Underground » Health and Safety
Coal workers' pneumoconiosis (CWP) is an irreversible lung disease associated with inhalation of coal dust. Recent epidemiological disease patterns suggest that the chemical properties of coal dust can influence disease risk. However, to date, no studies have been able to identify which chemical components of the coal dusts might be driving the geographical variation in disease risk, nor have they considered the potential for other lung disease to modify the response to inhaled coal dusts.
The aim of this project was to address these gaps in knowledge. The capacity of 19 different coal samples, from coal seams within the Sydney and Bowen basins, to induce CWP associated responses in lung cells was first assessed. By examining the link between coal chemistry and the lung cell response, a strong association between the potassium content of coal dust and cell cytotoxicity (cell death) was demonstrated. Based on previous studies, and the probable mineralogy, this is likely to be linked to potassium alumino-silicates in the coal samples. This observation requires further laboratory investigations and a wider review of the literature to determine if these minerals are driving adverse responses in lung cells that are related to CWP. If confirmed, further epidemiological studies in identified cases of CWP are required to determine whether there are situations in the coal mining environment where the risk of CWP may be enhanced.
An assessment was made whether coal dust exposure exacerbated the response to bacterial infection. Broadly, coal dust exposure increased the response to bacterial infection. However, this was highly dependent on coal chemistry and the bacterial pathogen used; a complexity that could not be untangled within the bounds of this project.
Finally, an assessment was made whether the response to coal dust was greater in individuals with pre-existing cigarette smoke-induced lung disease (chronic obstructive pulmonary disease; COPD). It was found that, in the coal samples that increased the production of pro-fibrotic (scar forming) mediators, the response was greater in cells from individuals with COPD. This suggests that COPD may increase the risk of CWP. Importantly, the samples that drove these pro-fibrotic responses were the same as those that we identified in the initial experiments. Collectively, studies identified the importance of coal chemistry in influencing the lung response and showed that assessment of the risk of coal dust inhalation to lung health should consider pre-existing lung conditions.