HistoryThis section has been translated automatically.
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).
DefinitionThis section has been translated automatically.
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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ClassificationThis section has been translated automatically.
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).
Occurrence/EpidemiologyThis section has been translated automatically.
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.)
- 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).
EtiopathogenesisThis section has been translated automatically.
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 featuresThis section has been translated automatically.
- occasional slightly bloody sputum
- Reduction in performance
- Night sweat
The pleura reacts to chronic irritation by asbestos fibres in different ways (Müller 1996):
A so-called asbestos pleuritis can develop, which turns into a hyalinosis complicata with often bilateral, diffuse pleural fibrosis, which is mainly located in the mid and subfields and in the pleura pulmonalis. Often hyaline or calcified pleural plaques also occur in the area of the chest wall or diaphragm. Pulmonary asbestosis does not necessarily have to be present at this stage.
ImagingThis section has been translated automatically.
Sonography: Sonography often shows signs of pleural effusion (signs of asbestos pleuritis; the effusion is usually non-specific, without signs of inflammation and rich in fibrin)
Computed tomography: Frequently, in computed tomography pleural (often calcified) plaques of the parietal pleura occur, more rarely of the visceral pleura, often on both sides; sometimes these plaques are also found in the area of the heart contour. In the advanced stage, reticular to coarse-striped changes of the subfields up to the honeycomb form can be found. Furthermore, spherical atelectasis and compensatory emphysema of the upper fields (Piper 2007)
HistologyThis section has been translated automatically.
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).
DiagnosisThis section has been translated automatically.
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 diagnosisThis section has been translated automatically.
- 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).
Complication(s)This section has been translated automatically.
Pleural fibrosis: There is a dose-response relationship for the development of pleural fibrosis, but this does not apply to the carcinogenic effect of asbestos.
Bronchial carcinoma: After 16 - 18 years of exposure, 12% - 17% develop bronchial carcinoma. The risk is further increased if the person concerned smokes. In this case, the risk is greater than the sum of both risk factors (so-called multikative or over-additive effect). The term "fibre years" is used to better assess the tumour risk. 1 fibre year corresponds to 1 x106 fibres per m³ x 1 year The risk of developing lung carcinoma, for example, doubles with 25 fibre years (Herold 2018).
Remark: For the recognition of a lung carcinoma as an occupational disease caused by asbestos, the so-called "bridge symptoms" must be present. The bridge symptoms include:
- the presence of asbestosis (even minimal asbestosis is sufficient)
- the presence of pleural changes due to asbestosis (pleural plaques)
- proof of at least 25 fibre 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. It develops most frequently in the pleura, occasionally in the peritoneum and very rarely in the pericardium. Up to 90% of mesotheliomas are due to exposure to asbestos (Craighead 2011). They represent the so-called "asbestos-related signal tumour" for an exposure to asbestos fibres. Mesotheliomas can occur after only a short exposure to asbestos, even without the presence of minimal asbestosis (Herold 2018). As these tumours are extremely rare in the general population without asbestos exposure, any mesothelioma is considered asbestos-induced until the contrary is proven. With regard to insurance claims, an occupational exposure to asbestos must be present in the medical history.
Progression/forecastThis section has been translated automatically.
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).
ProphylaxisThis section has been translated automatically.
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.
LiteratureThis section has been translated automatically.
- Official Journal of the European Union. Directive 2009/148/EC of 30.11.2009
- Baur X et al (2005) Position paper of the German Society of Pneumology on the assessment of silicosis. Pneumology (59). Georg Thieme Publisher SS 549-553
- Baur X et al. (2009) Ethics in Occupational Medicine: Orientation Guide in Ethical Fields of Conflict.main topic Annual Conference DGAUM 2008. Publishing Group Hüthig Jehle Rehm GmbH S 111
- Bücheler E et al (1998) Introduction to Radiology: Diagnostics and Interventions Georg Thieme Verlag S 293
- Büttner J U (2004) Asbestos in pre-modern times - from myth to science. Waxmann Publishing House S 262
- Craighead J (2011) Epidemiology of mesothelioma and historical bachground. Rec Res Cancer Res 189: 13-25
- Dörfler H et al (2008) Medical reports Springer Verlag S187
- Heine J (1960) About asbestosis. Archive for industrial pathology and hygiene 18: 159-204
- Herold G et al (2018) Internal Medicine Herold Verlag S 397
- Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education S 1689
- Kasper D L et al (2015) Harrison's Internal Medicine. Thieme Publishing House SS 2063-2064
- Kirchner T et al (2018) Short textbook on pathology. Elsevier Health Sciences S 55
- Kotschy-Lang N (2011) Case studies. Fortschr Röntgenstr 183: RK 3143
- Müller K M et al (1996) Asbestos-related diseases. German Medical Journal 9: A 538- A 534
- Piper W (2007) Internal Medicine. Springer Publishing House S 238
- Ulmer W T et al (1976) Pneumoconioses. Springer publishing house SS 57-67, 546
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