Variation on Toxic and Inflammatory Potential of Coal Smoke of Different Sources From a Region With High Lung Cancer Risk.

Abstract

Excess lung cancer risk in Xuanwei and Fuyuan, China, has been attributed to household air pollution from use of a locally sourced smoky (bituminous) coal. However, the carcinogenic mechanisms remain unclear. Given the important role of inflammation in lung cancer development, this study compared the proinflammatory potentials of the particulate phase of smoky coal emissions with those of a locally sourced smokeless (anthracite) coal, which poses a lower lung cancer risk. A co-culture model of lung epithelial (Calu-3) and macrophage (differentiated THP-1) cells was exposed to aerosolized particulates, followed by analysis at 24 h exposure (R0) and after 24 h of recovery (R24). Cytotoxicity was minimal, with lactate dehydrogenase (LDH) release consistently under 15% of the total LDH content. Particulate exposure reduced transepithelial electric resistance (TEER) at R0, with partial recovery by R24, indicating sustained epithelial barrier damage. IL-6 release occurred at R0 in a dose-dependent manner but normalized by R24 for most samples. No significant IL-8 release was observed. The inflammatory and toxic potential (TEER reduction and IL-6/IL-8 changes) were similar across coal types and ventilation conditions. The observed potencies showed no correlation with polycyclic aromatic hydrocarbons (PAHs) content and the observed lung cancer risks of the coal samples. In summary, transient inflammation and lasting barrier damage were observed with little contrast between different coal samples. As these results do not explain the variation of lung cancer risks, further studies examining alternative cellular pathways and biological effects are needed to elucidate the mechanisms driving lung cancer in this population.