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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Short description of key information on bioaccumulation potential result:  No toxicokinetics and metabolism data are available for SAS or long chain LAS. SAS, being structurally similar to a long chain LAS, is likely to be oxidized to shorter chain length species in vivo. SAS is composed of both linear and branched alkyl chains, sulfonated in multiple places, and according to Michael (1968) systemically absorbed SAS would expected to some extent to be metabolized by omega/beta oxidation; the extent of metabolism may depend on the level of branched alkyl chains.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

No data exist on SAS or on similar long-chain Linear Alkylbenzene Sulfonate (LAS). However data are available for shorter chain LAS, which is likely to be more bioavailable than SAS (see below). If some of SAS linear and branched alkyl chains are bioavailable one would expect that their distribution, metabolism and excretion would be similar to shorter chain LAS. Therefore, toxicokinetic information on short chain LAS is considered in this section:

Studies on experimental animals have shown that short-chain LAS is readily absorbed, distributed throughout the body, and extensively metabolized. The parent compound and metabolites are excreted primarily via the urine and feces, although there are marked differences between the metabolite isomers in the route of excretion. The main urinary metabolites identified in rats are sulfo-phenylbutanoic acid and sulfophenylpentanoic acid, which are probably formed through omega-oxidation followed by beta-oxidation of LAS, although the metabolic pathways in primates may differ.

SAS has a high molecular weight compared to the sulfonates tested in the toxicokinetics studies described in Table 9, and because of this high molecular weight and low water solubility, it is probable that SAS will be absorbed generally to a much lower extent than shorter chain LAS. The low bioavailability of SAS is supported by the absence of significant toxicological effects following oral and inhalation administration of SAS (in the acute oral and inhalation toxicity studies and repeat dose oral toxicity study) which suggests that absorption from the gastrointestinal and respiratory tracts is minimal. In addition, acute dermal and inhalation studies on structural surrogates support this low bioavailability from other exposure routes as indicated by 4-hr LC50 that ranged from >1.9 to >50 mg/L; and a dermal LD50 of >2,000 mg/kg (ACC, 2005).

No dermal toxicokinetic studies on structural surrogates were available. Subcutaneous studies conducted in monkeys exposed either one time or single daily doses for 7 consecutive days showed that most of the dose is excreted in the urine and faeces within 48 hrs (Creswell et al, 1978). In addition, the high molecular weight (MW > 500) suggests minimal dermal absorption.