 previous studies on the reproductive toxicity of boric acid have indicated that male rodents suffer testicular atrophy after treatment . 
 there were , however , no studies of the potential effects on female fertility or on the neonate . 
 in addition , no study described the development of the testicular lesion , thought to be related to the mechanism of toxicity . 
 a reproductive assessment by continuous breeding ( racb ) study using mice exposed to boric acid at 1000 , 4500 , and 9000 ppm in the diet indicated that there are probably multiple sites of action , although male fertility appears very sensitive . 
 possible effects on female fertility can not be separated from potential developmental toxicity and need additional investigation . 
 decrements in sperm motility were observed at all exposure levels , and testicular atrophy was confirmed in high- and middle - dose - group males . 
 this was investigated further by timed serial - sacrifice studies using 9000 ppm in the diet of rats , which found that the first lesion seen in the testis was an inhibition of spermiation ( release of mature spermatids ) . with continued dosing , 
 this was followed by a disorganization of the normal ordered layering of the seminiferous epithelium , germ cell sloughing and death , and finally , atrophy . 
 subsequent studies using additional doses ( 2000 , 3000 , 4500 , 6000 , and 9000 ppm ) found that it was possible to observe inhibited spermiation that did not progress to atrophy ( 4500 ppm and below ) within the 9-week exposure period.(abstract truncated at 250 words)imagesfigure 1 . 
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