We collected tissues from herring gulls (Larus argentatus) nesting within and outside of the Great Lakes basin. Genotoxin exposure was assessed as fluorescent aromatic compounds (FACs) in bile and SOS Chromotest-inducing activity in muscle extracts. We determined whether these exposures were associated with decreased erythrocyte DNA strand length and/or induction of hepatic ethoxyresorufin-O-deethylase (EROD) activity. FACs were detected in all bile samples. Most muscle extracts produced a positive or marginal SOS response in the presence of S9. SOS induction potentials were strongly associated with dietary trophic level. The median molecular length of DNA isolated from erythrocytes for 14 of 17 adult and 10 of 11 prefledgling collections was reduced compared to the modal class for their respective age group suggesting widespread DNA damage. DNA damage was greatest in gulls from Saginaw Bay, Lake Huron. Median EROD activity in both adults and prefledglings from remote locations was significantly lower than that of gulls from the lower Great Lakes and was not associated with concentrations of benzo[a]pyrene (B[a]P)-like FACs. Our results indicate Great Lakes herring gulls were exposed to genotoxins and Ah-receptor activating agents in biologically significant concentrations in the early 1990s. These agents appear to be persistent bioaccumulative compounds and/or their metabolites.