Transcriptomic analyses of the biological effects of black carbon exposure to A549 cells

Abstract Ambient black carbon (BC) is found to be associated with increased risk of diverse pulmonary diseases, including acute respiratory inflammation and decreased lung function. Freshly emitted BC (FBC) can be transformed into oxidized BC (OBC) through the photochemical oxidization in the air. How this oxidization process influences the toxicity of BC particles is unclear. Previous studies found FBC and OBC could induce oxidative stress and inflammation. This study aimed to further compare the regulating pathways and tried to reveal the crucial target genes caused by FBC and OBC in A549 cells based on transcriptomic data. A total of 47,000 genes in A549 cells after treated with FBC and OBC were examined using Affymetrix Human U133 plus 2.0 chips. Gene ontology (GO) classification (functional enrichment of differentially expressed genes) and Kyoto encyclopedia of genes and genomes (KEGG) classification (pathway enrichment of differentially expressed genes) were conducted and crucial genes were screened. The results showed that top 50 GO terms of FBC and OBC were not completely consistent. The Go term of cation channel was only identified in OBC group, probably caused by the characteristic that zeta potential of OBC is negative, while, that of FBC is positive. In addition transient receptor potential melastatin 7 (trpm7) gene was suggested to be closely related to this process caused by OBC. There are 47 identical pathways in FBC and OBC group among the top 50 KEGG. The inconsistent pathways are mostly related to inflammation with different up-regulation or down-regulation trends of crucial genes. The KEGG results suggested that FBC and OBC both cause inflammatory responses, but through different regulating pathways. In conclusion, OBC and FBC could induce similar toxic endpoints in A549 cells, but the underline regulating processes are not exactly the same.