Swiss-Webster mice were exposed to diets containing 7 or 1000 microg aluminum (Al)/g as Al lactate from conception through maturity (45 days of age). This exposure has previously been shown to cause changes in CNS myelin composition and peroxidizability; in this study myelin sheath widths were measured. Initially, samples of epon embedded, toluidine blue stained cervical spinal cord sectioned at 0.5 mm were examined light microscopically. Qualitatively, Al-treated mice appeared to have a diffuse paleness in nerve tracts. No indication of myelin structural damage (splitting, degeneration) was noted. Quantitative microscopy was performed using images captured with Scion Image Dage 1.59 at 1000x with oil. Axon perimeters and sheaths were measured with NIH image using a standardized sampling pattern in the right medial dorsal and ventral regions of the cervical spinal cord in 6 mice (3 male, 3 female) per group. Mean myelin sheath widths were 16% smaller in the Al-treated group compared to controls (p=.03). There was no effect of sex or region (dorsal/ventral). Axon perimeters were also smaller on the average in the Al treated group but this difference was not significant (p=.16). The relationship between sheath width and axon diameter was similar in the two groups. The density of myelinated axons was greater in some areas for the Al-treated group. The data indicate that dietary aluminum exposure can interfere with myelination in the spinal cord.