Mutations to ouabain resistance (selecting for base modifications at the co-dominant Na+K+-dependent ATP-ase locus) and thioguanine resistance (selecting for a wide range of genetic changes at the recessive hypoxanthine-guanine phosphoribosyl transferase locus) were measured in a repair-proficient human lymphoblastoid line with defined monochromatic radiations in the UVC (254 nm), UVB (302 nm, 313 nm), UVA (334 nm, 365 nm) and visible (405 nm) ranges. No mutations were detected at wavelengths in the range 334-405 nm. At 254 nm and 313 nm, both mutations to thioguanine resistance and survival were consistent with those expected from the relative levels of cyclobutane-type pyrimidine dimers induced. However, at 313 nm, the ratio of ouabain-resistant to thioguanine-resistant mutants is 10 times higher than at 254 nm, indicating that a unique type of pre-mutagenic base damage is induced at the longer wavelength. Radiation in the UVA (334 nm) range reduced the induction of mutations by a UVC (254 nm) wavelength at both mutation markers. These results suggest, first, that distinct types of biologically expressed genetic damage may be induced in the UVB region of sunlight and, second, that strong interactions may occur between the different wavelength regions of sunlight that can modify the expression of this genetic damage in human cells.