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Administrative data

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Description of key information


Substance is Benzenesulfonic acid, mono-C10-13-alkyl derivatives, compounds with N1,N1-dimethyl-1,3-propanediamine, CAS No 1093628-27-3. We have no specific toxicokinetics data for this salt.


This salt is manufactured from Benzenesulfonic acid, mono-C10-13-alkyl derivatives CAS No 1093628-26-2 neutralised with 1,3-Propanediamine, N1,N1-dimethyl (EINECS name 3-Aminopropyldimethylamine) CAS No 109-55-7.


It is anticipated that there would dissociation of the test substance in the stomach due to the high pH, therefore the test animals would be exposed to both substances.

For both substance parts much data is available:

Benzenesulfonic acid, mono-C10-13-alkyl


C10 140-60-3 4-Decylbenzenesulfonic acid

C11 50854-94-9 Benzenesulfonic acid, undecyl-

C12 121-65-3 p-Dodecylbenzenesulfonic acid

C13 25496-01-9 Benzenesulfonic acid, tridecyl-


Much information is available on alkylbenzene sulphonic acid (LAS), sodium salt, in general considering chain lengths between C10-C13.

Linear benzene sulfonates


Studies in Animals

The absorption, distribution, metabolism and elimination of LAS has been studied in several species, including rats, mice, guinea pigs, pigs, and rhesus monkeys (Debane 1978; Michael 1968; Havermann and Menke 1959; Cresswell et al. 1978; Sunakawa et al. 1979). LAS was administered either topically (i.e., dermally) or orally. Results showed that LAS can be absorbed from the gastrointestinal tract. 

Absorbed LAS is then metabolized and excreted without accumulation in the major tissues or fat. Debane (1978) found that when 0.2 to 0.5% LAS was topically applied once to the back skin of rats and guinea pigs, approximately 0.1 to 0.6% was absorbed. No accumulation was observed in specific organs and LAS was quickly excreted in the urine after being metabolized. IPCS (1996) notes that prolonged contact with the skin may compromise the integrity of the epidermal barrier, thereby potentially permitting greater absorption from this route. Michael (1968) found that LAS administered orally as an aqueous solution was readily absorbed from the gastrointestinal tract (80-90% of the dose). Most of the absorbed dose was eliminated within 72 hours and 60-65% was eliminated via the urine, with sulfophenyl butanoic and sulfophenyl pentatonic acid as metabolites. Approximately 35% of the absorbed dose was excreted in the bile. Although the metabolites in the bile were not identified, it was shown that no unchanged LAS was eliminated via this pathway. In oral studies with pigs, Havermann and Menke (1959) found that at 200 hours after oral administration, the radiolabelled LAS was relatively high in bristles and bones, while low in liver, kidney and spleen. After 10 weeks only traces of radioactivity were still in the body. At 40 hours after administration, 40% of the dose was excreted into the urine and 60% of the dose via the faeces. In another study (Sunakawa et al. 1979), rats were dosed orally with 14C-LAS and radioactivity was detected 0.25 hours after administration, reaching a maximum at 2 hours. The biological half-life was calculated to be 10.9 hours. The distribution was high in the digestive tract and in the bladder at 4 hours after administration, with high concentrations also found in the liver, kidney, testis, spleen and lung. At 168 hours after administration, the rates of excreted radioactivity were 47% in the urine and 50% in the faeces.

Toxicokinetics has also been studied in adult rhesus monkeys (Cresswell et al. 1978). Two male and two female monkeys were given single or repeated oral (30, 150 or 300 mg/kg) or subcutaneous (0.1, 0.5 or 1 mg/kg) doses of 14C-LAS. For example, after single 30 mg/kg oral doses, the radioactivity was rapidly excreted, mostly during the first 24 hours. Means of 71.2% and 23.1% of the dose were excreted in the urine and faeces, respectively, during 5 days. During seven consecutive daily (30 mg/kg/day) or subcutaneous (1 mg/kg/day) doses, there was no accumulation of radioactivity in plasma. Mean peak concentrations and biological half-lives were similar after the first and seventh doses. No unchanged LAS was detected in the urine after oral or subcutaneous doses. Five metabolites were excreted but they were not identified.

Studies in Humans

Studies were conducted with isolated human skin preparations using two solutions of C12 LAS (Howes 1975). The results demonstrated that penetration through the skin and subsequent absorption does not occur to any significant extent (less than 1%) at 24 to 48 hours.


Debane, C. 1978.  National Hygiene Laboratory; in: "Report on Studies on Synthetic Detergents", October 1978, Japan's Science and Technology Agency [in Japanese].

IPCS. 1996. Environmental Health Criteria 169: Linear Alkylbenzene Sulfonates and Related Compounds. World Health Organization, Geneva, Switzerland.

Michael, W.R. 1968. Metabolism of linear alkylate sulfonate and alkylbenzene sulfonate in albino rats. Toxicology and Applied Pharmacology. 12:473-485.  

Havermann, H. and Menke, K.H. 1959. Biological study of the water-soluble surface-active substances. Fette. Seifen. Anstrichmittel 61:429-434. (in German); cited in IPCS. 1996. Environmental Health Criteria 169: Linear Alkylbenzene Sulfonates and Related Compounds. World Health Organization, Geneva, Switzerland. Original article in Japanese.

Sunakawa, T., Ikida, Y. and Okamoto, K. 1979. Absorption, distribution, metabolism, and excretion of linear alkylbenzene sulfonate in rats. J. Jpn. Oil Chem. Soc. 39:59-68 (in Japanese); cited in: IPCS (1996); Environmental Health Criteria 169: Linear Aklylbenzene Sulfonates (LAS) and Related Compounds. WHO, Geneva, Switzerland.

Cresswell, D.G., Baldock, G.A., Chasseaud, L.F. and Hawkins, D.R. 1978. Toxicology studies of linear alkylbenzene sulphonate (LAS) in rhesus monkeys. II. The disposition of [14C] LAS after oral or subcutaneous administration. Toxicology. 11:5-17.

Howes, D. 1975. The percutaneous absorption of some anionic surfactants. J. Soc. Cosmet. Chem. 26:47-63.



1,3-Propanediamine, N1,N1-dimethyl, CAS: 109-55-7


Mw = 102.18

Formulae.: C5-H14-N2



No studies on the metabolism of DMAPA were identified in the available literature. In general, lower primary aliphatic amines are metabolized to the corresponding carboxylic acid and urea. The tertiary site would be expected to be more resistant to metabolism (Williams, 1959).

3-Aminopropyldimethylamine has been found to be harmful following oral administration to rats. Based on the results of the sensitisation test on the skin 3-Aminopropyldimethylamine has been classified as having a sensitising effect. 3-Aminopropyldimethylamine showed strong irritating or corrosive effects. In an oral 28-day subchronic toxicity study with rats, the no-observed-adverse effect-level (NOAEL) was 50 mg /kg bw/day. In the oral reproduction/developmental toxicity screening test the no-observed-adverse effect-level (NOAEL) was 50 mg /kg bw/day. In the oral reproduction/developmental toxicity screening test the no-observed-adverse effect-level (NOAEL) was 200 mg/kg bw/day. 3-minopropyldimethylamine was not mutagenic in the Ames Test and in a mouse micronucleus assay. The corrosive property of the compound prompts workers to limit the potential exposure to this chemical. (OECD SIDS 2003)



Williams, R.T. (1959) The metabolism of aliphatic amines and amides and various compounds derived from them. In:Detoxication Mechanisms. The Metabolism and Detoxication of Drugs, Toxic Substances and Other Organic Compounds, 2nded., London, Chapman & Hall, Ltd., p 128


OECD SIDS (2003) 3-aminopropyldiethylamine CAS No: 109-55-7

Key value for chemical safety assessment

Bioaccumulation potential:
low bioaccumulation potential
Absorption rate - oral (%):
Absorption rate - dermal (%):
Absorption rate - inhalation (%):

Additional information