The inter- and intrachromosomal distribution patterns of SCEs obtained with or without mutagen treatment are reviewed and compared, with each other as to their relation to heterochromatin and with the distribution patterns of chromatid aberrations that occurred either "spontaneously" in chromosomes of repair-defective human syndromes or after treatment with the mutagens (BrdU, ethylalcohol, DMBA, TMBA, maleic hydrazide, MMS, MMC). The conclusions are: No general rule is detectable for nonrandom involvement of heterochromatin in spontaneous SCEs. Mutagen-induced SCEs show the same or very similar distribution patterns as the spontaneous ones and are in no case as preferentially located as chromatid aberrations (which involve mainly the junctions between eu- and heterochromatin or other special regions). Therefore, a specific mutagen sensitivity of heterochromatin-aberrations does not exist (or is less pronounced) for SCEs. This supports the inference that different mechanisms underlie the origins of the two phenomena.