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EC number: 287-476-5
CAS number: 85535-84-8
human data currently available.
well-conducted study, Chlorparaffin 56 (a C12 chlorinated paraffin; 57%
chlorination) was assessed for its ability to induce gene mutations in
the Ames test. Seven concentrations (ranging from 4 -5000 ug/mL) of the
test substance were assessed in a plate incorporation assay with
Salmonella typhimurium strains TA1535, TA1537, TA1538, TA98 and TA100
and Eschericha coli WP2uvrA, both with and without a rat microsomal
activation fraction (S9). No increase in mutant frequency was evident
with the test substance, either with or without S9, compared to the
untreated controls. The positive control substances gave the expected
increases in the numbers of revertant colonies. Therefore, Chlorparaffin
56 showed no mutagenic potential in an Ames test for bacterial
mutagenicity when tested up to 5 mg/plate in the absence or presence of
S9 (Muller, 1988).
results were also obtained in an Ames test using S.
typhimurium strains TA97,
TA 98, TA 100 and TA 1535, when a C12 chlorinated paraffin (60%
chlorination) was tested at up to 3333 ug/plate, in the presence and
absence of Aroclor-induced rat or hamster liver S9. This study employed
a 20 minute preincubation period (NTP,
1986). [However, cytotoxicity was not observed and precipitation was not
reported; therefore it is possible that the maximum concentration tested
could have been increased further (up to 5000 ug/plate).]
C10-13 chlorinated paraffin (50% chlorination) did not produce an
increase in revertants in S. typhimurium strains
TA 98, TA 100, TA 1535 and TA 1538, in the absence or presence of
Aroclor-induced rat liver S9, when tested up to 2500 ug/plate (ICI,
1989; cited in Birtley et al. 1980
and EU, 2000). [As above, cytotoxicity was not observed and
precipitation was not reported and hence the maximum concentration
tested could have been increased.]
(a C10-13 chlorinated paraffin; 56% chlorination) at unspecified
concentrations was negative in an Ames assay with five strains of S.
typhimurium both in the presence
and absence of a mammalian metabolic activation fraction (Elliot, 1989).
Negative results were also claimed in another Ames test (ICI; 1977;
cited in the EU, 2000), but the results of this study and the Elliot
(1989) study provide very little experimental details, therefore there
reliability cannot be assessed.
A C10-13 chlorinated paraffin (50%
chlorination; containing 1% epoxy stabiliser) was assessed for its
mutagenic potential in the Ames test with S. typhimurium strains TA1535,
TA1537, TA1538, TA98 and TA100 and E. coli WP2uvrA. These bacterial
strains were incubated with up to 10 mg/plate of the test substance in
the presence or absence of a rat liver S9. Dose-related increases in
mutant frequency occurred with S9 in TA100 and without S9 in TA100 and
TA98. However, the increase in TA100 with S9 was just less than 2 -fold,
and in TA98 without S9 only just reached 2 -fold. Furthermore, the
presence of the epoxy stabiliser made it uncertain which substance was
responsible for the increase (Hoechst AG, 1986; cited in EU, 2000).
Overall it is not possible to draw firm conclusions from this study.
56 flϋssig (a C10-13 chlorinated paraffin; 56% chlorination) was
assessed for its mutagenic potential in mammalian cells using the HPRT
assay. After a preliminary study to determine cytotoxicity of the test
substance, it was tested at concentrations of up to 75 or 30 ug/mL with
or without a rat liver metabolic activation system (S9), respectively,
in cultures of Chinese hamster lung fibroblast (V79) cells. Mutants were
selected by their resistance to 6-thioguanine. Two independent
experiments were conducted. [According to an expert review (EU, 2000) on
SCCPs, the study was well-conducted and carried out to modern
protocols.] The test substance did not induce an increase in mutant
frequency; cytotoxicity was evident at levels of 50 or 20 ug/mL with or
without S9, respectively. In contrast positive control substances (not
specified in the available abstract of the report) performed as
expected, increasing the mutant frequency, thus demonstrating the
validity of the assay. In conclusion, in a gene mutation (HPRT) study in
Chinese hamster V79 cells, Chlorparaffin 56 flϋssig did not induce a
significant, reproducible increase in mutant frequency at doses of up to
75 or 30 ug/mL with or without S9, respectively (Muller, 1987).
No in vitro
cytogenetic studies on SCCPs in mammalian cells are available. In
accordance with column 2 of REACH Annex VIII, an in vitro cytogenicity
study in mammalian cells or an in vitro micronucleus study, do not
usually need to be conducted if adequate data from an in vivo
cytogenicity test are available. In this instance, two reliable in vivo
mammalian cytogenicity tests (Muller, 1989; IRDC, 1982) have been
performed with SCCPs. Both these in vivo bone marrow studies demonstrate
that C10-13 chlorinated paraffins
(58% chlorination) are not clastogenic at up to 5 g/kg bw to this
sensitive target tissue. The available toxicokinetic data demonstrate
that SCCPs undergo significant absorption following oral administration,
with one study (Darnerud et al. 1982; see IUCLID Chapter 7.1.1 for
further details) shows distribution to the bone marrow of three C12
chlorinated paraffins (17, 56 and 69% chlorination) following oral or
intravenous administration to mice; indicating the reliability of these
negative genotoxicity study results.
In a study
conducted to a protocol equivalent to OECD Guideline 478, a C10-13
chlorinated paraffin (58% chlorination) was tested for its ability to
induce dominant lethal mutations in the sperm of male Charles River COBS
CD rats. Groups
of 15 sexually mature male rats were treated with 0, 250, 750 or 2000
mg/kg bw/day (in corn oil) by gavage for 5 consecutive days followed 2
days later with the sequential mating with groups of 2 untreated virgin
females to provide a total of 20 mated females per male. This was to
cover all the various germ cell stages. The dams were sacrificed 15 days
after pairing and the uteri examined for foetal deaths and viable
embryos. No increase in foetal deaths or decrease in viable embryos were
evident in the treated groups compared to the untreated controls. In
contrast the positive control (cyclophosphamide) produced a dominant
lethal mutation affecting the post-meiotic stage of spermatogenesis.
Under the conditions of this study, a C10-13 chlorinated paraffin (58%
chlorination) showed no evidence of germ cell mutagenicity in a dominant
lethal assay in rats (IRDC, 1983).
mutagenicity assays, the results of two cell transformation assays,
using BHK21/C13 cells, have been summarised here for convenience. In the
first, cells were treated, in the presence of Aroclor-induced rat liver
metabolic activation, with up to toxic concentrations of a C10-13, 50%
chlorinated paraffin (cited in Birtley
and EU, 2000). There was no evidence of an increase in cell
transformation frequency. The test was not conducted in the absence of
metabolic activation mix. In contrast, increases in transformation
frequency were obtained in the presence and absence of Aroclor-induced
rat liver activation mix when cells were treated with Chlorowax 500C (a
C12 chlorinated paraffin; 58% chlorination) (ICI, 1982; cited in EU,
2000). Large increases (5 to1000-fold) in the transformation frequency
were obtained at both cytotoxic and nontoxic concentrations. The
relationship between this effect and neoplastic activity of chlorinated
Under EU CLP and
DSD regulations, SCCPs would not be classified as mutagenic based on the
information described above.
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
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