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No experimental data is available on the bioaccumulation potential of the target substance fatty acids, C16-18, isononyl esters (CAS 91031-57-1). Therefore, all available related data is combined in a Weight of Evidence (WoE) approach, in accordance with the REACh Regulation (EC) No 1907/2006, Annex XI General rules for adaptation of the standard testing regime set out in Annexes VII to X, 1.2, to cover the data requirements of Regulation (EC) No. 1907/2007 Annex IX and X (ECHA guidance section R.7.11.5.3, page 121).

Bioaccumulation refers to the uptake of a substance from all environmental sources including water, food and sediment. However, the accumulation of a substance in an organism is determined not only by uptake, but also by distribution, metabolism and excretion. Accumulation takes place if the substance is taken up faster than it can be metabolised and/or excreted.

In the case of the target substance fatty acids, C16-18, isononyl esters (CAS 91031-57-1), uptake of dissolved substance via water is expected to be low due to its poor water solubility (< 13.3 µg/L), high adsorption potential (log Koc > 5.0, KOCWIN v2.0) and ready biodegradability. According to Chapter R. 7b, “Endpoint specific guidance” (ECHA, 2016) a positive result in a test for ready biodegradability can be considered as indicative of rapid and ultimate degradation in most environments, including biological sewage treatment plants. Therefore, environmental concentrations of the substance are likely very low. Whatever fraction reaches the aquatic environment is expected to undergo rapid biodegradation and sorption to particles in soils and sediment, thereby reducing the bioavailability of the substance in the water phase. Thus, no significant uptake through the water phase is expected.

Consequently, the main potential route of uptake by aquatic organisms such as fish and sediment-dwelling organisms is likely to occur via contact with and ingestion of solid particles and contaminated sediment. In case of ingestion, it is known from literature that esters and their metabolites are readily metabolized. Esters of primary alcohols, containing 1 to 18 carbon atoms, with fatty acids containing 2 to 18 carbon atoms, have been shown to be hydrolysed by pancreatic lipases (Mattson and Volpenhein, 1972). Measured rates of enzymatically catalysed hydrolysis varied between 2 and 5 µeq/min/mg enzyme for different chain lengths (IUCLID section 7.1.1, Mattson and Volpenhein, 1972; and references therein). Only moderate differences in the rate of hydrolysis were observed for saturated and unsaturated fatty-acid esters of different chain lengths in studies investigating the fatty acid specificity of pancreatic lipases (Macrae and Hammond, 1985; and references therein). The resulting free fatty acids and alcohols are absorbed from the intestine into the blood stream. The alcohols are metabolised primarily in the liver through a series of oxidative steps, finally yielding carbon dioxide (Berg, 2001; HSDB).

Fatty acids are either metabolised via the beta-oxidation pathway in order to generate energy for the cell or reconstituted into glyceride esters and stored in the fat depots in the body (Berg et al., 2001). For fatty acids composed of up to 22 carbon atoms, beta-oxidation generally takes place in the mitochondria, resulting in the final product acetyl-CoA, which directly enters the citric acids cycle (Berg, 2002). Beta-oxidation of longer fatty acids takes place in the peroxisomes and is incomplete (Reddy and Hashimoto, 2001; Singh et al., 1987; Le Borgne and Demarquoy, 2012; and references therein), giving rise to medium chain acyl-CoA, which are then taken in charge by the carnitine octanoyl transferase and converted into acyl-carnitine that can leave the peroxisome and, at least some of them, can be fully oxidized in the mitochondria (Le Borgne and Demarquoy, 2012; and references therein). Peroxisomal β-oxidation has also been shown to take place in fish, mussels and algae (Rocha et al., 2003; and references therein; Frøyland et al., 2000; Bilbao et al., 2009; Winkler et al., 1988). Metabolic pathways in fish are generally similar to those in mammals. Lipids and their constituents, in particular fatty acids, are major organic constituents of fish and play major roles as sources of metabolic energy (Tocher, 2003).

Studies conducted with rats indicate that the main route of excretion in rats is via expired air in the form of CO2, and the second route of excretion is by biliary excretion and faeces. Exemplarily, experimental data of ethyl oleate (the ethyl ester of oleic acid) support this assumption: 14C-labeled carbon of 5 mL/kg of ethyl oleate (CAS No. 111-62-6) was rapidly excreted in respiration CO2 (approximately 70%), faeces (7 -10%), and urine (1-2%), with complete elimination within 72 hours after administration (Bookstaff, 2003).

In conclusion, the target substance fatty acids, C16-18, isononyl esters (CAS 91031-57-1) will be mainly taken up by ingestion and is digested through common metabolic pathways, providing a valuable energy source for the organism, such as dietary fats. The substance is thus not expected to bioaccumulate in aquatic or sediment organisms.

Biotransformation and biomagnification are processes that may occur once a chemical has bioaccumulated. As this substance is readily biodegradable and is considered to be rapidly metabolised, fatty acids, C16-18, isononyl esters (CAS 91031-57-1) will not be biomagnified within the food chain. Hence, fatty acids, C16-18, isononyl esters (CAS 91031-57-1) is not expected to pose a risk to organisms in regard to bioaccumulation/biomagnification. Therefore, and for reasons of animal welfare, further testing is neither considered necessary nor proposed.

The available literature supporting the assessment of bioaccumulation is presented in the IUCLID technical dossier and associated chemical safety report in a Weight of Evidence (WoE) approach, which is in accordance with the REACh Regulation (EC) No 1907/2006, Annex XI General rules for adaptation of the standard testing regime set out in Annexes VII to X, 1.2, to cover the data requirements of Regulation (EC) No. 1907/2007 Annex IX and X (ECHA guidance section R.7.11.5.3, page 121).