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Coal Miners' Lung Disease Guide

Coal worker's pneumoconiosis, also known as black lung disease, is caused by long-term exposure to coal dust in occupations like coal mining. Prolonged exposure can lead to simple coal worker's pneumoconiosis and complicated coal worker's pneumoconiosis, characterized by large dense lesions in the lungs. The disease is diagnosed based on a history of coal dust exposure, chest radiography findings, and ruling out other potential causes. Treatment focuses on restricting further exposure and managing symptoms, while prevention emphasizes eliminating dust exposure and vaccination.

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0% found this document useful (0 votes)
219 views4 pages

Coal Miners' Lung Disease Guide

Coal worker's pneumoconiosis, also known as black lung disease, is caused by long-term exposure to coal dust in occupations like coal mining. Prolonged exposure can lead to simple coal worker's pneumoconiosis and complicated coal worker's pneumoconiosis, characterized by large dense lesions in the lungs. The disease is diagnosed based on a history of coal dust exposure, chest radiography findings, and ruling out other potential causes. Treatment focuses on restricting further exposure and managing symptoms, while prevention emphasizes eliminating dust exposure and vaccination.

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viren thakkar
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Coal worker’s pneumoconiosis

Coal workers' pneumoconiosis (CWP), colloquially


referred to as black lung disease, 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.
Coal workers' pneumoconiosis, 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 coal
dust can result in more serious forms of the disease, simple
coal workers' pneumoconiosis and complicated coal
workers' pneumoconiosis (or Progressive massive
fibrosis, or PMF).

Pathogenesis
Coal dust is not as fibrogenic as is silica dust. 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. Coal dust provides a sufficient stimulus for
the macrophage to release various products, including
enzymes, cytokines, oxygen radicals, and fibroblast growth

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factors, which are important in the inflammation and
fibrosis of CWP. 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 ischemia, 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. The coal macule is the
basic pathological feature of CWP, and has a surrounding
area of enlargement of the airspace, known as focal
emphysema.
Continued exposure to coal dust following the
development of simple CWP may progress to complicated
CWP with progressive massive fibrosis (PMF), wherein
large masses of dense fibrosis develop, usually in the
upper lung zones, measuring greater than 1 cm in
diameter, with accompanying decreased lung function.
These cases generally require a number of years to develop.
Grossly, the lung itself appears blackened. Pathologically,

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these consist of fibrosis with haphazardly-arranged
collagen and many pigment-laden macrophages and
abundant free pigment. Radiographically, CWP can
appear strikingly similar to silicosis. In simple CWP,
small rounded nodules (see ILO Classification)
predominate, tending to first appear in the upper lung
zones. The nodules may coalesce and form large opacities
(>1 cm), characterizing complicated CWP, or PMF.
Diagnosis
There are three basic criteria for the diagnosis of CWP:
1. Chest radiography consistent with CWP
2. An exposure history to coal dust (typically
underground coal mining) of sufficient amount and
latency
3. Exclusion of alternative diagnoses (mimics of CWP)
Symptoms and pulmonary function testing relate to the
degree of respiratory impairment, but are not part of the
diagnostic criteria. As noted above, the chest X-ray
appearance for CWP can be virtually indistinguishable
from silicosis. Chest CT, particularly high-resolution
scanning (HRCT), are more sensitive than plain X-ray for
detecting the small round opacities.
Treatment
 Sometimes supplemental oxygen and pulmonary

rehabilitation
 Restriction from further exposure

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Treatment is rarely necessary in simple CWP,
although smoking cessation and TB surveillance are
recommended. Patients with pulmonary hypertension,
hypoxemia, or both are given supplemental oxygen
therapy.
Pulmonary rehabilitation can help more severely affected
workers carry out activities of daily living. Workers with
CWP, especially those with PMF, should be restricted
from further exposure, especially to high concentrations
of dust. TB is treated in accordance with current
recommendations.
Prevention
Preventive measures include eliminating exposure,
stopping smoking, and giving pneumococcal and
influenza vaccinations. CWP can be prevented by
suppressing coal dust at the coal face. Despite long-
standing regulations, exposures continue to occur in the
mining trade, resulting in increased rates of disease,
including severe forms.
Respiratory masks provide only limited protection.

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