SilicosisJ62.8

Silicosis (from Latin silex = pebble), also quartz dust lung, is the most common pneumoconiosis (dust lung disease). It is caused by inhalation of quartz dust (fine dust containing α-quartz or another crystalline modification of silica). In versch. Guidelines of the relevant professional societies, the term silicosis is also understood to include quartz dust pulmonary diseases triggered by other silicogenic dusts such as cristobalite and tridymite (Bauer X 2016). Silicosis is listed as a recognized and notifiable occupational disease under BK.Nr.4101, silico-tuberculosis, which is frequently associated with it, under BK.Nr.4102, COB or emphysema of appropriately disposed persons.

Under BK No. 4101, only those symptoms of illness are to be recognized as occupational diseases that were triggered by inhalation exposure to dust mixtures with varying proportions of alveolar quartz, cristobalite or tridymite dust particles. In this context, the risk of the disease depends on the dust concentration in the respiratory air, the proportion of the alveolar dust fraction, the content of free crystalline silica (SiO2), the type of accompanying dusts, the duration of exposure, the individual "sensitivity" to free crystalline silica, and the cleansing ability of the lungs. Furthermore, the type, extent and duration of dust exposure and the workplace conditions play a significant role (Bauer X 2016).

A distinction is made between:

• the quartz dust silicosis (caused by inhalation of almost pure quartz dust)

and the

• Mixed dust silicoses (also called silcatoses: formed by inhalation of dust mixtures; these contain other components besides quartz):

The most frequent mixed dust silicosis is the anthracosilicosis of the coal-mining miner (miner before coal). The triggering so-called coal pit dust is a highly complex mixture of different minerals and additives (e.g. building materials). It mainly consists of clay minerals, sulphides, carbonates and quartz. Note: Internationally, the term "silicosis" is only used for pneumoconiosis caused by crystalline dust types with a high silicic acid content.

The pneumoconiosis of coal miners is called mixed dust pneumoconiosis or "coal workersʼ pneumoconiosis" or anthracosilicosis. In the German law on occupational diseases on the other hand both the "pure" silicosis and the pneumoconiosis of the coal miner are subsumed under the term silicosis.

Another special form (usually only histologically clarified) is the interstitial disseminated fine-grained silicosis (pinhead/grain type). This type is most clinically impressive as unspecific interstitial pulmonary fibrosis. Dust deposits can be detected in the fibrotically widened septa, here partly free in the interstitium, partly bound in macrophages.

For the year 2013, 1497 notifications of a BK.Nr. 4101 were documented, as well as 768 recognitions, including 490 new BK pensions and 324 BK-related deaths. The majority (563 notifications) were for sick persons in the mineral extraction/construction professions, followed by metal workers/mechanics and related professions (84 notifications).

Only crystalline dust and the SiO2 high temperature modifications cristobalite and tridymite with an alveolar size of < 7um, lead to silicosis. Larger dust particles are retained in the bronchial system. The smaller quartz particles enter the alveoli, where they are phagocytized by the alveolar macrophages, but cannot be degraded by them. The alveolar macrophages perish and the quartz particles are released again in a kind of recycling process. In this way they initiate a perpetuating chronic alveolitis, which leads to the formation of silicotic granuloma and finally to fibrosis of the lung parenchyma. This mechanism explains the progression of silicosis even after the end of exposure, e.g. after the end of underground workings. Some of the silicogenic dust particles also penetrate the lung interstitium and are transported further into the lymph nodes, among other places. The individual granulomas can conflate into larger calluses. The calluses can soften centrally through ischemic necrosis. The characteristic calcifications of lymph nodes are called "eggshell silicosis".

The remodelling of the lung parenchyma leads to a reduction in the lung's ability to absorb oxygen. Finally, a lung damaged in this way is susceptible to other diseases such as lung cancer and tuberculosis (silicotuberculosis). Inhaled, fine-grained or powdered talc (talcum), which is used in the rubber and paper industry and in cosmetic products, among other things, can also trigger pulmonary fibrosis via contamination by quartz or asbestos (talc dust lung, talcosis).

Adit and tunnel workers, mine workers, sandblasters, quarry workers, casting cleaners, moulders, core makers, foundrymen, workers in the ceramic industry, workers in the cleaning industry; oven workers, workers in the clothing industry who blast e.g. blue jeans to give them a used look (Bloch KE et al 2017).

In the case of slowly progressing silicosis, the first sign of silicosis is chronic bronchitis with coughing, sputum, wheezing, whistling. Subjectively, dyspnoea dominates the clinical picture. The examination of the lung function shows above all the signs of obstruction of various degrees of severity. The restriction takes a back seat here.

Silicosis is usually diagnosed primarily by X-ray of the lungs (Bloch KE et al 2017) in conjunction with a subtle occupational history.

Characteristic are disseminated, more or less roundish shadows of different size and density, possibly with additional larger so-called callus formations, mainly localised in the upper and middle fields, possibly confluent and/or disintegrating. The diagnostic findings of the chest x-ray are standardized according to the dust lung classification of the ILO (International Labour Organization) (Bauer X et al. 2016). Initially, there is a mesh-like reinforcement of the lung drawing. This results in roundish spotted shadows, which are divided according to their diameter into P (up to 1.5mm), Q (up to 3mm) and R (up to 10mm). It is important to note that the radiological image does not allow a reliable conclusion to be drawn about the composition of the incorporated dust. Alternatively, silicosis can be defined primarily by computer tomographic or semi-quantitative macroscopic and histological findings (Baur X 2008). Larger callus formations are classified according to their size and extension according to A (0-5cm)-B (between A and C) and C (> right lung upper field).

Hilar lymph nodes: There is no close correlation between the involvement of the mediastinal lymph nodes and the severity of the silicotic lung involvement. More extensive conglomerating and indurating lymph node processes can lead to dislocations of the hilum with repercussions on the large bronchial and vascular trunks.

Other silicosis not caused by silicic acid but by silicate-containing dusts such as: asbestosis, kaolin lung, mica lung, aluminium lung, talc lung, berylliosis, ochre lung.

Also: sarcoidosis, hypersensitivity pneumonitis, viral pneumonia, histoplasmosis, adenocarcinoma with lepidic growth pattern, Kaposi's sarcoma of the lung, lymphomas and leukemias, bronchiectasis, cystic fibrosis, amyloidosis, storage diseases, Langerhans cell histiocytosis.

Silicosis and comorbidities

Increased susceptibility of the lungs to infections with frequent occurrence of broncho-pulmonary infections.

COB: Increased incidence of chronic obstructive bronchitis (COB) (J42.).

COPD: A doubling of risk of COPD of the kidney smoker results in coal mining with a cumulative exposure of about 100 particulate matter years; (particulate matter years= mg/m3 x work years).

Increased incidence of emphysema (J43.9), cor pulmonale (I27.9), silico-tuberculosis (10% of cases).

Lung cancer: doubling of the risk of lung cancer compared to the unaffected population.

Autoimmune diseases (data refer to Michigan's 1 022-case silicosis disease registry). For silicosis patients, there is:

• a two to eightfold risk of rheumatoid arthritis (Caplan syndrome)
• a two to eightfold risk of systemic lupus erythematosus
• a > than 24-fold risk for systemic scleroderma (M34.0)
• a > than 24-fold risk for ANCA+ vasculitis (Makol A et al. 2011).
• The most common autoimmune disease among silicosis patients is rheumatoid arthritis. ANCA-associated vasculitis is also much more common in silicosis patients than in the general population (Makol A et al. 2011) .

Preventive measures, treatment of infections and an existing COPD. S.u. bronchial asthma. Clarification and therapy of complicated diseases.

An early development of silicosis with considerable quartz dust exposure is possible. However, it takes 10-15 years until the clinical manifestation of silicosis. It is important to note that silicosis can continue to progress even after exposure to quartz dust has ended.

Lung diseases caused by the inhalation of organic dusts do not belong to the actual pneumoconioses.

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2. Attfield MD et al (1992) Pulmonary function of US coal miners related todust exposureestimates. Am Rev Respir Dis 145: 605-609
3. Bloch KE et al (2017) Structural lung changes. In: Battegay E: Differential diagnosis of internal diseases. Georg Thieme Publishers Suttart, New York pp 123-175.
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7. Makol A et al (2011) Prevalence of connective tissue disease in silicosis (1985-2006)-a report from the state of Michigan surveillance system for silicosis. Am J Ind Med 54:255-262.

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