MECHANISMS of formation of chromatid aberrations are not fully understood. The involvement of chromosome breakage and reunion1 or exchange2 has been suggested. DNA repair is a possible cause of aberrations and exchanges3–5, but a causal relationship between the two phenomena is not clear6,7. It is not known whether chromatid deletions derive from unrepaired chromatid breaks or from incomplete exchanges between sister chromatids. The origin of chromatid deletions can be studied by examining whether or not they occur just at the points of sister chromatid exchanges (SCE) (ref. 6). Differential labelling of sister chromatids with 5-bromodeoxyuridine (BUdR) has shown that X-ray-induced chromatid deletions are only infrequently associated with SCE, indicating that most chromatid deletions are not incomplete SCE but simple chromatid breakage8. On the other hand, the parallel distribution of SCE and chromosome aberrations induced by two different hydrocarbon carcinogens, 7,12-dimethylbenz (a) anthracene and 7,8,12-trimethylbenz (a) anthracene has been reported, suggesting that aberrations are incomplete SCE (ref. 9). The results presented here indicate that almost no chromatid deletions or gaps induced by irradiation of BUdR-substituted chromosomes with visible light represent incomplete SCE.