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The following remarks on secondary alkane sulfonates (SAS) are based on physicochemical properties of the compound and on toxicological data. Experimental toxicokinetic studies were not performed.

Paraffin oil, sulfochlorinated, saponified is a solid, white to yellowish substance (Lanxess, 2009) under normal ambient conditions with a very low vapour pressure (probably < 0.0001 Pa at 20°C, Laus GmbH, 2010), therefore vapour inhalation is an unlikely route of exposure.

The physicochemical data of the substance (UVCB; molecular weight range: approx. 315 – 343 g/mol; highly soluble in water: 469 g/l, Currenta 2010; estimated log Pow: 2.27, Currenta, 2010) suggest intestinal absorption subsequent to oral ingestion. However, no indications of systemic availability could be concluded from repeated dose studies, conducted with a structurally similar read across substance, where only unspecific effects have been reported (chronic feeding study: Ben-Dyke, 1977; study on reproductive function and intrauterine development: Tesh, Davidson, Newman, Levene, 1978). In fact, paraffin oil, sulfochlorinated, saponified, is an anionic surfactant, and is therefore expected to form negatively charged aggregates, so-called micelles (K. Holmberg, B. Jönsson, B. Kronberg, B. Lindman in “Surfactants and Polymers in aquous solution”, John Wiley & Sons Ltd., 2003) in the gastrointestinal fluid, which is probably prohibitive for the penetration through intestinal membranes. The formation of micelles should similarly lead to a negligible systemic availability after dermal exposure. In fact, no systemic availability could be concluded from an acute dermal toxicity study, where the LD50 was > 2000 mg/kg bw (OECD TG 402, Pößnecker, 1991).

Regarding the chemical nature of the substance, paraffin oil, sulfochlorinated, saponified, consists of a secondary aliphatic sulfonate and a counterion. The sulfonate is expected to have weak basic properties after contact to water or moisture, therefore the substance is assumed to have at least slight irritating properties. This was proven in acute studies (OECD TG 404, Pößnecker 1991; OECD TG 405, Maertins 1991, OECD TG 402, Pößnecker 1991).

The available in vitro and in vivo genotoxicity tests (OECD TG 471: Klunker, 1992; OECD TG 476: Wallner, 2010, OECD TG 474: Baeder/Weigand, 1978) indicate that DNA-reactive metabolites most probably will not be generated in mammalian organisms due to hepatic biotransformation.