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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

Workers - Hazard via inhalation route

Systemic effects

Long term exposure
Hazard assessment conclusion:
DNEL (Derived No Effect Level)
Value:
313 mg/m³
Most sensitive endpoint:
repeated dose toxicity
Route of original study:
Oral
DNEL related information
DNEL derivation method:
ECHA REACH Guidance
Overall assessment factor (AF):
10
Modified dose descriptor starting point:
NOAEC
Value:
3 127 mg/m³
Explanation for the modification of the dose descriptor starting point:

The following correction was made to the NOAEL (oral): Correction respiratory volume rat (8 hour) 1/0.38 m³/kg bw/day, Correction for respiratory volume (worker): 6.7 m³/10 m³. Correction for oral to inhaled 1/2. Alcohols, C14-15 90 d oral NOAEL = 3548 mg/kg bw/day. Therefore the corrected NOAEC for repeated-dose systemic effects via the inhalation route is: 3548*(1/0.38)*(6.7/10)*(1/2) = 3127 mg/m³

AF for dose response relationship:
1
Justification:
Default (starting point is NOAEL).
AF for differences in duration of exposure:
2
Justification:
Default (sub-chronic to chronic).
AF for interspecies differences (allometric scaling):
1
Justification:
Default (oral rat to inhalation human).
AF for other interspecies differences:
1
Justification:
The mammalian alcohol dehydrogenase system is a group of pathways which catalyse the conversion of alcohols and aldehydes, which includes different forms of the enzymes which vary in substrate specificity. The alcohol dehydrogenases (ADHs) are divided into six classes, denoted by ADH1-ADH6. Five of the six classes of alcohol dehydrogenase have been identified in humans. One of the classes, ADH3, is the ancestral form of all mammalian ADHs, and has been traced in all living species investigated. The alcohol dehydrogenase system is considered to be able to detoxify a wide range of alcohols and aldehydes without the generation of toxic radicals (Höög, J-O et al., 2001). Therefore the metabolism of all category members would be expected to follow the same pathway in rats and humans so an interspecies assessment factor to account for potential differences in metabolic pathway is not required and a value of 1 is appropriate. Reference: Höög, J-O, Hedberg, J. J., Strömberg, P., Svensson, S. (2001). Mammalian alcohol dehydrogenase - Functional and structural implications. Journal of Biomedical Science Volume 8, Issue 1, pp 71-76
AF for intraspecies differences:
5
Justification:
Default (worker).
AF for the quality of the whole database:
1
Justification:
Default (reliable study).
AF for remaining uncertainties:
1
Justification:
An assessment factor for remaining uncertainties is not required on the basis of the toxicological results: no adverse systemic effects were observed in any of the numerous reliable systemic toxicity studies that have been conducted for different endpoints for a wide range of alcohols with carbon chain lengths from C6 to C22; observations were consistent across the category. Furthermore, humans and test species are considered to respond to exposure to exogenous fatty alcohols in a similar way. Aliphatic alcohols show a chain-length dependant potential for gastro-intestinal and dermal absorption, with shorter chain aliphatic alcohols having a higher absorption potential than longer chain alcohols. Following inhalation exposure, absorption could occur for lower chain length alcohols, while little systemic exposure would be expected for the higher carbon number alcohols, from C9 upwards. Absorbed aliphatic alcohols potentially could be widely distributed within the body (OECD, 2006). As a result of the rapid and efficient metabolism, it is not anticipated that aliphatic alcohols would remain in the body for any significant length of time. Long chain (LC) fatty alcohols are synthesised within cells and are therefore found within organisms and occur naturally in the environment. Endogenous and exogenous LC alcohols are metabolised in catabolic (breakdown) and anabolic (synthesis) pathways. Cellular metabolism can cycle between LC alcohols and their corresponding acids. Alcohols are used as building blocks in the synthesis of lipids for energy storage. It is therefore concluded that, should systemic exposure occur to anthropogenic LC alcohols, mammals including test species and humans share common pathways for their metabolism and the products of metabolism are naturally-occurring metabolites. The LC aliphatic carboxylic acids are efficiently eliminated and aliphatic alcohols are therefore not expected to have a tissue retention or bioaccumulation potential (Bevan, 2001).
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

Local effects

Long term exposure
Hazard assessment conclusion:
DNEL (Derived No Effect Level)
Value:
178 mg/m³
Most sensitive endpoint:
irritation (respiratory tract)
DNEL related information
DNEL derivation method:
other: The German national maximum exposure limit (AGW) for tetradecan-1-ol, is 178 mg/m³
Overall assessment factor (AF):
1
Dose descriptor:
other: The German national maximum exposure limit (AGW) for tetradecan-1-ol
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

Workers - Hazard via dermal route

Systemic effects

Long term exposure
Hazard assessment conclusion:
DNEL (Derived No Effect Level)
Value:
89 mg/kg bw/day
Most sensitive endpoint:
repeated dose toxicity
Route of original study:
Oral
DNEL related information
DNEL derivation method:
ECHA REACH Guidance
Overall assessment factor (AF):
40
Modified dose descriptor starting point:
NOAEL
Value:
3 548 mg/kg bw/day
Explanation for the modification of the dose descriptor starting point:

Alcohols, C14-15 90 d oral NOAEL 3548 mg/kg bw/day  Oral rat to dermal human no correction to dose descriptor starting point required.

AF for dose response relationship:
1
Justification:
Default (starting point is NOAEL).
AF for differences in duration of exposure:
2
Justification:
Default (sub-chronic to chronic)
AF for interspecies differences (allometric scaling):
4
Justification:
Default (dermal rat to dermal human)
AF for other interspecies differences:
1
Justification:
The mammalian alcohol dehydrogenase system is a group of pathways which catalyse the conversion of alcohols and aldehydes, which includes different forms of the enzymes which vary in substrate specificity. The alcohol dehydrogenases (ADHs) are divided into six classes, denoted by ADH1-ADH6. Five of the six classes of alcohol dehydrogenase have been identified in humans. One of the classes, ADH3, is the ancestral form of all mammalian ADHs, and has been traced in all living species investigated. The alcohol dehydrogenase system is considered to be able to detoxify a wide range of alcohols and aldehydes without the generation of toxic radicals (Höög, J-O et al., 2001). Therefore the metabolism of all category members would be expected to follow the same pathway in rats and humans so an interspecies assessment factor to account for potential differences in metabolic pathway is not required and a value of 1 is appropriate. Reference: Höög, J-O, Hedberg, J. J., Strömberg, P., Svensson, S. (2001). Mammalian alcohol dehydrogenase - Functional and structural implications. Journal of Biomedical Science Volume 8, Issue 1, pp 71-76
AF for intraspecies differences:
5
Justification:
Default (worker)
AF for the quality of the whole database:
1
Justification:
Default (reliable study)
AF for remaining uncertainties:
1
Justification:
An assessment factor for remaining uncertainties is not required on the basis of the toxicological results: no adverse systemic effects were observed in any of the numerous reliable systemic toxicity studies that have been conducted for different endpoints for a wide range of alcohols with carbon chain lengths from C6 to C22; observations were consistent across the category. Furthermore, humans and test species are considered to respond to exposure to exogenous fatty alcohols in a similar way. Aliphatic alcohols show a chain-length dependant potential for gastro-intestinal and dermal absorption, with shorter chain aliphatic alcohols having a higher absorption potential than longer chain alcohols. Following inhalation exposure, absorption could occur for lower chain length alcohols, while little systemic exposure would be expected for the higher carbon number alcohols, from C9 upwards. Absorbed aliphatic alcohols potentially could be widely distributed within the body (OECD, 2006). As a result of the rapid and efficient metabolism, it is not anticipated that aliphatic alcohols would remain in the body for any significant length of time. Long chain (LC) fatty alcohols are synthesised within cells and are therefore found within organisms and occur naturally in the environment. Endogenous and exogenous LC alcohols are metabolised in catabolic (breakdown) and anabolic (synthesis) pathways. Cellular metabolism can cycle between LC alcohols and their corresponding acids. Alcohols are used as building blocks in the synthesis of lipids for energy storage. It is therefore concluded that, should systemic exposure occur to anthropogenic LC alcohols, mammals including test species and humans share common pathways for their metabolism and the products of metabolism are naturally-occurring metabolites. The LC aliphatic carboxylic acids are efficiently eliminated and aliphatic alcohols are therefore not expected to have a tissue retention or bioaccumulation potential (Bevan, 2001).
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

Local effects

Long term exposure
Hazard assessment conclusion:
no hazard identified
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified

Workers - Hazard for the eyes

Local effects

Hazard assessment conclusion:
low hazard (no threshold derived)

Additional information - workers

In summary of the toxicological properties of tetradecan-1-ol:

Acute toxicity tests of tetradecan-1-ol do not indicate any potential hazard for acute, dermal or inhalation toxicity, and would not be classified for acute toxicity endpoint under DSD or Regulation 1272/2008 (CLP).

Tetradecan-1-ol is classified as an eye irritant (Cat 2) but is not irritating to skin, nor is it sensitising by skin contact.

Tetradecan-1-ol is not classified for repeated dose toxicity effects (STOT-RE) or for reproductive toxicity.

In vitro and in vivo studies indicate that tetradecan-1-ol is not genotoxic.

In summary, tetradecan-1-ol is classified as an eye irritant under Regulation 1272/2008 (CLP). 

On the basis of the toxicological results for tetradecan-1-ol no adverse systemic effects were observed in any of the numerous systemic toxicity studies that have been conducted for the different endpoints. Nevertheless, systemic DNEL values have been derived for systemic effects based on the highest dose tested. The DNELs are therefore indicative only and are derived as a precautionary approach to enable quantitative risk assessment with overestimation in RMM

The German regulatory authority imposes a statutory national workplace limit concentration of several analogous alcohols in air in industrial workplaces (AGW); the value set for tetradecan-1-ol is 178 mg/m³.

Overall it would however be prudent to recommend the precautionary use of gloves. Studies indicate that tetradecan-1-ol is irritating to eyes. However, a DNEL for this endpoint cannot be derived and therefore quantitative risk characterisation is not possible. Instead qualitative risk characterisation is required and risk management measures (such as the limitation of concentration in consumer formulations) to minimise any potential eye contact would be required.

General Population - Hazard via inhalation route

Systemic effects

Long term exposure
Hazard assessment conclusion:
DNEL (Derived No Effect Level)
Value:
77 mg/m³
Most sensitive endpoint:
repeated dose toxicity
Route of original study:
Oral
DNEL related information
DNEL derivation method:
ECHA REACH Guidance
Overall assessment factor (AF):
20
Modified dose descriptor starting point:
NOAEC
Value:
1 543 mg/m³
Explanation for the modification of the dose descriptor starting point:

The following correction was made to the NOAEL (oral): Correction respiratory volume rat (24 hour) 1/1.15 m³/kg bw. Correction for oral to inhaled 1/2. Alcohols, C14-15 90 d oral NOAEL = 3548 mg/kg bw/day. Therefore the corrected NOAEC for repeated-dose systemic effects via the inhalation route is: 3548*(1/1.15)*(1.2) = 1543 mg/m³

AF for dose response relationship:
1
Justification:
Default (NOAEL)
AF for differences in duration of exposure:
2
Justification:
Default (sub-chronic to chronic)
AF for interspecies differences (allometric scaling):
1
Justification:
Default (oral rat to inhalation human)
AF for other interspecies differences:
1
Justification:
The mammalian alcohol dehydrogenase system is a group of pathways which catalyse the conversion of alcohols and aldehydes, which includes different forms of the enzymes which vary in substrate specificity. The alcohol dehydrogenases (ADHs) are divided into six classes, denoted by ADH1-ADH6. Five of the six classes of alcohol dehydrogenase have been identified in humans. One of the classes, ADH3, is the ancestral form of all mammalian ADHs, and has been traced in all living species investigated. The alcohol dehydrogenase system is considered to be able to detoxify a wide range of alcohols and aldehydes without the generation of toxic radicals (Höög, J-O et al., 2001). Therefore the metabolism of all category members would be expected to follow the same pathway in rats and humans so an interspecies assessment factor to account for potential differences in metabolic pathway is not required and a value of 1 is appropriate. Reference: Höög, J-O, Hedberg, J. J., Strömberg, P., Svensson, S. (2001). Mammalian alcohol dehydrogenase - Functional and structural implications. Journal of Biomedical Science Volume 8, Issue 1, pp 71-76
AF for intraspecies differences:
10
Justification:
Default (general population)
AF for the quality of the whole database:
1
Justification:
Default (reliable study)
AF for remaining uncertainties:
1
Justification:
An assessment factor for remaining uncertainties is not required on the basis of the toxicological results: no adverse systemic effects were observed in any of the numerous reliable systemic toxicity studies that have been conducted for different endpoints for a wide range of alcohols with carbon chain lengths from C6 to C22; observations were consistent across the category. Furthermore, humans and test species are considered to respond to exposure to exogenous fatty alcohols in a similar way. Aliphatic alcohols show a chain-length dependant potential for gastro-intestinal and dermal absorption, with shorter chain aliphatic alcohols having a higher absorption potential than longer chain alcohols. Following inhalation exposure, absorption could occur for lower chain length alcohols, while little systemic exposure would be expected for the higher carbon number alcohols, from C9 upwards. Absorbed aliphatic alcohols potentially could be widely distributed within the body (OECD, 2006). As a result of the rapid and efficient metabolism, it is not anticipated that aliphatic alcohols would remain in the body for any significant length of time. Long chain (LC) fatty alcohols are synthesised within cells and are therefore found within organisms and occur naturally in the environment. Endogenous and exogenous LC alcohols are metabolised in catabolic (breakdown) and anabolic (synthesis) pathways. Cellular metabolism can cycle between LC alcohols and their corresponding acids. Alcohols are used as building blocks in the synthesis of lipids for energy storage. It is therefore concluded that, should systemic exposure occur to anthropogenic LC alcohols, mammals including test species and humans share common pathways for their metabolism and the products of metabolism are naturally-occurring metabolites. The LC aliphatic carboxylic acids are efficiently eliminated and aliphatic alcohols are therefore not expected to have a tissue retention or bioaccumulation potential (Bevan, 2001).
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

Local effects

Long term exposure
Hazard assessment conclusion:
no hazard identified
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

General Population - Hazard via dermal route

Systemic effects

Long term exposure
Hazard assessment conclusion:
DNEL (Derived No Effect Level)
Value:
44.4 mg/kg bw/day
Most sensitive endpoint:
repeated dose toxicity
Route of original study:
Oral
DNEL related information
DNEL derivation method:
ECHA REACH Guidance
Overall assessment factor (AF):
80
Modified dose descriptor starting point:
NOAEL
Value:
3 548 mg/kg bw/day
Explanation for the modification of the dose descriptor starting point:

Alcohols, C14-15 90 d oral NOAEL 3548 mg/kg bw/day  Oral rat to dermal human no correction to dose descriptor starting point required.

AF for dose response relationship:
1
Justification:
Default (NOAEL)
AF for differences in duration of exposure:
2
Justification:
Default (sub-chronic to chronic)
AF for interspecies differences (allometric scaling):
4
Justification:
Default (dermal rat to dermal human)
AF for other interspecies differences:
1
Justification:
The mammalian alcohol dehydrogenase system is a group of pathways which catalyse the conversion of alcohols and aldehydes, which includes different forms of the enzymes which vary in substrate specificity. The alcohol dehydrogenases (ADHs) are divided into six classes, denoted by ADH1-ADH6. Five of the six classes of alcohol dehydrogenase have been identified in humans. One of the classes, ADH3, is the ancestral form of all mammalian ADHs, and has been traced in all living species investigated. The alcohol dehydrogenase system is considered to be able to detoxify a wide range of alcohols and aldehydes without the generation of toxic radicals (Höög, J-O et al., 2001). Therefore the metabolism of all category members would be expected to follow the same pathway in rats and humans so an interspecies assessment factor to account for potential differences in metabolic pathway is not required and a value of 1 is appropriate. Reference: Höög, J-O, Hedberg, J. J., Strömberg, P., Svensson, S. (2001). Mammalian alcohol dehydrogenase - Functional and structural implications. Journal of Biomedical Science Volume 8, Issue 1, pp 71-76
AF for intraspecies differences:
10
Justification:
Default (general population)
AF for the quality of the whole database:
1
Justification:
Default (reliable study)
AF for remaining uncertainties:
1
Justification:
An assessment factor for remaining uncertainties is not required on the basis of the toxicological results: no adverse systemic effects were observed in any of the numerous reliable systemic toxicity studies that have been conducted for different endpoints for a wide range of alcohols with carbon chain lengths from C6 to C22; observations were consistent across the category. Furthermore, humans and test species are considered to respond to exposure to exogenous fatty alcohols in a similar way. Aliphatic alcohols show a chain-length dependant potential for gastro-intestinal and dermal absorption, with shorter chain aliphatic alcohols having a higher absorption potential than longer chain alcohols. Following inhalation exposure, absorption could occur for lower chain length alcohols, while little systemic exposure would be expected for the higher carbon number alcohols, from C9 upwards. Absorbed aliphatic alcohols potentially could be widely distributed within the body (OECD, 2006). As a result of the rapid and efficient metabolism, it is not anticipated that aliphatic alcohols would remain in the body for any significant length of time. Long chain (LC) fatty alcohols are synthesised within cells and are therefore found within organisms and occur naturally in the environment. Endogenous and exogenous LC alcohols are metabolised in catabolic (breakdown) and anabolic (synthesis) pathways. Cellular metabolism can cycle between LC alcohols and their corresponding acids. Alcohols are used as building blocks in the synthesis of lipids for energy storage. It is therefore concluded that, should systemic exposure occur to anthropogenic LC alcohols, mammals including test species and humans share common pathways for their metabolism and the products of metabolism are naturally-occurring metabolites. The LC aliphatic carboxylic acids are efficiently eliminated and aliphatic alcohols are therefore not expected to have a tissue retention or bioaccumulation potential (Bevan, 2001).
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

Local effects

Long term exposure
Hazard assessment conclusion:
no hazard identified
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified

General Population - Hazard via oral route

Systemic effects

Long term exposure
Hazard assessment conclusion:
DNEL (Derived No Effect Level)
Value:
44.4 mg/kg bw/day
Most sensitive endpoint:
repeated dose toxicity
Route of original study:
Oral
DNEL related information
DNEL derivation method:
ECHA REACH Guidance
Overall assessment factor (AF):
80
Modified dose descriptor starting point:
NOAEL
Explanation for the modification of the dose descriptor starting point:

Alcohols, C14-15 90 d oral NOAEL 3548 mg/kg bw/day  Oral rat to oral human no correction to dose descriptor starting point required.

AF for dose response relationship:
1
Justification:
Default (NOAEL)
AF for differences in duration of exposure:
2
Justification:
Default (sub-chronic to chronic)
AF for interspecies differences (allometric scaling):
4
Justification:
Default (dermal rat to dermal human)
AF for other interspecies differences:
1
Justification:
The mammalian alcohol dehydrogenase system is a group of pathways which catalyse the conversion of alcohols and aldehydes, which includes different forms of the enzymes which vary in substrate specificity. The alcohol dehydrogenases (ADHs) are divided into six classes, denoted by ADH1-ADH6. Five of the six classes of alcohol dehydrogenase have been identified in humans. One of the classes, ADH3, is the ancestral form of all mammalian ADHs, and has been traced in all living species investigated. The alcohol dehydrogenase system is considered to be able to detoxify a wide range of alcohols and aldehydes without the generation of toxic radicals (Höög, J-O et al., 2001). Therefore the metabolism of all category members would be expected to follow the same pathway in rats and humans so an interspecies assessment factor to account for potential differences in metabolic pathway is not required and a value of 1 is appropriate. Reference: Höög, J-O, Hedberg, J. J., Strömberg, P., Svensson, S. (2001). Mammalian alcohol dehydrogenase - Functional and structural implications. Journal of Biomedical Science Volume 8, Issue 1, pp 71-76
AF for intraspecies differences:
10
Justification:
Default (general population)
AF for the quality of the whole database:
1
Justification:
Default (reliable study)
AF for remaining uncertainties:
1
Justification:
An assessment factor for remaining uncertainties is not required on the basis of the toxicological results: no adverse systemic effects were observed in any of the numerous reliable systemic toxicity studies that have been conducted for different endpoints for a wide range of alcohols with carbon chain lengths from C6 to C22; observations were consistent across the category. Furthermore, humans and test species are considered to respond to exposure to exogenous fatty alcohols in a similar way. Aliphatic alcohols show a chain-length dependant potential for gastro-intestinal and dermal absorption, with shorter chain aliphatic alcohols having a higher absorption potential than longer chain alcohols. Following inhalation exposure, absorption could occur for lower chain length alcohols, while little systemic exposure would be expected for the higher carbon number alcohols, from C9 upwards. Absorbed aliphatic alcohols potentially could be widely distributed within the body (OECD, 2006). As a result of the rapid and efficient metabolism, it is not anticipated that aliphatic alcohols would remain in the body for any significant length of time. Long chain (LC) fatty alcohols are synthesised within cells and are therefore found within organisms and occur naturally in the environment. Endogenous and exogenous LC alcohols are metabolised in catabolic (breakdown) and anabolic (synthesis) pathways. Cellular metabolism can cycle between LC alcohols and their corresponding acids. Alcohols are used as building blocks in the synthesis of lipids for energy storage. It is therefore concluded that, should systemic exposure occur to anthropogenic LC alcohols, mammals including test species and humans share common pathways for their metabolism and the products of metabolism are naturally-occurring metabolites. The LC aliphatic carboxylic acids are efficiently eliminated and aliphatic alcohols are therefore not expected to have a tissue retention or bioaccumulation potential (Bevan, 2001).
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

General Population - Hazard for the eyes

Local effects

Hazard assessment conclusion:
low hazard (no threshold derived)

Additional information - General Population

In summary of the toxicological properties of tetradecan-1-ol:

Acute toxicity tests of tetradecan-1-ol do not indicate any potential hazard for acute, dermal or inhalation toxicity, and would not be classified for acute toxicity endpoint under Regulation 1272/2008 (CLP).

Tetradecan-1-ol is classified as an eye irritant (Cat 2) but is not irritating to skin. Nor is it sensitising by skin contact.

Tetradecan-1-ol is not classified for repeated dose toxicity effects (STOT-RE) or for reproductive toxicity.

In vitro and in vivo studies indicate that tetradecan-1-ol is not genotoxic.

In summary, tetradecan-1-ol is classified as an eye irritant under Regulation 1272/2008 (CLP).

On the basis of the toxicological results for tetradecan-1-ol no adverse systemic effects were observed in any of the numerous systemic toxicity studies that have been conducted for the different endpoints. Nevertheless, systemic DNEL values have been derived for systemic effects based on the highest dose tested. The DNELs are therefore indicative only and are derived as a precautionary approach to enable quantitative risk assessment with overestimation in RMM

Overall it would however be prudent to recommend the precautionary use of gloves. Studies indicate that tetradecan-1-ol is irritating to eyes. However, a DNEL for this endpoint cannot be derived and therefore quantitative risk characterisation is not possible. Instead qualitative risk characterisation is required and risk management measures (such as the limitation of concentration in consumer formulations) to minimise any potential eye contact would be required.