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Silica dust a driving force behind rising rates of black lung, study suggests

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Chicago — The lung tissue of contemporary coal miners contains higher levels of respirable crystalline silica dust than was found in miners of past generations – which may explain an ongoing surge in cases of the most severe form of black lung disease, researchers at University of Illinois Chicago say.

Progressive massive fibrosis is caused by exposure to respirable coal mine dust. Workers can inhale silica dust while cutting, sawing, drilling or crushing materials such as rock and stone. OSHA estimates that 2.3 million workers are exposed to silica dust annually.

The researchers analyzed lung pathology specimens of 85 coal miners with the condition. They compared cases of those born in or after 1930 (contemporary group) with those born between 1910 and 1930 (historical group). They found a “significantly higher proportion” of silica-type progressive massive fibrosis among the contemporary miners compared with those in the historical group – 57% vs. 18%. Additionally, on average, the contemporary miners were younger at time of tissue collection (age 61 vs. 65) and had fewer years in underground mining (30 vs. 35 years).

UIC research released in May 2018 shows that more than 4,600 coal miners have developed severe black lung disease since 1970, with nearly half of the cases surfacing after 2000. The study cites previous research showing cases of black lung disease have tripled since 2005, while tenured miners in Kentucky, Virginia and West Virginia have experienced a tenfold increase in the condition.

“Historical miners worked mainly with conventional mining technology that relied on drilling and blasting, whereas contemporary miners spent at least a substantial portion of their mining tenure working with mechanized equipment which employ high-powered cutting heads to shear the coal from the mine face,” the study states.


Robert Cohen, lead study author and director of the UIC Mining Education and Research Center, said in a press release that the findings “provide the first direct evidence that silica is a causative agent” behind the rise in progressive massive fibrosis and “can be used to determine health-protective permissible exposure limits” for miners.

“We’ve known that silica is highly toxic and exposure contributes to coal workers’ pneumoconiosis, but we haven’t known why coal workers were suddenly experiencing more disease and more severe forms of it,” Cohen said. “Regulations have remained in place, minerals in the Earth have not changed and there is no evidence suggesting people have become more vulnerable to coal dust, so the rise in cases among young workers that started in the late ’90s was baffling.”

The study was published online in the journal Annals of the American Thoracic Society.

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