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Silicosis is a respiratory disease caused by breathing in (inhaling) silica dust. It is an occupational lung disease that develops over time when dust that contains silica is inhaled into the lungs. Other examples of occupational lung disease include coalworker’s pneumoconiosis and asbestosis.
The name silicosis (from the Latin silex, or flint) was originally used in 1870 by Achille Visconti (1836-1911), prosector in the Ospedale Maggiore of Milan. The recognition of respiratory problems from breathing in dust dates to ancient Greeks and Romans. Agricola, in the mid-16th century, wrote about lung problems from dust inhalation in miners. In 1713, Bernardino Ramazzini noted asthmatic symptoms and sand-like substances in the lungs of stone cutters. With industrialization, as opposed to hand tools, came increased production of dust. The pneumatic hammer drill was introduced in 1897 and sandblasting was introduced in about 1904, both significantly contributing to the increased prevalence of silicosis.
Classification of silicosis is made according to the disease’s severity (including radiographic pattern), onset, and rapidity of progression. These include:
Chronic simple silicosis
Usually resulting from long-term exposure (10 years or more) to relatively low concentrations of silica dust and usually appearing 10–30 years after first exposure. This is the most common type of silicosis. Patients with this type of silicosis, especially early on, may not have obvious signs or symptoms of disease, but abnormalities may be detected by x-ray. Chronic cough and exertional dyspnea are common findings. Radiographically, chronic simple silicosis reveals a profusion of small (<10 mm in diameter) opacities, typically rounded, and predominating in the upper lung zones.
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Silicosis that develops 5–10 years after first exposure to higher concentrations of silica dust. Symptoms and x-ray findings are similar to chronic simple silicosis, but occur earlier and tend to progress more rapidly. Patients with accelerated silicosis are at greater risk for complicated disease, including progressive massive fibrosis (PMF).
Silicosis can become “complicated” by the development of severe scarring (progressive massive fibrosis, or also known as conglomerate silicosis), where the small nodules gradually become confluent, reaching a size of 1 cm or greater. PMF is associated with more severe symptoms and respiratory impairment than simple disease. Silicosis can also be complicated by other lung disease, such as tuberculosis, non-tuberculous mycobacterial infection, and fungal infection, certain autoimmune diseases, and lung cancer. Complicated silicosis is more common with accelerated silicosis than with the chronic variety.
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Silicosis that develops a few weeks to 5 years after exposure to high concentrations of respirable silica dust. This is also known as silicoproteinosis. Symptoms of acute silicosis include more rapid onset of severe disabling shortness of breath, cough, weakness, and weight loss, often leading to death. The x-ray usually reveals a diffuse alveolar filling with air bronchograms, described as a ground-glass appearance, and similar to pneumonia, pulmonary edema, alveolar hemorrhage, and alveolar cell lung cancer.
Because chronic silicosis is slow to develop, signs and symptoms may not appear until years after exposure. Signs and symptoms include:
*Dyspnea (shortness of breath) exacerbated by exertion
*Cough, often persistent and sometimes severe
*Tachypnea (rapid breathing) which is often labored
*Loss of appetite and weight loss
*Gradual dark shallow rifts in nails eventually leading to cracks as protein fibers within nail beds are destroyed.
In advanced cases, the following may also occur:
*Cyanosis (blue skin)
*Cor pulmonale (right ventricle heart disease)
Patients with silicosis are particularly susceptible to tuberculosis (TB) infection—known as silicotuberculosis. The reason for the increased risk—3 fold increased incidence—is not well understood. It is thought that silica damages pulmonary macrophages, inhibiting their ability to kill mycobacteria. Even workers with prolonged silica exposure, but without silicosis, are at a similarly increased risk for TB.
Pulmonary complications of silicosis also include Chronic Bronchitis and airflow limitation (indistinguishable from that caused by smoking), non-tuberculous Mycobacterium infection, fungal lung infection, compensatory emphysema, and pneumothorax. There are some data revealing an association between silicosis and certain autoimmune diseases, including nephritis, Scleroderma, and Systemic Lupus Erythematosus, especially in acute or accelerated silicosis.
In 1996, the International Agency for Research on Cancer (IARC) reviewed the medical data and classified crystalline silica as “carcinogenic to humans.” The risk was best seen in cases with underlying silicosis, with relative risks for lung cancer of 2-4. Numerous subsequent studies have been published confirming this risk. In 2006, Pelucchi et al. concluded, “The silicosis-cancer association is now established, in agreement with other studies and meta-analysis
Silica in crystalline form is toxic to the lining of the lungs. When the two come into contact, a strong inflammatory reaction occurs. Over time this inflammation causes the lung tissue to become irreversibly thickened and scarred – a condition known as fibrosis.
Common sources of crystalline silica dust include:
•Pure silica sand
People who work with these materials, as well as foundry workers, potters and sandblasters, are most at risk. Other forms of silica, such as glass, are less of a health risk as they aren’t as toxic to the lungs.
Men tend to be affected more often than women, as they are more likely to have been exposed to silica.
Silicosis is most commonly diagnosed in people over 40, as it usually takes years of exposure before the gradually progressive lung damage becomes apparent.
There are now fewer than 100 new cases of silicosis diagnosed each year in the UK. This is mostly the result of better working practices, such as wet drilling, appropriate ventilation, dust-control facilities, showers and the use of face masks. Many foundries are also replacing silica sand with synthetic materials.
With these measures and an increased awareness of the risks of silica exposure, the number of cases should fall even further in the future.
When silicosis is suspected, a chest x-ray will look for any damaged areas of the lungs to confirm the diagnosis. Lung function tests are often performed to assess the amount of damage the lungs have suffered and to guide treatment.
•Connective tissue disease, including rheumatoid arthritis, scleroderma (also called progressive systemic sclerosis), and systemic lupus erythematosus
•Progressive massive fibrosis
There are three key elements to the diagnosis of silicosis. First, the patient history should reveal exposure to sufficient silica dust to cause this illness. Second, chest imaging (usually chest x-ray) that reveals findings consistent with silicosis. Third, there are no underlying illnesses that are more likely to be causing the abnormalities. Physical examination is usually unremarkable unless there is complicated disease. Also, the examination findings are not specific for silicosis. Pulmonary function testing may reveal airflow limitation, restrictive defects, reduced diffusion capacity, mixed defects, or may be normal (especially without complicated disease). Most cases of silicosis do not require tissue biopsy for diagnosis, but this may be necessary in some cases, primarily to exclude other conditions.
For uncomplicated silicosis, chest x-ray will confirm the presence of small (< 10 mm) nodules in the lungs, especially in the upper lung zones. Using the ILO classification system, these are of profusion 1/0 or greater and shape/size “p”, “q”, or “r”. Lung zone involvement and profusion increases with disease progression. In advanced cases of silicosis, large opacity (> 1 cm) occurs from coalescence of small opacities, particularly in the upper lung zones. With retraction of the lung tissue, there is compensatory emphysema. Enlargement of the hilum is common with chronic and accelerated silicosis. In about 5-10% of cases, the nodes will calcify circumferentially, producing so-called “eggshell” calcification. This finding is not pathognomonic (diagnostic) of silicosis. In some cases, the pulmonary nodules may also become calcified.
A computed tomography or CT scan can also provide a mode detailed analysis of the lungs, and can reveal cavitation due to concomitant mycobacterial infection.
Silicosis is an irreversible condition with no cure. Treatment options currently focus on alleviating the symptoms and preventing complications. These include:
*Stopping further exposure to silica and other lung irritants, including tobacco smoking.
*Antibiotics for bacterial lung infection.
*TB prophylaxis for those with positive tuberculin skin test or IGRA blood test.
*Prolonged anti-tuberculosis (multi-drug regimen) for those with active TB.
*Chest physiotherapy to help the bronchial drainage of mucus.
*Oxygen administration to treat hypoxemia, if present.
*Bronchodilators to facilitate breathing.
*Lung transplantation to replace the damaged lung tissue is the most effective treatment, but is associated with severe risks of its own.
*For acute silicosis, Whole-lung lavage (see Bronchoalveolar lavage) may alleviate symptoms, but does not decrease overall mortality.
Experimental treatments include:
*Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.
*The herbal extract tetrandine may slow progression of silicosis.
Joining a support group where you can meet other people with silicosis or related diseases can help you understand your disease and adapt to its treatments.
The outcome varies depending on the amount of damage to the lungs.
The best way to prevent silicosis is to identify work-place activities that produce respirable crystalline silica dust and then to eliminate or control the dust (“primary prevention”). Water spray is often used where dust emanates. Dust can also be controlled through dry air filtering.
Following observations on industry workers in Lucknow (India), experiments on rats found that jaggery (a traditional sugar) had a preventive action against silicosis.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
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