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Description of key information

In a reliable co- carcinogenicity study by Ando (1969; rel 2), the co-carcinogenicity potential of dodecan-1-ol was investigated in mice. The study concluded that treatment with dodecan-1-ol extended the survival time of mice implanted intraperitoneally with Ehrlich ascites tumour cells. In addition other numerous carcinogenic-related studies involving dodecan-1-ol do not indicate any carcinogenic potential; although reporting is limited and the reliability is poor in some of them.

Key value for chemical safety assessment

Carcinogenicity: via oral route

Endpoint conclusion
Endpoint conclusion:
no study available

Carcinogenicity: via inhalation route

Endpoint conclusion
Endpoint conclusion:
no study available

Carcinogenicity: via dermal route

Endpoint conclusion
Endpoint conclusion:
no study available

Justification for classification or non-classification

Based on the weight of evidence, thedata is waived as testing is not a scientifically necessary option.

Additional information

Although Column 2 of REACH Annex X requires a carcinogenicity study (required in Section 8.9.1) if the substance has a wide dispersive use, the weight of evidence across the category suggests that dodecan-1-ol is not carcinogenic. This is based on a large set of various types of repeated dose studies across the category which do not offer any evidence of treatment-related induction of hyperplasia / pre-neoplastic lesions for dodecan-1-ol or structurally related alcohols (though reporting is limited in many cases). In addition, dodecan-1-ol does not have any genotoxic effects.

Hexan-1-ol, octan-1-ol, decan-1-ol, dodecan-1-ol, tetradecan-1-ol, hexadecan-1-ol and octadecan-1-ol were tested in one or more mouse skin painting studies using applications two to three times weekly for periods up to sixty to seventy weeks. Development of local skin tumours was not reported in any of these assays. All of these experiments were conducted as part of investigative studies into co-carcinogenicity or tumour promotion properties of LCAAs (Sicé, 1966; Bingham, 1969; Van Duuren, 1976).

The aliphatic alcohols were applied repeatedly over periods up to 60 weeks to the skin of mice that had been initiated or were co-exposed with carcinogens such as 7, 12-dimethylbenz(a)-anthracene or benzo(a)pyrene (B(a)P). In most of the experimental protocols the application of aliphatic alcohols induced significant dermal irritation at the site of treatment and led to formation of local tumours; in some cases a decrease in latency of tumour development or co-carcinogenicity was reported (Sicé, 1966; Van Duuren et al., 1976; Bingham, 1969).

Discussion of trends in the Category of C6-24 linear and essentially-linear aliphatic alcohols:

Several members of the category of the LCAAs have been tested as control substances in skin painting studies. Even taking into account the limitations of these experiments, the data show that none of aliphatic alcohols tested have a potential to induce local skin tumours upon repeated dermal application at or above the maximum tolerated (irritant) dose. However, these data are unsuitable to assess properties such as co-carcinogenicity or tumour promotion for this category. Most of the study protocols considered here have almost certainly induced considerable local effects, however details of the irritation responses are limited and were reported only in a few cases. Irrespective of the causative agent, irritation at the site of application is a significant confounder in skin painting studies and its role in the tumour development of non-genotoxic chemicals has been well established (for examples see Nessel et al., 1998, 1999; Argyris, 1985). LCAAs are non-genotoxic and lack structural elements of concern for interaction with DNA (Ashby and Tenant, 1991). Together with the lack of response upon repeated application the skin painting studies LCAAs are regarded to be of little concern regarding carcinogenicity. The large set of various types of repeated dose studies across the category which do not offer any evidence of treatment-related induction of hyperplasia/pre-neoplastic lesions for any of the structurally related alcohols (though reporting is limited in many cases), and the lack of genotoxic effects demonstrated across the category, suggest that none of the category members are likely to be carcinogenic. A full discussion of the Category and considerations of RAAF Assessment Entities can be found in the Human Health Alcohols C6-24 Category report (PFA, 2016).


Argyris T.S. 1985, Regeneration and the mechanism of epidermal tumor promotion. Crit Rev Toxicol: 14(3):211-58.

Ashby, J., Tennant, R.W., 1991. Definitive relationships among chemical structure, carcinogenicity, and mutagenicity for 301 chemicals tested by the US NTP. Mutation Research 257, 229–306.

Bingham, E. and Falk, H.L. 1969. Environmental carcinogens: the modifying effect of cocarcinogens on the threshold response. Arch. Environ. Health 19:779-783.

Nessel, C.S., Freeman, J.L et al. 1999. The role of dermal irritation in the skin tumor promoting activity of petroleum middle distillates. Toxicological Sciences 49: 48-55.

Nessel, C.S.; Priston, R.A.J.; et al. 1998 A comprehensive evaluation of the mechanism of skin tumorigenesis by straight-run and cracked petroleum middle distillate. Toxicological Sciences 44: 22-31.

Sicé, J., 1966. Tumor-promoting activity of n-alkanes and l-alkanols. Toxicology and Applied Pharmacology 9:70-74.

Van Duuren, B.L. and Goldschmidt, B.M. 1976. Cocarcinogenic and tumor-promoting agents in tobacco carcinogenesis. Journal of the National Cancer Institute 56(6):1237-1242.