Impact of reactive iron in coal mine dust on oxidant generation and epithelial lung cell viability

Abstract

Coal workers' pneumoconiosis (CWP) is a preventable occupational lung disease caused by the chronic inhalation of coal mine dust. The inhalation of coal mine dusts can result in the development of a range of lung diseases termed coal mine dust lung diseases, which is not limited to CWP and includes silicosis, bronchitis, emphysema and cancer. For decades, the presence of elemental Fe, C and Si has been proposed to be the causal factors underlying CWP. The recent resurgence of CWP globally with examination of cases in the United States suggesting a potential but inconclusive role of Fe(II)-sulfide minerals. To obtain a better understanding of Australian coals, the existence and potential adverse impacts of iron minerals were examined using 24 representative Australian coal samples. The results of this work revealed that reduced iron minerals were widely distributed within samples obtained from Australian coal mines with pyrite and siderite being particularly abundant. Compared with carbon and crystalline silica, the presence of these specific iron minerals were negatively correlated to the viability of both alveolar macrophages (NR8383) and human lung epithelial cells (A549) (R2 = 0.689) under scenarios reflecting biologically-relevant inflammatory response conditions. Further analysis using Welch's unpaired t-test indicated that the presence of reduced iron minerals statistically enhanced acellular oxidant production (90% CI [0.74 to 2.55]) and inflammatory response (90% CI [0.15 to 36.96]). Compared with Fe(II)-hydroxide, Fe(II)- and Fe(III)-(phyllo)silicate and Fe(II)-sulfate mineralogies, pyrite and siderite bearing dusts are likely to have greater adverse impacts on epithelial lung cells under inflammatory response conditions in view of both their iron content and reactivity.