Over 500,000 workers in the United States are exposed to ethylene oxide and propylene oxide. These two solvents are used as chemical intermediates, as well as components in the manufacture of fumigants and food preparation. The neurophysiologic and neuropathologic effects of these two organic oxides were investigated in five groups of 12 primates after exposure to 50 or 100 ppm ethylene oxide, 100 or 300 ppm propylene oxide, or no chemical (sham-exposed). Animals were exposed for 7 h/day, 5 days/wk for 24 months. Body weights, electroencephalograms, and motor nerve conduction velocities of the sciatic and ulnar nerves were assessed six times throughout the exposure period. Although the monkeys exposed to 100 ppm ethylene oxide had significantly lower mean weights, nerve conduction velocities did not differ significantly among the groups. Following termination of exposures, ten animals (two from each exposure group) were sacrificed for neuropathological examinations. Multiple axonal bodies were found in the nucleus gracilis in seven of eight oxide-exposed animals, and demyelination was found in two monkeys exposed to ethylene oxide. In contrast, a single axonal body was found in one of the two sham-control monkeys. However, the lack of a dose-response relationship suggests that this effect may not be related to oxide exposure. In a follow-up study, nerve conduction velocity and neuropathology were assessed in the remaining monkeys seven years after exposure terminated, but again, treatment-related effects could not be detected.