Despite being on the decline after the 1970s, the prevalence of black lung has been on the rise over the last 2 decades, and the federal government has issued a new rule on miners' safety. With changes in mining technology, miners can dig deeper, exposing them more to silica, which is highly toxic and is driving rising rates of black lung
Pneumoconiosis, which encompasses the family of interstitial lung diseases—those that cause progressive scarring of lung tissue and eventually a lack of oxygen in the blood—can result from an autoimmune condition. It can also develop after an individual has inhaled either organic or nonorganic compounds that include bird and animal droppings, cotton or other fibers, silica, asbestos, diacetyl, beryllium, and talc.
Common forms of pneumoconiosis are asbestosis, silicosis, mixed-dust pneumoconiosis, and byssinosis, and they all are considered occupational lung diseases. One of the most well-known types of pneumoconiosis and potentially the best-known occupational illness in the US—perhaps infamous—is coal workers’ pneumoconiosis, also known as miner’s lung and black lung disease.
As its eponymous name states, this subtype of pneumoconiosis results from inhalation of coal dust and is most often seen in coal miners.
It entails both inflammation and fibrosis of the lung tissue, and cases can be simple or complicated.
Described as far back as the 16th century as a blue-black marbling of the lung and in the 19th century as black pigmentation and darkening of the lungs, black lung disease is most often seen in miners of hard coal but can also be found among those who work in soft-coal or graphite mines.