Buccal epithelial gene expression in smoky and smokeless coal users

Exposure to indoor air pollution generated from the combustion of solid fuels is a major risk factor for a spectrum of cardiovascular and respiratory diseases, including lung cancer. In China’s rural counties of Xuanwei and Fuyuan, lung cancer rates are among the highest in the country. While the elevated disease risk in this population has been linked to the widespread usage of bituminous (smoky) coal as compared to anthracite (smokeless) coal, the underlying physiologic mechanism that smoky coal induces in comparison to other fuel types is unclear. As we have previously used airway gene-expression profiling to gain molecular insights into the physiologic effects of cigarette smoke, here we profiled the buccal epithelium of residents exposed to the burning of smoky and smokeless coal in order to understand the physiologic effects of solid fuels. Buccal mucosa scrapings were collected from healthy, non-smoking female residents of Xuanwei and Fuyuan counties who burn coal indoors. RNA was isolated and hybridized onto Affymetrix Human gene 1.0 ST GeneChips, capturing the gene-expression response of (n=26) smoky coal users and (n=9) smokeless coal users. 24-hour indoor personal exposure levels (PM2.5, Polycyclic Aromatic Hydrocarbons) were also captured during this sampling period.