• small airway disease;
  • pneumoconiosis;
  • spirometry;
  • obstructive lung disease;
  • coal mining;
  • bronchial hyperreactivity



Coal mine dust exposure can cause both pneumoconiosis and chronic airflow limitation. The contributions of various pathophysiologic mechanisms to dust-related lung function decrements remain unclear.


Clinical and physiological findings were assessed for 15 underground coal miners who had demonstrated accelerated FEV1 losses (decliners) over 6–18 years. Decliners' findings were evaluated in comparison to a group of 11 miners who had shown relatively stable lung function (referents) during the same period.


At follow-up examination, the decliners showed significantly greater mean airway resistance (10.47 vs. 6.78 cmH2O/L/s; P = 0.05) and more air trapping (RV/TLC = 37.5 vs. 29.1%; P < 0.01) compared to the referents. Decliners also demonstrated more evidence of small airways dysfunction and tended to have more bronchospasm than the referent group. Total lung capacity, lung compliance, diffusing capacity, and chest radiography did not differ significantly between the two groups. After cessation of mine dust exposures, the decliners' mean rate of FEV1 loss normalized.


In a series of working coal miners, accelerated lung function declines were associated with air trapping and evidence of small airways dysfunction. A preventive benefit from controlling dust exposures was suggested. Am. J. Ind. Med. 56:1107–1112, 2013. © 2013 Wiley Periodicals, Inc.