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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Link to relevant study record(s)

Description of key information

Key value for chemical safety assessment

Additional information

No experimental data are available for the assessment of the toxicokinetics, metabolism and distribution of tetrahydrogeraniol.

Based on its physicochemical properties, i.e. small molecular weight, moderate LogPow and low to moderate water solubility at room temperature (MW=158.28, Log Kow = 3.9; Water solubility = 64 mg/L), tetrahydrogeraniol is considered to become readily bioavailable via the dermal and oral route. In acute dermal toxicity studies in rabbits, dermal administration of tetrahydrogeraniol resulted in systemic toxicity including mortality providing an indication for relevant dermal absorption. On the basis of the low vapour pressure at room temperature (Vapour pressure=1.44 Pa), the exposure via inhalation of tetrahydrogeraniol as a vapour is low.

According to the OECD SIDS for members of the Oxo Alcohols C9 to C13 Category as structurally analogs to tetrahydrogeraniol,  linear and branched chain alcohols exhibit similar patterns of absorption, metabolism, and excretion. Both linear and branched aliphatic alcohols are absorbed through the gastrointestinal tract and are rapidly eliminated from the blood. Plasmatic half-lives are normally difficult to measure since many of the low molecular weight metabolites (e.g. aldehydes, carboxylic acids) are endogenous in humans. Linear and branched chain alcohols are initially oxidized to their corresponding aldehydes and further to their corresponding carboxylic acids by high capacity NAD+/NADH-dependent enzymes, which are then metabolized to carbon dioxide via the fatty acid pathways and the tricarboxylic acid cycle. Alcohol dehydrogenase (ADH) enzymes are the cytosolic enzymes that are primarily responsible for the oxidation of alcohols to their corresponding aldehydes. Alcohols also can be oxidized to aldehydes by non-ADH enzymes present in the microsomes and peroxisomes, but these are generally quantitatively less important than ADH. Aldehyde dehydrogenases (ALDH) oxidize aldehydes to their corresponding carboxylic acids. Branched-chain aliphatic alcohols and aldehydes have been shown to be excellent substrates for ADH and ALDH. As carbon chain length increases, the rates of ALDH-mediated oxidation also increase. The metabolism of branched-chain alcohols, aldehydes, and carboxylic acids containing one or more methyl substituents is determined primarily by the position of the methyl group on the branched-chain. Higher molecular weight homologues (>C10) may also undergo a combination of ω, ω-1 and β-oxidation and selective dehydrogenation and hydration to yield polar metabolites which are excreted as the glucuronic acid or sulfate conjugates in the urine and, to a lesser extent, in the feces. Thus, the principal metabolic pathways utilized for detoxification of these branched-chain substances are determined primarily by four structural characteristics: carbon chain length, and the position, number, and size of alkyl substituents. Most of the substances in the Oxo Alcohols C9 to C13 category are mixed branched-chain alcohols. Based on the similar metabolism of linear and branched-chain alcohols within this carbon number range, it can be concluded that the members of the Oxo Alcohols C9 to C13 category will undergo metabolism similar to those of the analogue linear substances mentioned above (SIDS INITIAL ASSESSMENT PROFILE, attached to 7.12).