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Keywords:

  • iron;
  • calcium;
  • coal workers' pneumoconiosis (CWP);
  • epithelial mesenchymal transition (EMT);
  • fibrosis

Abstract

Background

Bioavailable iron (BAI) in coal, which may play a key role in causing coal workers' pneumoconiosis (CWP), is present at relatively high levels in Appalachian coals. Calcite decreases BAI and is more plentiful in Western coals than in Appalachian coals, possibly explaining the lower CWP prevalence among Western miners.

Methods

We measured effects of calcite on BAI in non-cellular and cellular systems involving Pennsylvania (PA) coal dust. We also tested in vivo effects of calcite on transferrin receptor and markers of epithelial mesenchymal transition (EMT) and inflammation in mice exposed to PA coal.

Results

Calcite rapidly eliminated BAI in an aqueous suspension of PA coal. Ferritin induction in human lung epithelial cells exposed to PA coal was effectively eliminated by calcite. Mouse lung tissue markers indicated increased EMT after exposure to PA coal dust, but not after exposure to PA coal plus calcite. Markers of inflammation increased following exposure to PA coal alone, but not following exposure to PA coal plus calcite.

Conclusion

Additional research may lead to the use of supplemental calcite in coal mining as a safe and effective way to prevent CWP among Appalachian coal miners. Am. J. Ind. Med. 56:292–299, 2013. © 2012 Wiley Periodicals, Inc.