HistoryThis section has been translated automatically.
Asbestos disease; benign disease due to asbestos dust; malignant disease due to asbestos dust; asbestosis; asbestos pulmonary disease;
Observations of an asbestos-induced disease, asbestosiswere first made in England in 1900 by Montague Murray, in Canada in 1912 by Wedler, and in Germany in 1914 by Fahr and Feigl.
The first writings on asbestosis were from England in 1924 by Cooke (Heine 1960).
In 1938, the first two cases of occupational cancer in asbestos workers were described by M. Nordmann. First protective measures for Germany were issued during the 2nd World War (Büttner 2004).
DefinitionThis section has been translated automatically.
Asbestos-related diseases are reportable occupational diseases caused by asbestos fibers (Herold 2022) and include the following spectrum:
- 1. classical asbestosis with interstitial fibrosis
- 2. asbestos-related changes in the pleura and other mesothelia
- 3. asbestos-related tumors, e.g., of the lung and pleura (Rehbock 2016).
You might also be interested in
ClassificationThis section has been translated automatically.
The following diseases can be caused by exposure to asbestos:
- Pulmonary fibrosis
- Pleural diseases (benign such as: Pleural effusions, diffuse pleural fibrosis with diffuse thickening of the lateral chest wall, pleuritis, spherical atelectasis, pleural plaques, hyalinosis complicata [Kraus 2020 / Teschler 2008] )
- Carcinomas of the:
Mesotheliomas of the:
- Pericardium (Herold 2022)
OccurrenceThis section has been translated automatically.
Asbestos-related diseases occur in the asbestos manufacturing and asbestos processing industries such as:
- Asbestos textile
- Asbestos cement
- Asbestos insulation industry (Herold 2022).
Currently, according to the GVS (Zentralstelle asbestgefährdeter Arbeitnehmer), about 500,000 people are registered there. It is estimated that the number of unreported cases is just as high.
In Germany, asbestos-induced malignancies are the most common occupational cancer.
Due to the long latency period (15 - 50 years), it is expected that the number of diseases will peak around 2020 (Herold 2022).
Asbestos-related diseases occur not only in workers in asbestos mining or processing, but also in the general population such as those who wash clothing that has come into contact with asbestos (Nowak 2018), painters, electricians, those exposed through road surfacing or playground materials, etc. (Kasper 2015). Indirect exposures such as washing work clothes are not eligible for recognition because they are not occupational exposures (Nowak 2018).
Although the neoplastic effects of asbestos were already known since the mid-1930s, asbestos itself was used medically until the 2nd half of the 20th century, among other things, e.g., in spontaneous pneumothorax or it was applied preoperatively to the pleural space to make it stick together(Ulmer 1976).
Mesothelioma can occur after a relatively short exposure to asbestos of ≥ 1 - 2 years after a latency period of up to 40 years. In those suffering from mesothelioma, up to 80% were found to have been exposed to asbestos (Kasper 2015).
EtiologyThis section has been translated automatically.
The cause is inhaled asbestos dust consisting of various silicates such as amosite, anthophyllite, chrysotile, crocidolite, etc., which have a fiber width of less than 3 µg in diameter and a length of more than 10 µg. Only with these size ratios do the fibers succeed in penetrating into the alveoli on the one hand, and on the other hand their elimination by the macrophages is significantly more difficult due to this (Piper 2007).
PathophysiologyThis section has been translated automatically.
Asbestos is understood to be fibrous crystallized silicate minerals that have a fibrinogenic and carcinogenic effect (Fritze 2008).
After inhalation of dusts containing asbestos fibers, they are deposited in the peripheral airways and alveoli. From there, they enter the parenchyma of the lungs up to the area of the pleura. There they can be visualized by scanning electron microscopy as protruding fiber ends consisting of phagocytosing cells (Matthys 2009).
In the further course, a chronic inflammatory and fibrosing process with fibroblast proliferation and macrophage activation occurs. Edema with histiocytic and giant cell reaction occurs in the terminal bronchial area, followed by interstitial collagen fiber proliferation. This spreads to the septa and alveoli, resulting in progressive fibrosis of the alveoli, alveolar ducts, and bronchioli. However, the elastic structures are typically preserved in the process (Kraus 2020).
- Fibrinogenic effect:
Fibrinogenic action results in asbestosis (see d. for more details).
This results in asbestos-induced pulmonary fibrosis with fibrosing alveolitis, activation of fibroblasts, and proliferation of alveolar macrophages. There is a dose-response relationship for the fibrinogenic effect (Herold 2022).
- Carcinogenic effect:
The carcinogenic effect can lead to lung carcinoma, mesothelioma, laryngeal carcinoma, and ovarian carcinoma.
In lung carcinoma, the risk is multiplicative from exposure to asbestos plus smoking.
Mesothelioma is so rare in the general population that it is always considered to be asbestos-induced until proven otherwise (so-called "signal tumor").
Smoking and alcohol are additional risk factors in laryngeal carcinoma. There is NO dose-response relationship for the carcinogenic effect (Herold 2022).
Clinical pictureThis section has been translated automatically.
Clinical symptoms depend on the type of disease (Herold 2022).
- Pleural plaques:
Pleural plaques do not cause any symptoms. They are signs of asbestos exposure but do not represent a precancerous condition (Herold 2022).
It manifests as small, recurrent pleural effusions often without other symptoms (Herold 2022)
The earliest form of asbestosis is the so-called "asbestos airways disease", in which fibrosis associated with asbestos bodies, exclusively affecting the wall of the bronchioli, occurs.
Patients initially complain of irritable cough, dyspnea, and chest tightness. As the disease progresses, chronic bronchitis, persistent hypoxemia, and cor pulmonale are added (Kraus 2020).
Typical of asbestosis is the symptom triad of dyspnea, fibrosis on x-ray, and auscultatory crackles over the lungs (Herold 2022).
Symptoms are usually absent in the early stages. Later, they may be joined by: cough, dyspnea, chest pain, and hemoptysis.
Occurs most commonly in the pleura, less commonly in the peritoneum and very rarely in the pericardium. When the pleura is involved, dyspnea, cough are found. Pleural effusion, chest pain, and if the peritoneum is involved, ascites, unexplained abdominal discomfort (Herold 2022), and constipation (Kraus 2020).
- Laryngeal carcinoma:
Hoarseness represents an early symptom (Herold 2022). Other symptoms may include: foreign body sensation, tumor fetor, bloody sputum (Kraus 2020).
- Ovarian Cancer:
- abdominal pain
- circumferential increase of the abdomen
- weight loss
- abnormal bleeding
- Micturition difficulties, etc. (Kaufmann 2012)
DiagnosticsThis section has been translated automatically.
- Occupational history
- Examination with equipment, e.g. X-ray thorax, HRCT (see below)
- bronchoalveolar lavage to detect alveolitis and asbestos fibers (Herold 2022). This is not suitable for confirming the diagnosis and does not require participation (Kraus 2020).
- Bronchoscopic tissue sampling (this is also not required for confirming the diagnosis and is not subject to cooperation [(Kraus 2020)]).
- In V. a. laryngeal carcinoma:
- Microlaryngoscopy usually performed by the ENT physician (Kraus 2020).
According to CAP (College of American Pathologist) / NIOSH (National Institute of Occupational Safety and Health), only the detection of one asbestos body is required in the histological section. If this is not possible in the case of typical interstitial fibrosis or lung carcinoma, more sensitive methods such as lung dust analysis (LSA) should be performed. If light microscopic detection is not possible, electron microscopy is recommended (Kraus 2020).
For recognition as an occupational disease caused by asbestos, evidence of the so-called "bridge symptoms" is required. These are:
- in conjunction with asbestosis
- in connection with disease of the pleura caused by asbestos
- Evidence of exposure to a cumulative dose of asbestos dust for at least 25 years in the workplace (Herold 2022).
In asbestosis, both auscultatory and percutorial findings are uncharacteristic. Evidence of fibrosis includes a fine crackling rattle at the end of the inspiratory over the lateral and lower parts of the lungs (Kraus 2020).
ImagingThis section has been translated automatically.
- recurrent small pleural effusions (Herold 2022)
- The changes occur mostly bilaterally, but not symmetrically (Kraus 2020)
- Pleural plaques: Pleural plaques with thickening or calcification of the parietal pleura are visible in the x-ray, especially along the lower lung fields, the cardiac border and the diaphragm.
- benign pleural effusions with bloody or serous exudate
- opacities: linear or irregular opacities appearing at the beginning in the lower lung fields
- indistinct cardiac border (Kasper 2015)
- Round focus (there is no reduction in transparency that cannot be caused by lung carcinoma [Herold 2022]).
HRCT (High-resolution CT)
- Pleural plaques:
- predominant involvement of the lateral and diaphragmatic pleura
- occurring bilaterally (Herold 2022)
Changes in the subpleural curve lines parallel to the surface with a length of 5 - 10 mm (Kasper 2015).
LaboratoryThis section has been translated automatically.
Pulmonary function testing:
Asbestosis typically shows:
- restrictive ventilation disorder
- decrease in lung volume (especially FVC and TLC [Kraus 2020])
- decrease of diffusion capacity
- mild airway obstruction due to peribronchial fibrosis possible (Kasper 2015)
- arterial hypoxemia
- decreased oxygen uptake
- FEV1 / FVC (the function of the large airways) is typically well preserved (Kraus 2020)
HistologyThis section has been translated automatically.
Non granulomatous fibrosis of the lung with acinar involvement and concomitant chronic inflammatory changes (Kraus 2020).
In lung cancer due to asbestos exposure, all known histological tumor forms occur (Kasper 2015).
- Laryngeal carcinoma:
It is squamous cell carcinoma in > 90% of cases (Kraus 2020).
- Ovarian carcinoma:
Epithelial tumors derived from the surface epithelium are found in 65-70% of cases. Germ cell tumors occur between 15 - 20 % and stromal tumors are the least common tumors with 5 - 15 %. Histologically, they belong to the adenocarcinomas (Kraus 2020).
Differential diagnosisThis section has been translated automatically.
Metastases from other primary tumors (Kraus 2020).
Complication(s)This section has been translated automatically.
- Lung carcinoma
- respiratory insufficiency
- Cor pulmonale (Herold 2022)
TherapyThis section has been translated automatically.
The therapy depends on the type of disease.
PrognoseThis section has been translated automatically.
The prognosis depends on the organ affected and the type of disease.
Mesothelioma, for example, has a very poor prognosis. It represents 50% of all occupational deaths. The median survival time is only 1 year (Herold 2022).
Note(s)This section has been translated automatically.
The term "fiber years" is used to estimate tumor risk. One fiber year = 1 x 10 to the power of 6 fibers / m³ x 1 year.
The risk of lung cancer, for example, doubles after 25 fiber years, whereas mesothelioma can occur without evidence of minimal asbestosis and even after a low level of exposure (Herold 2022).
The latency period between exposure and the onset of lung cancer ranges from a minimum of 15-19 years (Kasper 2015) to a maximum of 60 years (Matthys 2009). The higher the exposure was, the greater the risk of disease (Kasper 2015).
As early as the turn of the 19th / 20th century, health problems caused by inhaling asbestos were recognized. But it was not until 1972 that the WHO's International Agency on Cancer confirmed a direct link between the inhalation of asbestos dust and the incidence of cancer (Dyllick 2013).
In Germany, a regulation on hazardous working materials was issued in 1972, and in 1973 the employers' liability insurance associations issued a regulation on "protection against mineral dust hazardous to health" (Büttner 2004).
Asbestosis, for example, has been part of the Occupational Diseases Ordinance since 1929 (Baur 2005).
Mesothelioma ofthe pleura and peritoneum resulting from asbestos exposure was added to the Occupational Diseases Ordinance (BKV) in 1977 (Büttner 2004).
In 1987, the International Agency for Research on Cancer (IARC) classified asbestos as a Class I carcinogen (Huang 2021).
In 1992, lung cancer was recognized after 25 fiber years of asbestos exposure.
Laryngeal carcinoma was added to the BK- list with amendment in 1997, and ovarian cancer in 2017 (Kraus 2020).
Nowadays, in developed countries, asbestos has been largely replaced by synthetic mineral fibers such as glass fibers, refractory ceramic fibers. However, it is still used in developing countries (Kasper 2015).
- Primary prevention:
In Germany, both the manufacture and use of asbestos have been banned since the Hazardous Substances Ordinance of 1993 came into force - with the exception of its use as diaphragms for chlorine potassium electrolysis (Büttner 2004), EU-wide only since 2005 (Herold 2022).
As of 2019, asbestos is banned in 66 countries or regions of the world (Huang 2021).
- Secondary prevention:
Secondary prevention is for unavoidable exposure. As materials containing asbestos are still present in many buildings nowadays, demolition, renovation 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. The Official Journal contains detailed information on dust control measures, wearing of special protective work suits, use of fine dust filters and regular occupational medical examinations (Büttner 2004).
LiteratureThis section has been translated automatically.
- Baur X et al. (2005) Position paper of the German Society of Pneumology on the assessment of silicosis. Pneumology (59). Georg Thieme Verlag 549-553
- Büttner J U (2004) Asbestos in pre-modern times - from myth to science. Waxmann Verlag 19, 24 - 26, 262
- Dyllick T (2013) Managing environmental relations: public disputes and challenge. Springer Fachmedien Wiesbaden 313 - 333, 362 - 363.
- Fritze J et al (2008) The medical appraisal: legal issues - functional tests - assessments. Steinkopff Publishers 278 - 281
- Heine J (1960) On asbestosis. Archiv für Gewerbepathologie und Gewerbehygiene (18) Springer Verlag 159-204.
- Herold G et al (2022) Internal medicine. Herold Publishers 398 - 399, 404 - 405.
- Huang X Y et al (2021) Asbestos exposure and asbestos-related malignant diseases:an epidemiological review. Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 39 (3) 233 - 236.
- Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 1688 - 1689
- Kaufmann M et al (2012) Gynecology. Springer Verlag Berlin / Heidelberg 538
- Kraus T et al. (2020) Interdisciplinary S2k-guideline of the German Society for Pneumology and Respiratory Medicine e. V. and the German Society for Occupational and Environmental Medicine e. V.
- Matthys H et al (2009) Clinical pneumology. Springer Verlag Berlin / Heidelberg 183 - 185
- Nowak D et al. (2018) Essentials occupational medicine: the essentials for physicians of all specialties. Elsevier Urban and Fischer Publishers 57
- Piper W (2007) Internal medicine. Springer Verlag 238
- Rehbock B et al (2016) Asbestos-related diseases and their time course - a pathological-radiological discussion. Rofo 188 RK 401_1
- Teschler H (2008) Asbestos-related lung diseases. The pulmonologist (5) 111 - 119.
- Ulmer W T et al (1976) Handbook of internal medicine. Volume 4 respiratory organs 1st part: pneumoconioses. Springer Verlag Berlin / Heidelberg / New York 392