The carcinogen 7-methylbenz[a]anthracene (7-MBA) is considered to be metabolically activated via its bay-region dihydrodiol-epoxide, trans-3,4-dihydro-3,4-dihydroxy-7-methyl-benz[a]anthracene 1,2-oxide (7-MBA-3,4-diol 1,2-oxide). When tested on mouse skin, a target tissue for polycylic aromatic hydrocarbon carcinogenesis, 7-ethylbenz[a]anthracene (7-EBA) was much less active than 7-MBA, and this difference may be due to differences in the pathways by which the two compounds are metabolized and activated. In the present work, the metabolism by mouse-skin microsomes of both hydrocarbons to dihydrodiols has been examined. Both were metabolized to a similar extent with the 8,9-dihydrodiols being detected as the predominant metabolites. The 3,4-, 5,6-and 10,11-dihydrodiols of 7-MBA and the 3,4- and 10, 11-dihydrodiols of 7-EBA, were also detected. 7-MBA was found to bind covalently to microsomal protein at 10 times the level of 7-EBA. The covalent binding of benz[a]anthracene (BA), 7-EBA and 7-MBA to DNA in mouse skin following topical application was determined using the 32P-postlabelling assay. The results correlated with the relative carcinogenic activities of the compounds with 7-MBA binding at five and nine times the level of 7-EBA and BA respectively. For all three hydrocarbons, the major hydrocarbon: 32P-labelled nucleoside bisphosphate, eluted in the same area of the TLC maps, suggesting the involvement of a common type of bay-region dihydrodiol-epoxide intermediate.