pneumoconiosis

pneumoconiosis
/nooh'meuh koh'nee oh"sis, nyooh'-/, n. Pathol.
any chronic lung disease, including anthracosis, asbestosis, and silicosis, caused by the inhalation of particles of coal, asbestos, silica, or similar substances and leading to fibrosis and loss of lung function.
[1880-85; syncopated var. of PNEUMONOCONIOSIS]

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Any lung disease caused by inhalation of organic or inorganic dusts or chemical irritants, usually over time.

Some dusts (e.g., silica minerals, asbestos) produce grave reactions in small quantities. Dust collects in the pulmonary alveoli, causing inflammation that scars lung tissue, reducing its elasticity. Chest tightness and shortness of breath may progress to chronic bronchitis and emphysema. Cigarette smoking worsens many types. The most common cause of severe disease is silica (see silicosis). Asbestos (see asbestosis), beryllium, and aluminum dusts can cause worse disease, often on brief exposure. Organic causes include mold spores (see allergy) and textile fibres. Chemical irritants such as ammonia, acid, and sulfur dioxide are soon absorbed by the lung lining; their irritant effect can cause pulmonary edema, and they can lead to chronic bronchitis.

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      any of many lung diseases caused by the inhalation of a variety of organic or inorganic dusts or chemical irritants, usually over a prolonged period of time. The type and severity of disease depends on the composition of the dust; small quantities of some substances, notably silica and asbestos, produce grave reactions, while milder irritants produce symptoms of lung disease only with massive exposure. Much evidence indicates that the smoking of cigarettes in particular aggravates the symptoms of many of the pneumoconiosis diseases.

      Typically, the early symptoms of mild pneumoconioses include chest tightness, shortness of breath, and cough, progressing to more serious breathing impairment, chronic bronchitis, and emphysema in the most severe cases. Inhaled dust collects in the alveoli, or air sacs, of the lung, causing an inflammatory reaction that converts normal lung tissue to fibrous scar tissue and thus reduces the elasticity of the lung. If enough scar tissue forms, lung function is seriously impaired, and the clinical symptoms of pneumoconiosis are manifested. The total dust load in the lung, the toxic effects of certain types of dust, and infections of the already damaged lung can accelerate the disease process.

      Among inorganic dusts, silica, encountered in numerous occupations including mining, quarrying, sand blasting, and pottery making, is the most common cause of severe pneumoconiosis. As little as 5 or 6 grams (about 0.2 ounce) in the lung can produce disease (see silicosis). Graphite, tin, barium, chromate, clay, iron, and coal dusts (see black lung) are other inorganic substances known to produce pneumoconiosis, although silica exposure is also involved in many cases. Pneumoconioses associated with these substances usually result only from continued exposure over long periods. asbestos (see asbestosis), beryllium (see berylliosis), and aluminum dusts can cause a more severe pneumoconiosis, often after relatively brief exposure to massive amounts of dust. Asbestosis has also been associated with cancers of the lung and other organs.

      Prolonged exposure to organic dusts such as spores of molds from hay, malt, sugarcane, mushrooms, and barley can produce lung disease through a severe allergic response within a few hours of exposure, even in previously nonallergic persons. Brown lung disease (see byssinosis) in textile workers is also a form of pneumoconiosis, caused by fibres of cotton, flax, or hemp that, when inhaled, stimulate histamine release. Histamines cause the air passages to constrict, impeding exhalation.

      Chemical (chemical industry) irritants that have been implicated in lung disease include sulfur dioxide, nitrogen dioxide, ammonia, acid, and chloride, which are quickly absorbed by the lining of the lungs. The chemicals themselves may scar the delicate lung tissues, and their irritant effect may cause large amounts of fluid to accumulate in the lungs. Once exposure to the chemical ceases, the patient may recover completely or may suffer from chronic bronchitis or asthma.

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Universalium. 2010.

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