A research team from the University of Illinois Chicago has linked silica exposure to recent high rates of severe cases of pneumoconiosis in coal workers.
What did scientists investigate throughout this study?
Silica exposure is currently behind the rising rates of cases of pneumoconiosis among coal workers, according to a new collaborative study published by occupational health experts at the University of Illinois Chicago.
This study is the first to compare the pathology and mineralogy of pneumoconiosis, which is commonly called black lung disease, across generations. It is also the first to offer scientific evidence explaining why progressive massive fibrosis, the most severe form of black lung disease, is occurring more frequently and among younger coal workers in West Virginia, Virginia, and Kentucky.
Before 2005, when the increase was first reported, incidences of pneumoconiosis had been on the decline since the 70s, which was when modern coal dust controls were introduced. Subsequent investigations have reported that cases of pneumoconiosis have tripled and that tenured miners in central Appalachia, the epicentre of the disease, have experienced a tenfold increase in severe black lung disease.
“We have known that silica is highly toxic, and exposure contributes to coal workers’ pneumoconiosis, but we have not known why coal workers were suddenly experiencing more disease and more severe forms of it,” explained Dr Robert Cohen, Clinical Professor of Environmental and Occupational Health Sciences and Director of the Mining Education and Research Centre at UIC.
“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.”
How were the rising cases of pneumoconiosis considered?
Scientists collected lung tissue samples from coal miners with severe pneumoconiosis to further understand this phenomenon. Then, they compared the samples from miners born between 1910 and 1930 with those from miners born in or after 1930, both historical and contemporary coal miners, respectively.
The researchers considered the samples’ physical characteristics of the diseased lungs – or the pathology. It was discovered that the tissues that had more than 75% silicotic nodules – which are round with whirls of pinkish scar tissue – were classified as having silica-type disease. While tissues with fewer silicotic nodules and a greater number of grey or black-pigmented nodules were classified as coal-type (less than 25%) or mixed-type (25%-75%).
Additionally, scientists also examined other lesions, such as mineral dust‐related alveolar proteinosis, which presents as fluid-like material on lung tissue and is caused by silica exposure.
Advanced analytic techniques like scanning electron microscopy and X-ray spectroscopy were utilised to measure the chemistry, crystal structure, and physical properties of the mineral particles in the samples.
What was discovered from this examination?
Cohen and his team found a clear link between silica exposure and severe black lung disease in contemporary miners:
- Contemporary miners had significantly higher rates of silica-type disease compared to their historical counterparts (57% vs 18%). In contrast, historical miners had a significantly higher proportion of both coal‐type (50% vs 17%) and mixed‐type (33% vs 26%) diseases;
- Mineral dust alveolar proteinosis was more common in contemporary miners (70% vs 37%);
- The percentage (26% vs 18%) and concentration (4.7 vs 2.6 billion particles per cubic centimetres) of silica particles were significantly greater in contemporary miners; and
- The concentration of silica particles was significantly greater (more than 50%) when silica‐type severe black lung, mineral dust alveolar proteinosis, silicotic nodules or immature silicotic nodules were present.
“These findings provide the first direct evidence that silica is a causative agent behind the increasing incidence of progressive massive fibrosis — severe pneumoconiosis. This is critical information that can be used to determine health-protective permissible exposure limits for coal miners,” noted Cohen.
He attributes silica-driven resurgence as likely due to changes in mining technology like the mechanised coal extraction devices introduced in the US in the 1950s, when miners born in or after 1930 would have begun their careers.
“Silica is a mineral found in rock and technology that allows for more mining below and above the coal seam, which is profitable, means more cutting through rock and more silica exposure,” Cohen added. “Our findings underscore the importance of controlling workplace silica exposure to prevent the disabling and untreatable adverse health effects afflicting US coal miners.”
What do these results mean for coal miners?
In 2019, the Mine Safety and Health Administration initiated a request for information to inform its silica rules, but the standard established in 1969 remains in effect. The rule permits 100 micrograms per cubic centimetre for silica exposure. The Occupational Safety and Health Administration, which sets occupational health standards for nearly all other industries, allows 50 micrograms per cubic centimetre.
These findings were published in the Annals of the American Thoracic Society article, the paper titled: ‘Pathology and Mineralogy Demonstrate Respirable Crystalline Silica is a Major Cause of Severe Pneumoconiosis in US Coal Miners.’
