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EC number: 203-458-1
CAS number: 107-06-2
Ethylene dichloride (EDC) induces tumors in rats and mice when
administered chronically by gavage. However, chronic inhalation of EDC
vapor failed to induce any treatment-related tumors. To help understand
the consequences of environmental exposure to EDC by either route,
14C-EDC was administered to male Osborne-Mendel rats by gavage (150
mg/kg in corn oil) or inhalation (150 ppm, 6 hr). EDC was extensively
metabolized following either exposure. No significant differences were
observed in the route of excretion of nonvolatile metabolites. In each
case, -85% of the total metabolites appeared in the urine, with 7 to 8,
4, and 2% found in the CO,, carcass, and feces, respectively. The major
urinary metabolites were thiodiacetic acid and thiodiacetic acid
sulfoxide, suggesting a role for glutathione in biotransformation of
EDC. Gross macromolecular binding (primarily protein binding) was
studied after inhalation or gavage. No marked differences were noted
between the two routes, or between “target” and “nontarget” tissues,
after in vivo administration of EDC. Covalent alkylation of DNA by EDC
was studied in Salmonella typhimurium and rats. DNA alkylation in S.
typhimurium was directly related to the frequency of mutation in these
bacteria. However, when DNA was purified from the organs of rats exposed
in vivo to EDC, very little alkylation was observed after either gavage
or inhalation (2 to 20 alkylations per million nucleotides). DNA
alkylation after gavage was two to five times higher than after
inhalation, but no marked differences were noted between target and
nontarget organs. Pharmacokinetic studies indicated that peak blood
levels of EDC were approximately five times higher after gavage than
after inhalation. When pharmacokinetic data were modeled, it appeared
that the elimination of EDC may become saturated when high blood levels
are produced and that such saturation is more likely to occur when
equivalent doses are administered by gavage versus inhalation. Since
toxicity often occurs when the normal detoxification pathways are
overwhelmed, this toxicity may represent the most reasonable explanation
for the apparent differences between the two bioassays.
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