Propylene oxide (PO) has been produced commercially since 1925. The main uses of PO are (1) as intermediates in the synthesis of polyurethane foams and polyester resins (via propylene glycol), and (2) as a fumigant for sterilizing plastic medical equipment and foodstuffs (IARC, Vol. 11, 1976). PO has (a) rate constants for chemical reactivity with water and other nucleophils, (b) mutagenicity, and (c) estimates of risk to man, all similar to those observed for ethylene oxide (EO). (For detailed review, see Ehrenberg and Hussain, 1981.) Both PO and EO are carcinogenic in mammals, and EO has also been implicated as a human carcinogen (Hogstedt et at., 1979a, b). Recently we have shown that exposure, both in vivo and in vitro, of an individual's lymphocytes to EO inhibited unscheduled DNA synthesis (UDS), a step in the enzymatic repair of DNA lesions (Pero et al., 1981). Here we report a verification of these earlier results of EO exposure, and further extend our results to include another closely related epoxide, PO, which we have now found also caused inhibition of UDS after occupational exposure. According to our knowledge, this is the first report of the genotoxic effects of PO in man.