approx. 25% and 50% (Herold 2018).

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We distinguish between primary and secondary prevention.

As measures for primary prevention, the production and use of asbestos was banned at the beginning of 1994 when the Ordinance on Hazardous Substances of 26.10.1993 came into force (Büttner 2004).

Secondary prevention serves to prevent unavoidable exposure. Since even today materials containing asbestos are still present in many buildings, demolition, refurbishment and maintenance of asbestos are now legally regulated by the Official Journal of the European Union, EU Directive 2009/148/EC on the protection of workers at work from asbestos (formerly: Directive 83/477/EEC). The Official Journal contains detailed information on dust control measures, the wearing of special protective suits, the use of fine dust filters and regular occupational health checks.

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  1. Official Journal of the European Union. Directive 2009/148/EC of 30.11.2009
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Last updated on: 06.01.2023