The invention relates to the role of Acr-DNA adducts in p53 mutagenesis in CS- related lung cancer. The distribution of Acr-DNA adducts was mapped at the sequence level in the p53 gene of lung cells using the UvrABC incision method in combination with ligation-mediated PCR. It was determined that Acr preferentially binds at methylated CpG sites. Also, Acr can greatly reduce the DNA repair capacity for damage induced by benzo(a)pyrene diol epoxide. Together these results suggest that Acr is a major etiological agent for CS-related lung cancer and that it contributes to lung carcinogenesis through DNA damage and inhibition of DNA repair. Methods and compositions are provided for either removing an exogenous toxic agent from a combustion product or for preventing the toxic or mutagenic effect of these toxic agents on cells and tissues. Methods are also provided for screening for candidate compounds that protect cells from toxic combustion products.
