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Environmental Carcinogenesis Division (MD-68) [D. M. D., S. L., N. M. H., B. C. R., M. J. M.], and Human Studies Division [J. L. M.], United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711; Program in Lung Biology, University of North Carolina, Chapel Hill, North Carolina 27599 [D. T.]; Institute of Environmental Health and Engineering, Chinese Academy of Preventive Medicine, Beijing, China [X. L.]; Yunnan Provincial People’s Hospital, Kunming, Yunnan, China [F. H.]; Department of Environmental and Occupational Health and Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, Pennsylvania 15261 [P. K., W. G.]; and International Agency for Research on Cancer (WHO), 150 Cours Albert Thomas, 69372 Lyon Cedex, France [M. O., P. H.]
We determined the TP53 and codon 12 KRAS mutations in lung tumors from 24 nonsmokers whose tumors were associated with exposure to smoky coal. Among any tumors studied previously, these showed the highest percentage of mutations that (a) were G 
T transversions at either KRAS (86%) or TP53 (76%), (b) clustered at the G-rich codons 153–158 of TP53 (33%), and (c) had 100% of the guanines of the G T transversions on the nontranscribed strand. This mutation spectrum is consistent with an exposure to polycyclic aromatic hydrocarbons, which are the primary component of the smoky coal emissions. These results show that mutations in the TP53 and KRAS genes can reflect a specific environmental exposure.
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