Registration Dossier

Administrative data

Key value for chemical safety assessment

Genetic toxicity in vitro

Description of key information

The available data indicate that hydrocarbons, C7-C9, isoalkanes are not genotoxic.

Negative Ames test with S. typhimurium TA 1535, TA 1537, TA 1538, TA 98 and TA 100, and E. coli WP2 and WP2 uvr A, with and without metabolic activation.


Negative results in mammalian chromosomal aberration and gene mutation tests, the latter with and without metabolic activation.

Link to relevant study records

Referenceopen allclose all

Endpoint:
in vitro gene mutation study in bacteria
Remarks:
Type of genotoxicity: gene mutation
Type of information:
experimental study
Adequacy of study:
key study
Study period:
September - October 1982
Reliability:
1 (reliable without restriction)
Rationale for reliability incl. deficiencies:
other: Test procedure according to national standards
Justification for type of information:
The justification for read across is provided as an attachment in IUCLID Section 13.
Reason / purpose:
read-across: supporting information
Reason / purpose:
reference to same study
Qualifier:
equivalent or similar to
Guideline:
OECD Guideline 471 (Bacterial Reverse Mutation Assay)
Deviations:
yes
Remarks:
- limited documentation of cytotoxicity data
GLP compliance:
no
Type of assay:
bacterial reverse mutation assay
Target gene:
S. typhimurium strains: his-operon
E. coli strains: tryptophan-operon
Species / strain / cell type:
S. typhimurium, other: TA 1535, TA 1537, TA 1538, TA 98, TA 100
Additional strain / cell type characteristics:
not specified
Species / strain / cell type:
E. coli, other: WP2, WP2 uvr A
Additional strain / cell type characteristics:
not specified
Metabolic activation:
with and without
Metabolic activation system:
Rat liver homogenate S9 activation, 10 % S9 liver homogenate from Aroclor treated rats
Test concentrations with justification for top dose:
TA 1538 (-S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000; (+S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000 µg/mL
TA 1538 (-S) mix): 0, 15.62, 31.25, 62.5, 125, 250, 500, 1000; (+S9 mix): 0, 31.25, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000 µg/mL
TA 1537 (-S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000; (+S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000 µg/mL
TA 1537 (-S9 mix): 0, 3.9, 7.81, 15.62, 31.25, 62.5, 125; (+S9 mix): 0, 31.25, 62.5, 125, 250, 500, 1000, 2000 µg/mL
TA 1535 (-S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000; (+S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000 µg/mL
TA 100 (-S9 mix): 0, 0.31, 0.62, 1.25, 2.5, 5, 10; (+S9 mix): 0, 7.81, 15.62, 31.25, 62.5, 125, 250 µg/mL
TA 100 (-S9 mix): 0, 31.25, 62.5, 125, 250, 500; (+S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000 µg/mL
TA 100 (-S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000; (+S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000 µg/mL
TA 98 (-S9 mix): 0, 0.31, 0.62, 1.25, 2.5, 5, 10; (+S9 mix): 0, 7.81, 15.62, 31.25, 62.5, 125, 250 µg/mL
TA 98 (-S9 mix): 0, 3.9, 7.81, 15.62, 31.25, 62.5, 125; (+S9 mix): 0, 31.25, 62.5, 125, 250, 500, 1000, 2000 µg/mL
TA 98 (-S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000; (+S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000 µg/mL
EC WP2 (-S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000; (+S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000 µg/mL
EC WP2uvrA (-S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000; (+S9 mix): 0, 62.5, 125, 250, 500, 1000, 2000, 4000, 8000 µg/mL
Vehicle / solvent:
- Vehicle(s)/solvent(s) used: Tween 80 and ethanol
Untreated negative controls:
yes
Negative solvent / vehicle controls:
yes
True negative controls:
not specified
Positive controls:
yes
Positive control substance:
other: TA 1538, TA 98, TA 100: benzo(a)pyrene; TA 1537: neutral red; TA 1535: Sodium azide; and E. coli strains: 4-nitroquinoline-N-oxide
Details on test system and experimental conditions:
METHOD OF APPLICATION: preincubation

DURATION
- Preincubation period: 30 min
- Incubation period: 48-72 hours

NUMBER OF REPLICATIONS: All test were carried out in triplicate.

Two replicate assays were carried out on different days to confirm reproducibility of results.
Statistics:
none
Key result
Species / strain:
S. typhimurium, other: TA 1535, TA 1537, TA 1538, TA 98, TA 100
Metabolic activation:
with and without
Genotoxicity:
negative
Remarks:
Concentrations up to 8000 µg/mL in agar layer cultures did not increase the reverse mutation frequency of S. typhimurium strains either in the presence or absence of a rat liver microsomal activation system.
Cytotoxicity / choice of top concentrations:
other: There was a differential toxicity of the test material to individual strains of Salmonella and the reduction of toxicity in the presence of an S9 mix
Vehicle controls validity:
valid
Untreated negative controls validity:
valid
Positive controls validity:
valid
Key result
Species / strain:
E. coli, other: WP2, WP2 uvr A
Metabolic activation:
with and without
Genotoxicity:
negative
Remarks:
Concentrations up to 8000 µg/mL in agar layer cultures did not increase the reverse mutation frequency of E. coli strains either in the presence or absence of a rat liver microsomal activation system
Cytotoxicity / choice of top concentrations:
not specified
Untreated negative controls validity:
valid
Positive controls validity:
valid
Additional information on results:
There was no evidence of test compound precipitation in the assay system.
Remarks on result:
other: all strains/cell types tested
Remarks:
Migrated from field 'Test system'.

Table: Relative Mutation Rate – Bacterial Experiment I without Metabolic Activation

Concentration

E. coli WP2

E. coli WP2 uvr A

S. typhimurium TA 1535

S. typhimurium TA 1537

S. typhimurium TA 1538

S. typhimurium TA 98

S. typhimurium TA 100

Without S9

3.91

-

-

-

-

-

-

-

7.81

-

-

-

-

-

-

-

15.6

-

-

-

-

-

-

-

31.3

-

-

-

-

-

-

-

62.5

0.8

0.7

1.2

0.1

0.7

0.2

1.4

125

0.9

0.6

0.7

0

0.4

0

0.7

250

0.7

0.8

0.6

0

0

0

0.3

500

0.7

0.7

0.9

0

0

0

0.1

1000

0.8

0.5

0.9

0

0

0

0

2000

0.7

0.6

0.7

0

0

0

0

4000

0.8

0.6

0.6

0

0

0

0

8000

0.6

0.5

0.7

0

0

0

0

Sodium azide 2 µg

-

-

89.8

-

-

-

-

Benzo(a)-pyrene 7 µg

-

-

-

-

1.0

0.7

0.9

4-nitroquinoline-N-oxide 3 µg

39.8

3.2

-

-

-

-

-

Neutral red 7 µg

-

-

-

1.8

-

-

-

Table: Relative Mutation Rate – Bacterial Experiment I with Metabolic Activation

Concentration

E. coli WP2

E. coli WP2 uvr A

S. typhimurium TA 1535

S. typhimurium TA 1537

S. typhimurium TA 1538

S. typhimurium TA 98

S. typhimurium TA 100

Without S9

31.3

-

-

-

-

-

-

-

62.5

0.7

1.3

1.4

0.3

1.5

0.7

1.0

125

0.8

1.0

1.1

0.2

1.3

1.3

0.8

250

0.9

1.0

0.8

0.6

1.5

1.2

1.0

500

0.7

0.8

1.0

0.2

1.0

0.7

1.3

1000

0.7

0.7

1.0

0.4

0.7

0.2

1.4

2000

1.1

0.9

1.1

0

0.4

0

1.2

4000

1.0

1.0

1.0

0

0.7

0

1.1

8000

0.8

1.0

0.5

0

0.7

0

1.1

Sodium azide 2 µg

-

-

15.2

-

-

-

-

Benzo(a)-pyrene 7 µg

-

-

-

-

3.7

5.3

3.1

4-nitroquinoline-N-oxide 3 µg

1.2

3.6

-

-

-

-

-

Neutral red 7 µg

-

-

-

4.4

-

-

-

Table: Relative Mutation Rate – Bacterial Experiment II without Metabolic Activation

Concentration

E. coli WP2

E. coli WP2 uvr A

S. typhimurium TA 1535

S. typhimurium TA 1537

S. typhimurium TA 1538

S. typhimurium TA 98

S. typhimurium TA 100

Without S9

3.91

-

-

-

1.1

-

0.8

-

7.81

-

-

-

0.6

-

0.9

-

15.6

-

-

-

0.7

0.9

0.8

-

31.3

-

-

-

0.4

1.0

0.8

1.1

62.5

1.0

1.0

1.2

0.4

0.7

0.4

1.0

125

1.0

1.0

0.9

0

0.5

0

0.9

250

0.7

0.8

1.4

-

0.2

-

1.0

500

0.9

0.7

1.1

-

0

-

0.7

1000

1.0

0.8

0.9

-

0

-

-

2000

0.7

0.9

0.7

-

-

-

-

4000

0.9

0.8

0.9

-

-

-

-

8000

0.8

0.7

0.9

-

-

-

-

Sodium azide 2 µg

-

-

86.6

-

-

-

-

Benzo(a)-pyrene 7 µg

-

-

-

-

1.1

1.1

1.3

4-nitroquinoline-N-oxide 3 µg

36.7

5.3

-

-

-

-

-

Neutral red 7 µg

-

-

-

1.2

-

-

-

Table: Relative Mutation Rate – Bacterial Experiment II with Metabolic Activation

Concentration

E. coli WP2

E. coli WP2 uvr A

S. typhimurium TA 1535

S. typhimurium TA 1537

S. typhimurium TA 1538

S. typhimurium TA 98

S. typhimurium TA 100

Without S9

31.3

-

-

-

1.1

0.9

0.8

-

62.5

0.9

0.9

0.7

1.2

1.1

1.0

1.1

125

1.1

1.0

1.2

1.1

1.1

0.9

1.0

250

1.4

0.8

0.8

1.4

1.1

0.8

1.1

500

1.2

1.0

0.9

1.0

1.1

0.8

1.2

1000

1.0

1.1

0.8

0.5

0.9

0.4

0.9

2000

0.8

1.0

1.1

0

0.9

0.1

0.9

4000

0.8

0.9

0.8

-

0.5

-

0.9

8000

1.0

0.7

0.7

-

0.4

-

0.9

Sodium azide 2 µg

-

-

18.2

-

-

-

-

Benzo(a)-pyrene 7 µg

-

-

-

-

9.7

6.1

6.5

4-nitroquinoline-N-oxide 3 µg

1.1

2.8

-

-

-

-

-

Neutral red 7 µg

-

-

-

5.2

-

-

-

Conclusions:
Interpretation of results:
negative with metabolic activation
negative without metabolic activation

The purpose of this study was to determine the mutagenicity of the test substance hydrocarbons, C7-C9, n-alkanes, isoalkanes, cyclics. An Ames reverse mutation assay was done on S. typhimurium strains, TA 1535, TA 1537, TA 1538, TA 98 and TA 100, and E. coli strains WP2 uvr A and WP2, both with and without metabolic activation. Species were tested at concentrations ranging from 0.31 to 8000 ug/plate. The test plates were incubated for 48 -72 hrs, and then the number of colonies were counted. For all species, there was no significant increase in the number of revertants as compared to negative controls. Positive controls showed a significant increase in mutations. The test substance is not mutagenic.
Executive summary:

The purpose of this study was to determine the mutagenicity of the test substance hydrocarbons, C7-C9, n-alkanes, isoalkanes, cyclics. An Ames reverse mutation assay was done on S. typhimurium strains, TA 1535, TA 1537, TA 1538, TA 98 and TA 100, and E. coli strains WP2 uvr A and WP2, both with and without metabolic activation. Species were tested at concentrations ranging from 0.31 to 8000 ug/plate. The test plates were incubated for 48 -72 hrs, and then the number of colonies were counted. For all species, there was no significant increase in the number of revertants as compared to negative controls. Positive controls showed a significant increase in mutations. The test substance is not mutagenic.

Endpoint:
in vitro cytogenicity / chromosome aberration study in mammalian cells
Remarks:
Type of genotoxicity: chromosome aberration
Type of information:
experimental study
Adequacy of study:
key study
Study period:
September - October 1982
Reliability:
1 (reliable without restriction)
Rationale for reliability incl. deficiencies:
other: Test procedure according to national standards.
Justification for type of information:
The justification for read across is provided as an attachment in IUCLID Section 13.
Reason / purpose:
read-across: supporting information
Reason / purpose:
reference to same study
Qualifier:
equivalent or similar to
Guideline:
OECD Guideline 473 (In Vitro Mammalian Chromosome Aberration Test)
GLP compliance:
no
Type of assay:
in vitro mammalian chromosome aberration test
Species / strain / cell type:
mammalian cell line, other: Rat liver epithelial-type line (RL4) cells
Details on mammalian cell type (if applicable):
- Type and identity of media: Stock culture media and assay media was Minimal Essential Medium supplemented with 10% fetal calf serum and 1% non-essential amino acids.
Additional strain / cell type characteristics:
other: metabolic competent
Metabolic activation:
without
Metabolic activation system:
RL4 cells are metabolically competent.
Test concentrations with justification for top dose:
0, 2.5, 5.0, and 10 mg/mL
Vehicle / solvent:
- Vehicle(s)/solvent(s) used: Tween 80 and ethanol
Untreated negative controls:
yes
Negative solvent / vehicle controls:
yes
Positive controls:
yes
Positive control substance:
7,12-dimethylbenzanthracene
Details on test system and experimental conditions:
see "Any other information on materials and methods"
Key result
Species / strain:
mammalian cell line, other: RL4 cells, metabolic competent
Metabolic activation:
not applicable
Genotoxicity:
negative
Remarks:
There was no significant increase in chromosome damage
Cytotoxicity / choice of top concentrations:
cytotoxicity
Remarks:
Exposure of RL4 cells to 20 µg/mL test substance resulted in inhibition of cell proliferation by 50 %. Therefore final test concentrations of 2.5, 5, and 10 µg/mL were chosen
Vehicle controls validity:
valid
Untreated negative controls validity:
valid
Positive controls validity:
valid
Additional information on results:
A maximum dose level of 10 µg/mL was determined in the chromosome assay. There was no significant increase beyond control limits in the frequency of chromatid breaks or total chromatid aberrations in rat liver cells exposed to the test material up to 10 µg/mL indicating that the compound did not induce chromosome damage in rat liver cells. A small increase in the percentage of cells showing gaps in exposed cultures was well within historical control ranges. Cultures exposed to the positive control material, DMBA, showed an increase in the frequency of chromosome damage.
Remarks on result:
other: all strains/cell types tested
Remarks:
Migrated from field 'Test system'.

Table: Metaphase chromosome analysis of RL4cells

0 µg/ml

2.5 µg/ml

5.0 µg/ml

10.0 µg/ml

1.0 µg/ml 7,12-dimethylbenzanthracene

Polyploidy (% cells)

1.3

1.3

1.3

1.3

0.5

Chromatid gaps (% cells)

0.3

0.7

0.9

1.0

5.5

Multiple aberrations (% cells)

-

-

-

-

-

Severe damage (% cells)

-

-

-

-

-

Chromatid aberrations (% cells)

0.7

-

0.9

-

4.0

Chromosome aberrations (% cells)

-

-

-

-

1.5

Chromatid gaps

(frequency per cell)

0.003

0.007

0.009

0.010

0.060

Chromatid breaks

(frequency per cell)

0.007

-

0.004

-

-

Chromatid exchange

(frequency per cell)

-

-

0.004

-

-

Chromosome breaks

(frequency per cell)

-

-

-

-

0.015

Chromosome exchange

(frequency per cell)

-

-

-

-

-

Conclusions:
Interpretation of results: negative

This study examined the potential for the test substance, hydrocarbons, C7-C9, n-alkanes, isoalkanes, cyclics, to cause chromosomal aberrations in rat liver RL4 cells. Cells were exposed to concentrations of 0, 2.5, 5.0, and 10 ug/mL of test substance, and then examined for chromosomal aberrations including polyploidy, chromatid gaps, and chromatid exchanges. The positive control substance was 7,12 -dimethylbenzanthracene. No significant increase in the frequency of chromosomal damage was observed. Based on the study design the test substance showed no genetic toxicity.
Executive summary:

This study examined the potential for the test substance, hydrocarbons, C7-C9, n-alkanes, isoalkanes, cyclics, to cause chromosomal aberrations in rat liver RL4 cells. Cells were exposed to concentrations of 0, 2.5, 5.0, and 10 ug/mL of test substance, and then examined for chromosomal aberrations including polyploidy, chromatid gaps, and chromatid exchanges. The positive control substance was 7,12 -dimethylbenzanthracene. No significant increase in the frequency of chromosomal damage was observed. Based on the study design the test substance showed no genetic toxicity.

Endpoint:
in vitro gene mutation study in mammalian cells
Remarks:
Type of genotoxicity: gene mutation
Type of information:
experimental study
Adequacy of study:
key study
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: Acceptable, well documented publication which meets basic scientific principles
Justification for type of information:
The justification for read across is provided as an attachment in IUCLID Section 13.
Reason / purpose:
read-across: supporting information
Qualifier:
according to
Guideline:
OECD Guideline 476 (In Vitro Mammalian Cell Gene Mutation Test)
Deviations:
yes
Remarks:
- using microtiter plates
GLP compliance:
not specified
Type of assay:
mammalian cell gene mutation assay
Target gene:
thymidine kinase
Species / strain / cell type:
human lymphoblastoid cells (TK6)
Details on mammalian cell type (if applicable):
- Type and identity of media: RPMI 1640 medium supplemented with 15% heat-inactivated horse serum

Additional strain / cell type characteristics:
not specified
Metabolic activation:
with and without
Metabolic activation system:
with Aroclor induced-rat liver homogenate
Test concentrations with justification for top dose:
5 % v/v TMP in DMEM medium, administered undiluted or as 50 % (1:1 saturated to normal medium)
Vehicle / solvent:
- Vehicle(s)/solvent(s) used: DMEM medium
Untreated negative controls:
yes
Remarks:
with and without S9
Negative solvent / vehicle controls:
yes
Remarks:
DMEM medium
Positive controls:
yes
Remarks:
for S9 activated cultures
Positive control substance:
benzo(a)pyrene
Remarks:
Migrated to IUCLID6: 15 µM
Untreated negative controls:
yes
Remarks:
with and without S9
Negative solvent / vehicle controls:
yes
Remarks:
DMEM medium
Positive controls:
yes
Remarks:
for non-activated cultures
Positive control substance:
ethylmethanesulphonate
Remarks:
Migrated to IUCLID6: 0.2 mM
Details on test system and experimental conditions:
see "any other information on materials and methods"
Key result
Species / strain:
human lymphoblastoid cells (TK6)
Metabolic activation:
with and without
Genotoxicity:
negative
Remarks:
TMP did not induce significant increases in the mutation frequency at the thymidine kinase locus.
Cytotoxicity / choice of top concentrations:
cytotoxicity
Remarks:
Cell survival in TMP-saturated medium with and without metabolic activation was greater than 50-60 %.
Vehicle controls validity:
not specified
Untreated negative controls validity:
not specified
Positive controls validity:
valid
Additional information on results:
The elevated mutation frequencies of positive control compounds were as expected.

ADDITIONAL INFORMATION ON CYTOTOXICITY:
Cell survival in positive control treated cultures was 40 or 30% for benzo(a)pyrene and EMS, respectively
Remarks on result:
other: all strains/cell types tested
Remarks:
Migrated from field 'Test system'.
Conclusions:
Interpretation of results: negative

Based on the study design there is no incidence of increased genetic toxicity caused by the test substance.
Executive summary:

Based on the study design there is no incidence of increased genetic toxicity caused by the test substance.

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed (negative)

Genetic toxicity in vivo

Description of key information

The available data indicate that hydrocarbons, C7-C9, isoalkanes are not genotoxic.


Negative in dominant lethal, micronucleus and unscheduled DNA synthesis assays.

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed (negative)

Additional information

In vitro

There are no data available on the in vitro genotoxic potential of hydrocarbons, C7 -C9, isoalkanes. However, reliable data are available on structurally-related substances. Thus, read-across based on analogue approach was conducted.

A reliable bacterial reverse mutation assay (Ames test) was conducted with hydrocarbons, C7-C9, n-alkanes, isoalkanes, cyclics following a protocol similar to OECD 471.The pre-incubation procedure was performed with Salmonella typhimurium strains TA 1535, TA 1537, TA 1538, TA 98 and TA 100, and Escherichia coli strains WP2 uvr A and WP2.. The strains were exposed to concentrations ranging from 0.31 to 8000 µg/plate for 30 min both with and without metabolic activation prior to plating and further incubation for 48 -72 h.For all strains tested, there was no significant increase in the number of revertants as compared to negative controls. An initial cytotoxicity assay with S. typhimurium TA100 showed that the test substance was extremely cytotoxic, especially in the absence of S9 fraction. Therefore, initial mutation assays were conducted over a low dose range (0.31 -10 µg per mL) with strains TA100 and TA98. Virtually no cytotoxicity was observed at these concentrations, and so more appropriate concentrations were tested for all strains in subsequent assays. Salmonella strains were more sensitive to the cytotoxic effect of the test substance than E. coli strains, and cytotoxicity was greater in the absence of S9-fraction.

In conclusion, the test substance was not mutagenic in this assay (Shell Chemicals, 1983; Brooks et al., 1988).

The potential of hydrocarbons, C7-C9, n-alkanes, isoalkanes, cyclics to cause chromosomal aberrations in rat liver RL4 cells was tested with a method comparable to OECD 473. Cells were exposed to concentrations of 0, 2.5, 5, and 10 µg/mL of test substance for 22 h, and then examined for chromosomal aberrations including polyploidy, chromatid gaps, and chromatid exchanges. Exposure of RL4 cells to 20 µg/mL test substance resulted in inhibition of cell proliferation by 50%. Therefore 10 µg/mL was chosen as the maximum dose level. No significant increase in the frequency of chromosomal damage was observed. Under the conditions of this study, the test material was not clastogenic (Shell Chemicals, 1983; Brooks et al., 1988).

Iso-octane (CAS No. 540-84-1) was tested in a mammalian cell gene mutation assay performed according to OECD 476. The test material was prepared by adding iso-octane at a final concentration of 5 % v/v in culture (DMEM) medium and stirred overnight at room temperature in a foil wrapped, capped parafilm-sealed bottle to saturate the medium. Human lymphoblastoid cells (TK6) were exposed to 100 or 50 % of this saturated DMEM medium with and without metabolic activation for 3 h and allowed for expression for 4 to 8 days. Both with and without metabolic activation, iso-octane did not induce significant increases in the mutation frequency at the thymidine kinase locus and cell survival in iso-octane-saturated medium was greater than 50-60 %. Based on the study design there was no incidence of increased genetic toxicity caused by the test substance (Richardson et al., 1986).

 

In vivo

Hydrocarbons, C7-C9, isoalkanes tested in a dominant lethal study (similar to OECD 478) showed no evidence of genotoxicity in the germ cells of treated male rats exposed to 400 or 1200 ppm by inhalation (ExxonMobil Chemical,1980).

The in vivo genotoxicity of other analogues has been tested.

Hydrocarbons, C7-C9, n-alkanes, isoalkanes, cyclics were not clastogenic to mouse bone marrow cells. Iso-octane did not induce unscheduled DNA synthesis in rat hepatocyte cultures.

Based on an analogue approach, these results suggest that hydrocarbons, C7 -C9, isoalkanes are not expected to induce genotoxicity in vivo.

Justification for classification or non-classification

The available data on the genotoxic potential of hydrocarbons, C7 -C9, isoalkanes and structurally related substances are conclusive but not sufficient for classification.