The induction of sister-chromatid exchanges (SCEs) and micronuclei (MN) was used as an endpoint to evaluate the cytogenetic effects of benzo[a]pyrene (B(a)P) activated by human red blood cells and S9 mix. Human erythrocytes can metabolically activate B(a)P. It was shown that both human erythrocytes and S9 mix activate B(a)P and that the resulting excess SCE and MN depend in a linear manner on the B(a)P dose. HPLC analysis suggested that quinone derivatives formed by the red blood cells are responsible for the cytogenetic abnormalities observed.