Benzene, mono-C10-13-alkyl derivs., distn. residues

Endpoint summary

Description of key information

Specific data on the absorption, distribution, elimination, and the potential for accumulation of Benzene, mono-C10-13-alkyl derivs., distn. residues (HAB) in the body are not available.  However, metabolism data on linear alkyl chains includes conversion of the terminal carbons of linear alkyl chains (alkanes) to carboxylic acids followed by metabolism of the resulting fatty acids.  Degradation of alkanes is a widespread phenomenon in nature, and numerous microorganisms capable of utilizing these substrates as a carbon and energy source have been isolated and characterized (Wentzel, A., Ellingsen, T.E., Kotlar, H.-K., Zotchev, S.B. and Throne-Holst, M.  2007. Bacterial metabolism of long-chain n-alkanes.  Appl. Microbiol. Biotechnol. 76:1209-1221).  Extensive knowledge of the microbiology of long-chain n-alkanes degradation has been accumulated.  In the most described cases, the n-alkane is oxidized to the corresponding primary alcohol by substrate-specific terminal monooxygenases/ hydroxylases.  Subterminal oxidation has also been described both for long-chain n-alkane substrates up to C16 and for n-alkanes of shorter chain lengths (Wentzel et al. 2007).

After initial oxidation of the n-alkane, the corresponding alcohol is subsequently oxidized further by alcohol dehydrogenases and aldehyde dehydrogenase to the corresponding aldehyde and carboxylic acid, respectively. The carboxylic acid then serves as a substrate for acyl-CoA synthetase, and the resulting acyl-CoA enter the β-oxidation pathway (Wentzel et al 2007).  Rates of these reactions vary depending on the composition of the mixtures and other factors.

It should be noted that this mechanism of linear alkyl chain metabolism applies to the initial metabolism of HAB, mainly to the linear alkyl chains of each component structure, but does not imply complete metabolism of the resulting aromatic alkyl carboxylic acids.  The data for Benzene, C10-13-alkyl derivs. (LAB) suggest that, in fish at least, the phenyl alkyl carboxylic acids are rapidly excreted. This metabolism and excretion mechanism, suggesting low bioaccumulation potential, is expected to cover all of the components of HAB because all contain at least one linear alkyl chain with unblocked terminal carbons that are known substrates for terminal monooxygenases/hydroxylases as described by Wentzel et al. (2007).

This mechanism has been demonstrated as the biotransformation mechanism for Benzenesulfonic acid, 4-C10-13-sec-alkyl derivs. (LAS), the sulfonated derivative of LAB (OECD. 2005. SIDS Initial Assessment Profile.  SIDS Initial Assessment Report.  Linear Alkylbenzene Sulfonate.  CAS No. 123-01-3 and 6742-54-7.  April 2005).  HAB is expected to be subject to similar metabolism due to the presence on all HAB components of C10-C14 linear alkyl chains with unhindered terminal carbons similar to those in LAB (and LAS).  This mechanism is consistent with the rapid elimination rate observed for LAB in bluegill sunfish as described in the bioaccumulation section above.  While no specific data are presented, HABs also would be subject to biotransformation by this metabolic mechanism, based on the presence of C10-C14 linear alkyl chains with unhindered terminal carbons in all structures.  However, given the complexity of the HABs, the rate of metabolism cannot necessarily be easily read across from the other compounds.

Thus, the metabolism and biodegradation data on linear alkyl chains as well as LAS and LAB, indicate that HAB will undergo metabolism and degradation in biological systems.