Abstract

Inhalation of coal dusts can invoke tissue damage and proinflammatory effects in the lungs which ultimately lead to the disease known as Coal Workers’ Pneumoconiosis (CWP). It is unknown if this is related to the amount of iron and silica found in different coals. Methods: We used X-ray Fluorescence and combustion techniques to determine the chemical composition of coals from 10 mines. Cytotoxicity was assessed by lactate dehydrogenase (LDH) release by cells at 2, 6 and 24 hours. Human alveolar (A549) and bronchial (Calu-3) epithelial cells were used to assess the cytotoxicity of coal dust in different regions of the lung. A549 cells were exposed to coal dust in suspension. Calu-3 cells differentiated at an air-liquid interface were exposed to coal dusts using a modified Andersen cascade impactor. LDH released into the media was measured at initial exposure then after coal dust exposure. Results: Carbon, iron (Fe) and silica (Si) contents were the major differences between coal samples. Most samples had carbon contents of 60-70%, Mine 5 had the highest Fe content (45-50%) and Mines 6 and 10 were predominantly Si (30-40%). Using 4 representative coal dusts differing in Fe and Si contents we found that in Calu-3 cells the greatest cytotoxicity was induced by the dust from Mine 5 (high Fe, minimal Si). Also in Calu-3 cells, coal dust samples from mines with low Fe/high Si, low Fe/minimal Si, and minimal Fe/low Si dusts had minimal cytotoxicity. In contrast, A549 cells showed similar cytotoxicity regardless of the Fe or Si content of the coal. Conclusions: Our results suggest that Fe and Si contents of coal warrant further investigation as they may exhibit different toxicities in different regions of the lung.

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