SPERMATOTOXICITY OF DIBROMOACETIC ACID IN RATS AFTER 14 DAILY EXPOSURES

Halogenated acetic acids are major disinfection by-products of water c hlorination and ozonation. Limited data in experimental animals indica te that repeated doses of dichloroacetic acid (DCA) or single doses of dibromoacetic acid (DBAA) cause testicular damage. In the present stu dy, spermatotoxic effects were investigated in rats given oral doses o f 0, 10, 30, 90, or 270 mg DBAA/kg/day for 14 days. In rats dosed with 270 mg/kg/day, there were marked effects on epididymal sperm motility and morphology including the flagellar fusion of 2 or more sperm. Tes tis weight, epididymis weight, and testicular sperm head counts were m ildly reduced relative to control, whereas epididymal sperm counts wer e substantially decreased. Histologic changes in the testis included r etention of Step 19 spermatids in Stages IX to XII, abnormal developme nt of late spermatids, and the formation of atypical structures resemb ling residual bodies that were observed predominantly in Stages X to X IV and I of the cycle of the seminiferous epithelium. At the dosage of 90 mg/kg/day, effects on spermiation, spermatid development, epididym al sperm counts, sperm motility, and sperm morphology were less severe than at the higher dosage. Reduced caput sperm counts and mild effect s on spermiation also occurred at 30 and 10 mg/kg/day. These studies i ndicate that subchronic exposure to DBAA has the potential to affect r eproductive outcome in the rat. Compared to previous studies of DCA (1 2), DBAA, on a molar basis, appears to be a stronger testicular toxica nt than the dichloro analogue.