Page 10

use (Brayton, 1986). There is no evidence that DMSO causes chromosomal aberrations at levels that are
not directly toxic to cells.

Reproductive and Developmental Toxicity

A mouse teratology NOEL of 12 g/kg/day has been established based on research with a 50% DMSO solution
administered orally. Additional teratogenicity studies of orally administered DMSO to pregnant mice, rats, rab-
bits and guinea pigs have demonstrated that DMSO is not a teratogen in mammals except at high levels that cause
overt maternal toxicity and are coincident with the maximum tolerated dose. The data suggest that DMSO is
not teratogenic at low levels regardless of the route of administration. Finally, the teratogenic potential of DMSO
is dependent on the route of administration, the dose level and gestation stage at exposure.

The one study (Robens, 1968) that did show evidence of teratogenic effects (in hamsters, one of three animal
species tested) from oral administration of DMSO is inappropriate to use for a teratologic evaluation of
DMSO for the following reasons:

DMSO was not the compound of interest but was used only as a solvent control at two very high dose

levels which precluded establishing a NOEL.

One of the DMSO levels tested resulted in maternal death and was clearly beyond the maximum toler-

ated dose (MTD).

DMSO is not considered to be directly embryotoxic and has been shown to be a successful cryoprotectant
for mammalian semen and embryos (Brayton, 1986).

In summary, the evidence of the above teratology data suggests that:

1. DMSO is not a teratogen to mammals when administered via oral and dermal routes at dose levels that

do not produce overt maternal toxicity.

2. DMSO is not a teratogen at low dose levels regardless of the route of administration.
3. The teratogenic potential of DMSO is dependent on route of administration, the dose level and the gesta-

tional time of exposure.