The impact of mineralogy on coal dust toxicity: potassium as a proxy for illite and surface iron-driven oxidative stress.

Epidemiological evidence suggests that the chemical composition of coal dust influences its toxicity, although the underlying mechanisms remain unclear. We previously identified potassium content as a strong predictor of lung cell responses, likely reflecting the presence of potassium alumino-silicate minerals. In this study, we investigated the role of potassium and potassium alumino-silicates in coal dust-induced cellular responses and explored the mechanisms driving these effects. Forty-four coal samples and four potassium alumino-silicate minerals were assessed for their effects on cytotoxicity, cell proliferation, and inflammatory responses in epithelial cells and macrophages. Surface-associated iron was quantified, and intracellular reactive oxygen species (ROS) generation was measured to assess oxidative stress mechanisms. Our data showed that potassium oxide alone induced only minor cytotoxic effects, whereas specific potassium alumino-silicate minerals, particularly illite, elicited strong cytotoxic and pro-inflammatory responses. Higher potassium content in coal dust was associated with reduced epithelial cell proliferation. Illite exhibited elevated surface-associated iron and induced greater ROS production compared with muscovite and orthoclase. Increasing surface iron on these less reactive minerals enhanced inflammatory responses but did not replicate the cytotoxic effects of illite. These findings demonstrate that potassium alone does not directly drive coal dust toxicity, but instead reflects the presence of reactive mineral phases. Mineral-specific surface properties, particularly those related to iron-mediated oxidative stress, play a central role in determining biological responses to coal dust.