Metabolism studies were conducted using Fischer 344 and Sprague-Dawley
rats following inhalation exposure to 1.0% (v/v) air atmospheres of 1
,1-dichloro-2,2,2-trifluoroethane (HCFC-123),2-chloro-1,1,1,2-tetraflu
oroethane (HCFC-124), 1-chloro-1,1-difluoroethane (HCFC-142b), bromoch
lorodifluoromethane (Halon 1211), and perfluorohexane (PFH) for 2 h. T
here were no remarkable differences in results between the two strains
of rats. Animals exposed to HCFC-123 or HCFC-124 excreted trifluoroac
etic acid in their urine. Urinary fluoride concentrations were increas
ed in rats exposed to HCFC-124, and urinary bromide levels were increa
sed in rats exposed to Halon 1211. Small quantities of volatile metabo
lites 2-chloro-1,1,1-trifluoroethane (HCFC-133a) and 2-chloro-1,1-difl
uoroethylene were observed in the livers of rats exposed to HCFC-123.
Rats exposed to HCFC-142b excreted chlorodifluoroacetic acid in their
urine; no volatile metabolites were detected in tissue samples. For PF
H studies, no metabolites were detected in the urine or tissues of exp
osed animals. These results are consistent with proposed oxidative and
reductive pathways of metabolism for these chemicals. Pharmacokinetic
studies were carried out in rats exposed by inhalation to 1.0%, 0.1%,
or 0.01% of HCFC-123. Following exposure, blood concentrations of HCF
C-123 fell sharply, whereas trifluoroacetic acid levels rose for appro
x. 5 h and then declined gradually. Using a physiologically based phar
macokinetic model, saturation of HCFC-123 metabolism was estimated to
occur at approx. 0.2% (2000 ppm) HCFC-123.