Coal Worker’s Pneumoconiosis (CWP) was thought to be an archaic
disease, but after an initial decline because of the Coal Mine Health and Safety Act in
1969, there has been a resurgence of this disease in the 21st century. For centuries,
miners have been exposed to varied types and degrees of coal mine dust. Lung diseases
in coal miners are caused by the inhalation, retention, and tissue reaction to the mixed
constituents of this dust, which include carbon, silica, and silicates. Respirable dust
particles of less than 5 microns are deposited in the proximal and distal airways and the
smaller particles are deposited in the alveoli. The tissue reaction to these particles
results in a variety of pathologic lesions, including coal macules, silicotic nodules,
mixed dust pneumoconiosis, interstitial fibrosis, progressive massive fibrosis,
bronchitis, and emphysema. These disorders are recognized primarily through
occupational exposure history and characteristic radiographic imaging. With a latency
of approximately 20 years, cumulative lifetime exposures appear to be most predictive
of the disease severity. Prevention of these diseases should be the primary focus of the
industry, the workforce, and the public health agencies. In the US, federal programs of
screening and surveillance are in place and active. The treatment of these disorders as
with other chronic respiratory conditions, is focused on vaccinations against respiratory
infection, bronchodilator therapy when indicated, supplemental oxygen therapy when
required, pulmonary rehabilitation programs, smoking cessation, vigilant observation
for chronic respiratory infections, and if necessary, lung transplantation should be
considered as the last resort.
Keywords: Antifibrotics, Black Lung, CMDLD, CWP, ILO, Lung transplantation, NIOSH, PMF, Pneumoconiosis, Prevention, Pulmonary rehabilitation, Resurgence, Sea coal, Vaccinations.
