Silicosis (also known as phthisis miners , asthma grinder , destructive pottery and other work related names, or by name found pneumonoultramicroscopicsilicovolcanoconiosis ) is a form of occupational lung disease caused by the inhalation of crystalline silica dust, and is characterized by inflammation and scarring in the form of a nodular lesion in the upper lobe of the lung. This is a type of pneumoconiosis.
Silicosis (especially the acute form) is characterized by shortness of breath, cough, fever, and cyanosis (bluish skin). It may often be misdiagnosed as pulmonary edema (fluid in the lungs), pneumonia, or tuberculosis.
Silicosis resulted in 46,000 global deaths in 2013 down from 55,000 deaths in 1990.
The name silicosis (from Latin silex , or flint) was originally used in 1870 by Achille Visconti (1836-1911), prosecutor at Ospedale Maggiore Milan. The introduction of respiratory problems from breathing in the dust comes from ancient Greece and Rome. Agricola, in the mid-16th century, wrote about the lung problem from inhalation of dust in miners. In 1713, Bernardino Ramazzini recorded symptoms of asthma and sand-like substances in the lung cutters. With industrialization, instead of hand tools, comes an increased production of dust. Pneumatic hammer drill was introduced in 1897 and sandblasting was introduced in about 1904, both of which significantly contributed to the increased prevalence of silicosis.
Video Silicosis
Classification
The classification of silicosis is performed according to the severity of the disease (including the radiographic pattern), onset, and rate of progression. These include:
- Chronic simple silicosis
- Usually generated from long-term exposure (10 years or more) to relatively low concentrations of silica dust and usually appear 10-30 years after the first exposure. This is the most common type of silicosis. Patients with this type of silicosis, especially early on, may have no obvious signs or symptoms of the disease, but the abnormality may be detected by x-rays. Chronic cough and dyspnea during activity (shortness of breath) is a common finding. Radiographically, chronic sympathetic silicosis indicates a small (& lt; 10 mm) turbidity, usually rounded, and dominates in the upper lung zone.
- accelerated silicosis
- Silicosis develops 5-10 years after the first exposure to a higher concentration of silica dust. The symptoms and findings of x-rays are similar to those of chronic simple silicosis, but occur early and tend to develop more rapidly. Patients with accelerated silicosis have a greater risk for complicated diseases, including progressive massive fibrosis (PMF).
- Complicated silicosis
- Silicosis can be "complicated" by severe scar tissue development (progressive massive fibrosis, also known as silicosis conglomerate), where small nodules gradually become confluent, reaching a size of 1 cm or more. PMF is associated with more severe symptoms and respiratory problems than simple diseases. Silicosis can also be complicated by other lung diseases, such as tuberculosis, non-TB mycobacterial infections, and fungal infections, certain autoimmune diseases, and lung cancer. Complicated silicosis is more common in accelerated silicosis than with chronic variation.
- Acute silicosis
- Silicosis develops weeks to 5 years after exposure to high concentrations of inhaled silica dust. This is also known as silicoproteinosis. The symptoms of acute silicosis include a faster onset of severe respiratory distress, cough, weakness, and weight loss, often leading to death. X-rays usually reveal diffuse alveolar filling with an air bronchogram, described as a soil-glass view, and similar to pneumonia, pulmonary edema, alveolar bleeding, and alveolar cell lung cancer.
Maps Silicosis
Signs and symptoms
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) is exacerbated by exertion
- Cough, often persistent and sometimes severe
- Fatigue
- Tachypnoea (quickness of breath) that often works,
- Loss of appetite and weight loss
- Chest pain
- Fever
- The skin becomes dark gradually (blue skin)
- The gradual dark shallow cracks in the nails eventually lead to cracks because the protein fibers inside the nail lining are destroyed.
In advanced cases, the following may also occur:
- Cyanosis, pale along the top of the body (blue skin)
- Cor pulmonale (right ventricular heart disease)
- Respiratory insufficiency
Patients with silicosis are particularly susceptible to tuberculosis (TB) infection - known as silicotuberculosis. The reason for the increased risk - a 3-fold increase in incidence - is not well understood. It is thought that silica damages pulmonary macrophages, inhibiting their ability to kill mycobacteria. Even workers with prolonged exposure to silica, but without silicosis, have the same increased risk of TB.
Pulmonary complications of silicosis also include Chronic Bronchitis and airflow limitations (indistinguishable from those caused by smoking), non-tuberculous Mycobacterium infections, fungal lung infections, emphysema compensation, and pneumothorax. There are some data that reveal the relationship between silicosis and certain autoimmune diseases, including nephritis, scleroderma, and systemic lupus erythematosus, particularly in acute or accelerated silicosis.
In 1996, the International Agency for Research on Cancer (IARC) reviewed medical data and classified crystalline silica as "carcinogenic in humans." The risk is best seen in cases with underlying silicosis, with a relative risk for lung cancer 2-4. A number of further studies have been published that justify this risk. In 2006, Pelucchi et al. concluded, "The silicosis-cancer association is now established, according to other studies and meta-analysis."
Pathophysiology
When tiny silica dust particles are inhaled, they can deepen into small alveolar sacs and channels in the lungs, where oxygen and carbon dioxide gas are exchanged. There, the lungs can not clean the dust with mucus or cough.
When fine particles of crystalline silica dust are deposited in the lungs, macrophages that ingest dust particles will trigger an inflammatory response by releasing tumor necrosis factor, interleukin-1, leukotriene B4 and other cytokines. In turn, it stimulates fibroblasts to proliferate and produces collagen around the silica particles, resulting in fibrosis and the formation of nodular lesions. The inflammatory effect of crystalline silica appears to be mediated by NALP3 inflammation.
The characteristic lung tissue pathology of nodular silicosis comprises fibrotic nodules with fibrous "fibers" fibers arranged with collagen fibers, central hybridization, and peripheral zone cells, with light birefringent particles visible under polarized light. Silicotic nodules represent specific tissue responses to crystalline silica. In acute silicosis, microscopic pathology shows a positive alveolar exudate of Schiff-acid (alveolar lipoproteinosis) and cellular infiltration in alveolar walls.
Silica
Silicon (Si) is the second most common element in the Earth's crust (oxygen is the most common). The silica compound, also known as silicon dioxide (SiO 2 ), is made up of silicon and oxygen atoms. Because oxygen and silicon make up about 75% of the Earth's crust, silica compounds are very common. These are found in many stones, such as granite, sandstone, gneiss and slate, and in some metal ores. Silica can be a major component of sand. Can also be on the ground, mortar, plaster, and shingles. Drilling, cutting, crushing, drilling, milling, or abrasive blasting of these materials can produce ultra fine dust in very fine air.
Silica occurs in 3 forms: crystalline, microcrystalline (or cryptocrystalline) and amorphous (non-crystalline). The "Free" silica consists of pure silicon dioxide, not combined with other elements, while silicates (eg, talc, asbestos, and mica) are SiO 2 in combination with a considerable cation section.
- Silica crystal exists in 7 different shapes (polymorph), depending on the forming temperature. The 3 major polymorphs are quartz, cristobalite, and tridymite. Quartz is the second most common mineral in the world (in addition to feldspar).
- Microcrystalline silica consists of minute quartz crystals bonded together with amorphous silica. Examples include flint and rhizome.
- Amorphous silica consists of kieselgur (diatomite), from a diatomic framework, and vitreous silica, produced by heating and then rapid cooling of crystalline silica. Amorphous silica is less toxic than crystalline, but not biologically inert, and diatomite, when heated, can be transformed into tridymite or cristobalite.
The pure silica flour is almost pure SiO 2 finely ground. Silica flour has been used as a polisher or buffer, as well as paint extenders, abrasives, and fillers for cosmetics. Silica flour has been associated with all types of silicosis, including acute silicosis.
Silicosis is due to the settling of fine inhaled dust (less than 10 micrometers in diameter) containing crystalline silicon dioxide in the form of alpha-quartz, cristobalite, or tridymite.
Diagnosis
There are three key elements for the diagnosis of silicosis. First, the patient's history should reveal sufficient exposure to silica dust to cause the disease. Second, chest imaging (usually chest X-rays) that reveal findings consistent with silicosis. Thirdly, no underlying disease is more likely to cause abnormalities. Physical examination is usually mediocre unless there is a complicated disease. Also, the examination findings are not specific to silicosis. Pulmonary function tests may reveal airflow limitations, 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, especially to exclude other conditions.
For uncomplicated silicosis, chest x-rays will confirm the presence of small ( lt; 10 mm) nodules in the lungs, especially in the upper lung zone. Using the ILO classification system, this is profusion 1/0 or greater and the shape/size "p", "q", or "r". The participation and improvement of the lung zones increases with the progression of the disease. In advanced cases of silicosis, large opacities (& 1 cm) occur from a small turbidity blend, especially in the upper lung zone. With lung tissue retraction, there is emphysema compensation. Hilar enlargement is common in chronic silicosis and acceleration. In about 5-10% of cases, the nodes will harden in a circle, resulting in calcification of "eggshells". This finding is not pathognomonic (diagnostic) of silicosis. In some cases, pulmonary nodules may also be calcified.
Computed tomography or CT scan can also provide a detailed lung analysis mode, and may reveal cavitation due to concurrent mycobacterial infection.
Prevention
The best way to prevent silicosis is to identify workplace activity that produces inhalable crystalline silica dust and then to remove or control dust ("primary prevention"). Water spray is often used where the dust radiates. Dust can also be controlled through dry air filtration.
After an observation of industrial workers in Lucknow (India), experiments in mice found that jaggery (traditional sugar) had precautions against silicosis.
Treatment
Silicosis is a permanent disease without drugs. Treatment options currently available focus on reducing symptoms and prevent further progression of the condition. These include:
- Stopping further exposure to air silica, silica dust and other lung irritations, including tobacco smoking.
- Cough suppressant.
- Antibiotics for bacterial lung infections.
- Prophylactic tuberculosis (TB) 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 drain mucus bronchi.
- Giving of oxygen to treat hypoxemia, if present.
- Bronchodilator to facilitate breathing.
- Lung transplantation to replace damaged lung tissue is the most effective treatment, but is associated with a severe risk of lung transplant surgery as well as the long-term consequences of immunosuppression (eg, opportunistic infections).
- For acute silicosis, bronchoalveolar lavage may relieve symptoms, but does not reduce overall mortality.
Experimental treatments include:
- Inhalation of aluminum powder, d-penicillamine and polyvinyl pyridine-N-oxide.
- Corticosteroid therapy.
- Kombucha Chinese Herbs
- Tetrandrine herbal extract can slow the progression of silicosis. Epidemiology
- Reduce the permitted exposure limit (PEL) for the inhaled crystal silica to 50 micrograms per cubic meter of air, averaged over an 8 hour shift.
- Use technical controls (such as water or ventilation) to limit worker exposure to LED; provide respirators when technical controls can not limit exposure adequately; restrict workers' access to high exposure areas; develop a written exposure control plan, offer medical examinations to highly exposed workers, and train workers about the risk of silica and how to limit exposure.
- Provide a medical examination to monitor highly exposed workers and provide them with information about their lung health.
- Provide flexibility to help entrepreneurs - especially small businesses - protect workers from exposure to silica.
- Construction - June 23, 2017, one year after the effective date.
- General and Maritime Industry - June 23, 2018, two years after the effective date.
- Hydraulic Fracture - June 23, 2018, two years after the date of validity for all conditions except for Engineering Controls, which have compliance dates June 23, 2021.
- Pneumoconiosis
- Asbestosis
- Chronic obstructive pulmonary disease (COPD)
- Volcanic ash (health effects) - Although there are no documented cases of silicosis developed from exposure to volcanic ash (due to the relatively short period of time it remains in the air), it is theoretically possible.
- Philip D'Arcy Hart
- Hawks Nest Tunnel Nest
- John Scott Haldane
- Fortress
- Dust Pneumonia
- Pneumonoultramicroscopicsilicovolcanoconiosis - a synonym found for silicosis "found to mimic the polysllabic medical term"
- Imaging Findings in Silicosis by Daniel Powers, MD www.breader.com
- Estimated risk for silicosis: comparison of animal and human studies by CL Tran, BG Miller and CA Soutar. Research Report of Vocational Research Institute TM/05/02
Silicosis resulted in 46,000 deaths in 2013 dropped from 55,000 deaths in 1990.
Silicone occupation
Silicosis is the most common lung disease worldwide; it is happening everywhere, but it is very common in developing countries. From 1991 to 1995, China reported more than 24,000 deaths due to silicosis each year. In the United States, it is estimated that between one and two million workers exposed to the work of crystalline silica dust and 59,000 workers will develop silicosis at some time in their lives.
According to CDC data, silicosis in the United States is relatively rare. The incidence of silicosis deaths decreased 84% between 1968 and 1999, and only 187 deaths in 1999 had silicosis as an underlying or contributing cause. In addition, silicosis cases in Michigan, New Jersey, and Ohio are highly correlated with industry and employment.
Although silicosis has been known for centuries, industrialization of mining has led to an increase in cases of silicosis. Pneumatic drilling in the mine and less commonly, mining using explosives, will increase fine fine crystalline silica dust (stone dust). In the United States, the silicosis epidemic of 1930 due to the construction of the Hawk Nest Tunnel near Gauley Bridge, West Virginia caused the death of at least 400 workers. Other accounts place the death toll in more than 1000 workers, mainly temporary African American workers from the southern United States. Workers who get sick are fired and leave the area, making the right death account difficult. The Hawks Nest Tunnel Disaster is known as "the worst industrial disaster in America." The prevalence of silicosis causes some people to grow what are called miners whiskers, in an attempt to cut as much dust as possible.
Chronic simple silicosis has been reported to occur from environmental exposure to silica in areas with high silica soils and frequent dust storms.
Also, mining mining of the Delamar Ghost Town, Nevada is destroyed by a dry mining process that produces silicosis-causing dust. After hundreds of deaths due to silicosis, the city was nicknamed The Widowmaker . The problem at that time was somewhat resolved by the addition of a nozzle to a drill that sprayed water mist, converting dust generated by drilling mud, but this inhibited mining work.
Due to occupational exposure to silica dust, silicosis is a work hazard to mining, sandblasting, quarry, ceramics and foundry workers, as well as grinders, stone cutters, stone countertops, firework workers, gravestone workers, workers in oil and industrial gases, , manufacturing fiberglass, glass manufacturing, flint knappers and others. Short or casual exposure to low levels of crystalline silica dust is said to produce no clinically significant lung disease.
Protection measures such as respirators have brought a steady decline in mortality due to silicosis in Western countries. However, this is not true for less developed countries where poor working conditions and respiratory equipment are rarely used. For example, life expectancy for silver miners in PotosÃÆ', Bolivia is about 40 years due to silicosis.
Recently, silicosis in Turkish denim sandblaster was detected as a new cause of silicosis due to repetitive and poor working conditions.
Silicosis is seen in horses associated with inhaling dust from certain cristobalite-containing soils in California.
Social realist artist Noel Counihan describes people who worked in industrial mines in Australia in the 1940s who died of silicosis in their six-mold series, 'Miners' (1947 linocuts).
Desert Lung Disease
Non-working silicosis forms have been described that are caused by long-term exposure to sand dust in desert areas, with cases reported from Sahara, Libyan desert and Negev. The disease is caused by the deposition of this dust in the lungs. Lost desert disease may be associated with Al Eskan disease, a lung disorder thought to be caused by exposure to sand dust containing organic antigens, first diagnosed after the 1990 Gulf war. The relative importance of the silica particles themselves and the microorganisms they carry in the effects health is still unclear.
Rule
In March 2016, OSHA officially mandated that the company should provide certain security measures for employees working with or around silica, to prevent silicosis, lung cancer, and other silica related diseases.
Main Provisions
Compliance Schedule
The two standards contained in the final rule take effect on June 23, 2016, after which industries have one to five years to meet most requirements, based on the following schedule:
See also
References
External links
Source of the article : Wikipedia
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