Ethyl carbamate (EC, urethan) is carcinogenic probably because it is converted in vivo to vinyl carbamate and then to vinyl carbamate epoxide, which reacts with DNA bases. We hypothesized that vinyl carbamate arises from EC by oxidation to 2-hydroxy-EC (HEC) and dehydration of the HEC, rather than by direct dehydrogenation of EC. In that case, HEC should be more carcinogenic than EC. In a previous test, HEC showed only borderline initiating activity for mouse skin, but its synthesis was poorly described. In the present study, HEC was synthesized by reacting ethylene carbonate with ammonia and was characterized. A single dose of HEC or EC in saline was injected i.p. into adult male strain A mice, which were maintained for 16 weeks. HEC doses of 1.12, 4.6 and 11.2 mmol/kg induced 0.16, 0.32 and 0.32 lung adenomas/mouse, respectively. The 28% tumor incidence for the two highest doses was significantly (P < 0.05) greater than that in controls injected with saline alone. The number of tumors/mouse with 4.6 mmol HEC/kg was one-fortieth of that for an equimolar dose of EC. The weak activity of HEC supports the view that HEC is not a proximal carcinogenic metabolite of EC, i.e. that vinyl carbamate is produced directly from EC.