Abstract The mechanisms responsible for 300-fold higher levels of aldrin resistance in western corn rootworms relative to the closely related and sympatric northern corn rootworm were investigated. In vivo metabolism of [14C]aldrin by the resistant and susceptible rootworms proceeds similarly with a rapid conversion to its epoxide, dieldrin, which accounted for approximately 60% of the recovered dose in both species. Western corn rootworms exhibited 40% slower penetration and 40% greater excretion than aldrin-susceptible northern corn rootworms, but such differences alone are unlikely to account for overall susceptibility differences. Both species showed similar in vitro rates of aldrin metabolism within nervous tissue; however, western corn rootworm formed more aldrin trans-diol relative to dieldrin than northern corn rootworm. Aldrin trans-diol formation from aldrin in the central nervous system was much higher than its rate of production in the whole rootworm body. Western corn rootworms displayed low levels of cross-resistance to picrotoxinin, a compound thought to share a similar target site with cyclodiene insecticides, but such results are insufficient to ascribe resistance differences solely to target site insensitivity. It is proposed that the joint action of decreased penetration, increased excretion, increased detoxification at the nerve site, and mild nerve insensitivity are responsible for aldrin resistance in western corn rootworm. The possible influence of reduced alternative host plant feeding of the western compared to northern species on resistance mechanisms, particularly nerve site factors, are discussed.