Rates of DNA repair in ultraviolet (254 nm)-irradiated nondividing human diploid fibroblasts were determined at doses as low as 1 J/sq m using an enzymatic assay for pyrimidine dimers. In normal cells, initial rates (dimers removed per 24 hr) increased with dose to 20 J/sq m with no further increase at 40 J/sq m. At 10 J/sq m or less, repair occurred continuously over long postultraviolet periods until all the damage that could be detected was removed (for 10 J/sq m, this required 20 days; sensitivity of the assay was about 0.1 dimer/10(8) daltons). The overall rate curves appear as the sum of two first-order reactions with different rate constants (rapid, 1.7 dimers/10(8) daltons/day; slow, 0.25 dimer/10(8) daltons/day). The slow reaction extrapolates to 30 to 40% of the original dimers. Populations irradiated a second time after greater than 90% of the original damage had been removed repaired the newly added DNA damage with similar kinetics and to the same extent. Repair kinetics in a xeroderma pigmentosum strain (XP12BE, Complementation Group A, 1 J/sq m) lacks the rapid component and approximates the slow component of normal cells. If the slow component of normal cells is due to repair of less accessible dimers, as suggested by others, then by analogy, slow excision repair in XP12BE may be due to the poor accessibility of all dimers. This suggests that the XP12BE excision repair defect is in the enzymes that render dimers in chromatin accessible to repair.