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Coal workers' pneumoconiosis, in its most severe state, develops after the initial, milder form of the disease known as '''anthracosis''' (''anthrac'' - coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers<ref name="robspath">{{cite book | title=Robbins Pathologic Basis of Disease| last=Cotran| coauthors=Kumar, Collins| publisher=W.B Saunders Company| location=Philadelphia| id=0-7216-7335-X}}</ref> due to air pollution. Prolonged exposure to large amounts of carbon dust can result in more serious forms of the disease, ''simple coal workers' ]'' and ''complicated coal workers' ]''. Coal workers' pneumoconiosis, in its most severe state, develops after the initial, milder form of the disease known as '''anthracosis''' (''anthrac'' - coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers<ref name="robspath">{{cite book | title=Robbins Pathologic Basis of Disease| last=Cotran| coauthors=Kumar, Collins| publisher=W.B Saunders Company| location=Philadelphia| id=0-7216-7335-X}}</ref> due to air pollution. Prolonged exposure to large amounts of carbon dust can result in more serious forms of the disease, ''simple coal workers' ]'' and ''complicated coal workers' ]''.

==History and prevention efforts==
There are currently about 42,000 underground coal miners actively working in the United States. The mining and production of coal is a major part of the economy in several developed countries. In the past 10 years, over 10,000 American miners have died from CWP. Although this disease is preventable, many miners are still developing advanced and severe cases.

In the 25 years since the Federal Coal Mine Health and Safety Act of 1969 became law, the proportion of miners with black lung disease has gone down by about 90%. But the downward trend of this disease in coal miners has stopped. Rates of black lung are on the rise and have almost doubled in the last 10 years. From 2000 to 2004, over 4,000 miners died from black lung disease in the United States.

The National Institute for Occupational Safety and Health (NIOSH), with support of the Mine Safety and Health Administration (MSHA), has started a Mobile Health Screening Program. This Mobile Unit travels to mining regions around the United States. Miners who participate in the Program receive health evaluations once every five years, at no cost to themselves. Chest x-rays can detect the early signs of and changes in CWP, often before the miner is aware of any lung problems. The screening program is only available to current miners.<ref>{{cite web | title = Enhanced Coal Workers' Health Surveillance Program | publisher = National Institute for Occupational Safety and Health | date = November 12, 2008 | url = http://www.cdc.gov/niosh/topics/surveillance/ORDS/ecwhsp.html | accessdate = November 24, 2008}}</ref>

== Pathogenesis ==
Coal dust that enters the lungs can neither be destroyed nor removed by the body. The particles are engulfed by resident alveolar or interstitial ]s and remain in the lungs, residing in the connective tissue or pulmonary ]s. Aggregations of carbon-laden macrophages can be visualised under a microscope as granular, black areas. In serious cases, the lung may grossly appear black. These aggregations can cause inflammation and fibrosis, as well as the formation of nodular ]s within the lungs. The centres of dense lesions may become necrotic due to ], leading to large cavities within the lung

== Appearance ==
<!-- Image with unknown copyright status removed: ] -->
Simple CWP is marked by the presence of 1-2mm nodular aggregations of anthracotic macrophages, supported by a fine collagen network, within the lungs. Those 1-2mm in diameter are known as ''coal macules'', with larger aggregations known as ''coal nodules''. These structures occur most frequently around the initial site of coal dust accumulation - the upper regions of the lungs around ]s<ref name="robspath">{{cite book | title=Robbins Pathologic Basis of Disease| last=Cotran| coauthors=Kumar, Collins| publisher=W.B Saunders Company| location=Philadelphia| id=0-7216-7335-X}}</ref>.

Continued exposure to coal dust following the development of simple CWP may result in its progression to complicated CWP, which generally requires a number of years to develop. Large, black, fibrotic scars 2-10cm in diameter are present, with accompanying decreased lung function. The lung itself appears blackened. A minority of these cases progresses to ] (PMF), the most serious form of CWP.

== Symptoms ==
Both CWP and mild complicated CWP are often unsymptomatic or only affect lung function slightly. Shortness of breath and pain may be felt. However, progression to PMF is marked by lung dysfunction, ], and ].

== See also ==
* ]

==Additional resources==
*
* video
*
*
*
*
*
*
*
* The Courier-Journal (Louisville, Ky):

== References ==
{{reflist|1}}

<br>{{Respiratory pathology}}

]


]
]
]


==History and prevention efforts== ==History and prevention efforts==

Revision as of 00:21, 12 December 2008

Medical condition
Black lung disease
SpecialtyPulmonology Edit this on Wikidata

Black lung disease, also known as coal workers' pneumoconiosis (CWP), is caused by long exposure to coal dust. It is a common affliction of coal miners and others who work with coal, similar to both silicosis from inhaling silica dust, and to the long term effects of tobacco smoking. Inhaled coal dust progressively builds up in the lungs and is unable to be removed by the body, leading to inflammation, fibrosis, and in the worst case necrosis.

Coal workers' pneumoconiosis, in its most severe state, develops after the initial, milder form of the disease known as anthracosis (anthrac - coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers due to air pollution. Prolonged exposure to large amounts of carbon dust can result in more serious forms of the disease, simple coal workers' pneumoconiosis and complicated coal workers' pneumoconiosis.

History and prevention efforts

There are currently about 42,000 underground coal miners actively working in the United States. The mining and production of coal is a major part of the economy in several developed countries. In the past 10 years, over 10,000 American miners have died from CWP. Although this disease is preventable, many miners are still developing advanced and severe cases.

In the 25 years since the Federal Coal Mine Health and Safety Act of 1969 became law, the proportion of miners with black lung disease has gone down by about 90%. But the downward trend of this disease in coal miners has stopped. Rates of black lung are on the rise and have almost doubled in the last 10 years. From 2000 to 2004, over 4,000 miners died from black lung disease in the United States.

The National Institute for Occupational Safety and Health (NIOSH), with support of the Mine Safety and Health Administration (MSHA), has started a Mobile Health Screening Program. This Mobile Unit travels to mining regions around the United States. Miners who participate in the Program receive health evaluations once every five years, at no cost to themselves. Chest x-rays can detect the early signs of and changes in CWP, often before the miner is aware of any lung problems. The screening program is only available to current miners.

Pathogenesis

Coal dust that enters the lungs can neither be destroyed nor removed by the body. The particles are engulfed by resident alveolar or interstitial macrophages and remain in the lungs, residing in the connective tissue or pulmonary lymph nodes. Aggregations of carbon-laden macrophages can be visualised under a microscope as granular, black areas. In serious cases, the lung may grossly appear black. These aggregations can cause inflammation and fibrosis, as well as the formation of nodular lesions within the lungs. The centres of dense lesions may become necrotic due to ischaemia, leading to large cavities within the lung

Appearance

Simple CWP is marked by the presence of 1-2mm nodular aggregations of anthracotic macrophages, supported by a fine collagen network, within the lungs. Those 1-2mm in diameter are known as coal macules, with larger aggregations known as coal nodules. These structures occur most frequently around the initial site of coal dust accumulation - the upper regions of the lungs around respiratory bronchioles.

Continued exposure to coal dust following the development of simple CWP may result in its progression to complicated CWP, which generally requires a number of years to develop. Large, black, fibrotic scars 2-10cm in diameter are present, with accompanying decreased lung function. The lung itself appears blackened. A minority of these cases progresses to progressive massive fibrosis (PMF), the most serious form of CWP.

Symptoms

Both CWP and mild complicated CWP are often unsymptomatic or only affect lung function slightly. Shortness of breath and pain may be felt. However, progression to PMF is marked by lung dysfunction, pulmonary hypertension, and cor pulmonale.

See also

Additional resources

References

  1. ^ Cotran. Robbins Pathologic Basis of Disease. Philadelphia: W.B Saunders Company. 0-7216-7335-X. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  2. "Enhanced Coal Workers' Health Surveillance Program". National Institute for Occupational Safety and Health. November 12, 2008. Retrieved November 24, 2008.


Diseases of the respiratory system
Upper RT
(including URTIs,
common cold)
Head
sinuses
Sinusitis
nose
Rhinitis
Vasomotor rhinitis
Atrophic rhinitis
Hay fever
Nasal polyp
Rhinorrhea
nasal septum
Nasal septum deviation
Nasal septum perforation
Nasal septal hematoma
tonsil
Tonsillitis
Adenoid hypertrophy
Peritonsillar abscess
Neck
pharynx
Pharyngitis
Strep throat
Laryngopharyngeal reflux (LPR)
Retropharyngeal abscess
larynx
Croup
Laryngomalacia
Laryngeal cyst
Laryngitis
Laryngopharyngeal reflux (LPR)
Laryngospasm
vocal cords
Laryngopharyngeal reflux (LPR)
Vocal fold nodule
Vocal fold paresis
Vocal cord dysfunction
epiglottis
Epiglottitis
trachea
Tracheitis
Laryngotracheal stenosis
Lower RT/
lung disease
(including LRTIs)
Bronchial/
obstructive
acute
Acute bronchitis
chronic
COPD
Chronic bronchitis
Acute exacerbation of COPD)
Asthma (Status asthmaticus
AERD
Exercise-induced
Bronchiectasis
Cystic fibrosis
unspecified
Bronchitis
Bronchiolitis
Bronchiolitis obliterans
Diffuse panbronchiolitis
Interstitial/
restrictive
(fibrosis)
External agents/
occupational
lung disease
Pneumoconiosis
Aluminosis
Asbestosis
Baritosis
Bauxite fibrosis
Berylliosis
Caplan's syndrome
Chalicosis
Coalworker's pneumoconiosis
Siderosis
Silicosis
Talcosis
Byssinosis
Hypersensitivity pneumonitis
Bagassosis
Bird fancier's lung
Farmer's lung
Lycoperdonosis
Other
Obstructive /
Restrictive
Pneumonia/
pneumonitis
By pathogen
By vector/route
By distribution
IIP
Other
Pleural cavity/
mediastinum
Pleural disease
Pleural effusion
Hemothorax
Hydrothorax
Chylothorax
Empyema/pyothorax
Malignant
Fibrothorax
Mediastinal disease
Other/general

History and prevention efforts

There are currently about 42,000 underground coal miners actively working in the United States. The mining and production of coal is a major part of the economy in several developed countries. In the past 10 years, over 10,000 American miners have died from CWP. Although this disease is preventable, many miners are still developing advanced and severe cases.

In the 25 years since the Federal Coal Mine Health and Safety Act of 1969 became law, the proportion of miners with black lung disease has gone down by about 90%. But the downward trend of this disease in coal miners has stopped. Rates of black lung are on the rise and have almost doubled in the last 10 years. From 2000 to 2004, over 4,000 miners died from black lung disease in the United States.

The National Institute for Occupational Safety and Health (NIOSH), with support of the Mine Safety and Health Administration (MSHA), has started a Mobile Health Screening Program. This Mobile Unit travels to mining regions around the United States. Miners who participate in the Program receive health evaluations once every five years, at no cost to themselves. Chest x-rays can detect the early signs of and changes in CWP, often before the miner is aware of any lung problems. The screening program is only available to current miners.

Pathogenesis

Coal dust that enters the lungs can neither be destroyed nor removed by the body. The particles are engulfed by resident alveolar or interstitial macrophages and remain in the lungs, residing in the connective tissue or pulmonary lymph nodes. Aggregations of carbon-laden macrophages can be visualised under a microscope as granular, black areas. In serious cases, the lung may grossly appear black. These aggregations can cause inflammation and fibrosis, as well as the formation of nodular lesions within the lungs. The centres of dense lesions may become necrotic due to ischaemia, leading to large cavities within the lung

Appearance

Simple CWP is marked by the presence of 1-2mm nodular aggregations of anthracotic macrophages, supported by a fine collagen network, within the lungs. Those 1-2mm in diameter are known as coal macules, with larger aggregations known as coal nodules. These structures occur most frequently around the initial site of coal dust accumulation - the upper regions of the lungs around respiratory bronchioles.

Continued exposure to coal dust following the development of simple CWP may result in its progression to complicated CWP, which generally requires a number of years to develop. Large, black, fibrotic scars 2-10cm in diameter are present, with accompanying decreased lung function. The lung itself appears blackened. A minority of these cases progresses to progressive massive fibrosis (PMF), the most serious form of CWP.

Symptoms

Both CWP and mild complicated CWP are often unsymptomatic or only affect lung function slightly. Shortness of breath and pain may be felt. However, progression to PMF is marked by lung dysfunction, pulmonary hypertension, and cor pulmonale.

See also

Additional resources

References

  1. "Enhanced Coal Workers' Health Surveillance Program". National Institute for Occupational Safety and Health. November 12, 2008. Retrieved November 24, 2008.
  2. Cotran. Robbins Pathologic Basis of Disease. Philadelphia: W.B Saunders Company. 0-7216-7335-X. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)


Diseases of the respiratory system
Upper RT
(including URTIs,
common cold)
Head
sinuses
Sinusitis
nose
Rhinitis
Vasomotor rhinitis
Atrophic rhinitis
Hay fever
Nasal polyp
Rhinorrhea
nasal septum
Nasal septum deviation
Nasal septum perforation
Nasal septal hematoma
tonsil
Tonsillitis
Adenoid hypertrophy
Peritonsillar abscess
Neck
pharynx
Pharyngitis
Strep throat
Laryngopharyngeal reflux (LPR)
Retropharyngeal abscess
larynx
Croup
Laryngomalacia
Laryngeal cyst
Laryngitis
Laryngopharyngeal reflux (LPR)
Laryngospasm
vocal cords
Laryngopharyngeal reflux (LPR)
Vocal fold nodule
Vocal fold paresis
Vocal cord dysfunction
epiglottis
Epiglottitis
trachea
Tracheitis
Laryngotracheal stenosis
Lower RT/
lung disease
(including LRTIs)
Bronchial/
obstructive
acute
Acute bronchitis
chronic
COPD
Chronic bronchitis
Acute exacerbation of COPD)
Asthma (Status asthmaticus
AERD
Exercise-induced
Bronchiectasis
Cystic fibrosis
unspecified
Bronchitis
Bronchiolitis
Bronchiolitis obliterans
Diffuse panbronchiolitis
Interstitial/
restrictive
(fibrosis)
External agents/
occupational
lung disease
Pneumoconiosis
Aluminosis
Asbestosis
Baritosis
Bauxite fibrosis
Berylliosis
Caplan's syndrome
Chalicosis
Coalworker's pneumoconiosis
Siderosis
Silicosis
Talcosis
Byssinosis
Hypersensitivity pneumonitis
Bagassosis
Bird fancier's lung
Farmer's lung
Lycoperdonosis
Other
Obstructive /
Restrictive
Pneumonia/
pneumonitis
By pathogen
By vector/route
By distribution
IIP
Other
Pleural cavity/
mediastinum
Pleural disease
Pleural effusion
Hemothorax
Hydrothorax
Chylothorax
Empyema/pyothorax
Malignant
Fibrothorax
Mediastinal disease
Other/general
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