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EC number: 200-864-0
CAS number: 75-35-4
Short description of key information on bioaccumulation potential result: 1,1-dichloroethene is readily absorbed following inhalation or oral exposures. 1,1-dichlorethene can be metabolized by a system of mixed function oxidases (mainly CYP2E1). Excretion of 1,1-dichlorethene occurs via exhalation (as unchanged 1,1-dichloroethene or as CO2) or via feces or urine.1,1-dichloroethene shows no bioaccumulation potential.
1,1-dichloroethene is readily absorbed following inhalation or oral
exposures. 1,1-dichlorethene can be metabolized by a system of mixed
function oxidases (mainly CYP2E1). Excretion of 1,1-dichlorethene
occurs via exhalation (as unchanged 1,1-dichloroethene or as CO2) or via
feces or urine. 1,1-dichloroethene shows no bioaccumulation potential.
In vitro experiments on vinylidene chloride dermal absorption on
human skin revealed that it can potentially be well absorbed by dermal
route (Fasano et al., 2008).
Discussion on bioaccumulation potential result:
1,1-dichloroethene is readily absorbed following inhalation or
oral exposures, and can be metabolized by system of mixed-function
oxidases (mainly CYP2E1). With increasing doses of 1,1 -dichloroethene
and subsequent saturation of the metabolizing enzymes, the proportion of
1,1 -dichloroethene exhaled unchanged increased markedly. Several
pathways for metabolisation and excretion of 1,1-dichloroethene exist.
Metabolisation occurs through the formation of an expoxide which can be
further lead to the formation of CO2 which is excreted by exhalation or
to the formation of non-volatile metabolites. The relative importance of
these pathways depends on the dose, the route of administration, the
absorption rate, the activity of the enzyme systems (species
differences) and the body composition (fat content). When comparing the
metabolizing systems from humans, rats and mice, those of mice showed
most often the highest activity. Metabolites of 1,1 -dichloroethene can
bind covalently to biomolecules and cause cellular damage in kidney,
lung and liver which correlates with the high concentration of CYP2E1 in
certain cell populations in these tissues. The main detoxification
mechanism of reactive metabolites consists of glutathione conjugation.
Therefore, exposure to high 1,1 -dichloroethene doses influences the
glutathione concentration (in the liver) and the vice-versa the
occurrence of adverse effects due to 1,1 -dichloroethene exposure is
dependent on the glutathione levels. A conservative interpretation of a
PBPK-model showed that
despite limitations due to extrapolation issues from rat to human, it
can be reasonable assumed that the amount of epoxide formed from
1,1-dichloroethene is not higher in humans as compared to the rat at
equivalent oral or inhalation concentrations.
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