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EC number: 265-084-5
CAS number: 64741-82-8
A complex combination of hydrocarbons from the distillation of the products from a thermal cracking process. It consists predominantly of unsaturated hydrocarbons having carbon numbers predominantly in the range of C10 through C22 and boiling in the range of approximately 160°C to 370°C (320°F to 698°F).
Catalytically cracked light cycle oil with 8.7% 3 to 7 ring polycyclic aromatic compounds was carcinogenic when applied repeatedly to mouse skin. The evidence from 3 studies with cracked gas oils suggests that they are carcinogenic.
application tumours were observed. The
percentages of tumour bearing animals indicate that the development of
tumours is likely not dependent on dermal irritation. Data from the
experiments conducted with cracked gas oils indicate that they are
carcinogens, therefore they are classified as Carcinogenic Cat 1B, H350,
according to EU CLP Regulation (EC No. 1272/2008).
Mice were exposed
to a catalytically cracked light cycle oil (CAS No. 64741-59-9), as part
of a study to investigate the influence of skin irritation on tumour
development (Klimisch score = 2, EMBSI, 1996). The
dosing regimen used in this study was designed to allow investigation of
the carcinogenic potential of gas oil streams under conditions that
produced varying levels of skin irritation through manipulation of the
applied concentration and frequency of treatment. The treatment regime
was designed to deliver a constant total weekly dose of each distillate
while varying the extent of any local skin irritation by manipulating
test material concentration and frequency of application. For
example the 100 % (neat) material would be applied once a day whilst the
50% concentration would be applied twice a day to achieve an equivalent
dose of test material.
was observed in animals treated with test material and the positive and
negative control substances, and was generally greater after treatment
with neat distillate twice per week compared with more frequent
treatment with lower concentrations. Concentration-dependent increases
in dermal irritation were observed in all of the treatment groups (0.28,
1.59, 2.40). The pattern of mortality in animals from the 28.5%
treatment groups was generally similar to that of the mineral oil
(negative) control group, with slightly higher mortality in the 50% or
100% groups. This was statistically significant in the case of the
cracked gas oil, where estimated median survival was around 60-80 days
less than that of the controls. Survival in the positive control group
(median 300 days) was also significantly lower than the controls (median
There were no
significant treatment-related gross findings at necropsy other than skin
irritation and masses (tumours) at the treatment site. Tumours
(predominately papillomas or squamous cell carcinomas) occurred in all
groups treated with test material, affecting 1, 17 and 7 mice from the
high, intermediate or low dose groups respectively with a time to first
tumour of approximately 300 to 650 days.
cracked light cycle oil, containing moderate amounts of 3 to 7 ring
polycyclic aromatic compounds, was a dermal carcinogen with a short time
to tumour development, following dermal treatments that did not cause
appreciable skin irritation. These findings are consistent with a
genotoxic mechanism of action. The reason for the failure of undiluted
test material to produce clear evidence of carcinogenicity, despite the
much greater incidence of tumours in the 50% group, is unclear but it
may be due to widespread epidermal necrosis destroying initiated cells.
Hence the evidence suggests that cracked oils are dermal carcinogens
acting via a genotoxic mechanism.
support that cracked gas oils are carcinogens (Biles et al., 1988; API,
1989; Broddle et al., 1996;). This
information is presented in the dossier. In
Biles et al. (1988), the dermal carcinogenicity of 10 middle distillate
samples, including a light catalytic cycle oil with a boiling point <338
°C, was tested in this study. Some
individual PAH analysis was provided and very high phenanthrene levels
were found in the sample. In view of some large sensitivity values (e.
g. Chrysene <108 ppm), however, it would seem that the analysis method
was insufficiently sensitive to measure the critical levels of 4-6 ring
PAHs that may have been present in the samples. The results obtained
with the test material are: median survival of 78 weeks, 250 animals
bearing tumours (4%), 90 days to first tumour, and median time to first
tumour of 140 days. Clear
evidence of skin irritation/skin injury was seen with all the test
materials including hyperplasia, hyperkeratosis, dermatitis, epidermal
degeneration and epidermal necrosis. Tumour
incidences in internal organs were reported to be sporadic and, except
for hepatocellular carcinoma, to be of low frequency. No treatment
related increase in tumours in internal organs was reported. It
was noted by the authors that there was a significant increase in skin
tumour yield with the majority of samples tested, but that
non-neoplastic dermal changes including hyperplasia may have contributed
to the tumourigenic response. In
view of the questionable adequacy of the PAH analysis and the high
levels of phenanthrene and pyrene found in some samples it is uncertain
however whether a genotoxic mechanism can be ruled out.
API (1989), the dermal carcinogenicity
of eleven refinery streams, including three gas oils (one straight run
and two cracked), was investigated in mice. One
of the cracked gas oils showed 78% of mice developing tumours (72%
malignant, 6% benign), while the other cracked gas oil showed 52%
incidence of tumours (46% malignant, 6% benign). The
only conclusions drawn by the authors was that the test materials were
dermatotoxic and carcinogenic and that the degree of these effects
varied greatly. However examination of the tumour data suggests that the
first cracked gas oil might be active as a genotoxic carcinogen as it
produced a high incidence of tumours with a short latent period. The
results with the second gas oil are suggestive of a possible combination
of genotoxic and non-genotoxic
Justification for selection of carcinogenicity via dermal route endpoint:
One of 3 well conducted skin cancer studies
Carcinogenicity: via dermal route (target organ): other: skin
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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