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Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

Short description of key information on bioaccumulation potential result: 
The toxicokinetic characteristics of linear alkylbenzene sulfonates has been extensively reviewed by the World Health Organization [1996]. The substance being registered is a higher molecular weight compound which is likely to be less readily absorbed than the compounds reviewed. The chemical characteristics of the substance are unfavorable to dermal absorption. The high vapour pressure combines with high molecular weight and high viscosity to provide evidence the substance is not volatile. Inhalation exposure would only be likely if the substance sprayed in respirable droplets, an unlikely scenario for the applications where this chemistry is used. Indicators from available toxicology studies including human health and aquatic studies suggest very low toxicity. Taken together, evidence indicates the substance is no concern for health and is not a concern for bioaccumulation.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

An evaluation of the likely ADME characteristics of alkylbenzene sulfonate salts has been developed for the substances as a class of chemicals. That assessment I provided here as appropriate and applicable to the substance being registered.


The registered substance is produced, supplied and marketed in the presence of a liquid mineral oil solvent. The primary route of exposure to such alkaryl benzene sulfonates (ABS) is therefore anticipated to be via the dermal, primarily in the manufacture, processing and professional/consumer use as lubricant additives. Given that the ABS substances are manufactured and distributed as 60/40 inseparable mixtures of ABS/diluent oil it is not clear what role the diluent oil contributes to the dermal absorption of the aforementioned substances.

Whilst there exists no specific Adsorption Distribution Metabolism and Excretion (ADME) studies to this substance, this category of substances was subject to an evaluation by theWHO (World Health Organisation) in 1996[1], and is covered extensively in the paper “Linear alkylbenzene sulfonates and related compounds. Environmental health criteria 196, Geneva. International Program on Chemical Safety. World Health Organisation.” Information on short chain ABS is primarily considered within this report; however this data is considered relevant as longer chain ABS are likely to be oxidised to shorter chain length species in vivo (reported by Michael, 1968). It is likely that the substance, being a longer chain ABS, will be absorbed generally to a lesser extent than shorter chain ABS.

Absorption, distribution metabolism and excretion

WHO (1996) reports that in experimental animals, ABS are readily absorbed via the gastrointestinal tract. In Wistar rats following oral administration, radiolabelled calcium and sodium salts of ABS with chain length of C12 were detected in plasma after 0.25 hours, with levels reaching a maximum at 2 hours. Biological half-lives were calculated at 10.9 and 10.8 hours respectively. Excretion occurred equally via urine and faeces (Sunakawa et al, 1979, as cited in WHO, 1996).

A rat study of ABS isomers of similar chain length (C12) given orally or intravenously showed differential excretion in urine and faeces depending on the position of sulfonate moieties on the benzene ring (position 2 or 6). For either route of administration, after 48 hours around 75% of position 2 isomer was found in the urine, whereas 78% of the position 6 isomer was found in the faeces. In bile duct cannulated rats following intravenous administration, 89% of the 2 isomer was recovered in the urine whilst 83% of the 6 isomer was found in the bile (Rennison et al, 1987, as cited in WHO, 1996).

In an earlier series of rat studies of radiolabelled ABS of alkyl chain lengths C10-14, 40-58% was excreted in urine and 39-56% in faeces within 72 hours of oral (gavage) administration. Orally administered radiolabelled ABS in bile duct cannulated rats showed 46% recovered in urine, 29% in faeces and 25% in bile after 90 hours. Lymph levels (< 2%) in thoracic duct cannulated rats indicated little absorption of ABS via the lymphatic system (Michael, 1968).

In contrast, dermally applied ABS of chain length C10-14 are not well absorbed. Of radiolabelled ABS applied to dorsal skin of rats for 15 minutes, none was detected in urine or faeces 24 hours after application. An accompanying in vitro study showed no measurable penetration of ABS through isolated human epidermis or rat skin 24 or 48 hours after application (Howes, 1975, as cited in WHO (1996). Similarly, of radiolabelled ABS applied in white petrolatum to the dorsal skin of guinea-pigs, only 0.1% was found in urine and 0.01% in blood and main organs after 24 hours (Hasegawa and Sato, 1978, as cited in WHO, 1996).

This conclusion is further endorsed by three dermal repeat dose studies (28 day) in rats using variousABS products (CAS no. 68610-84-4; 68783-96-0; 71786-47-5)showed a consistently low pattern of subchronic toxicity with NOELs ranging from 500-1,000 mg/kg; NOAEL=1,000mg/kg respectively, suggest either low systemic toxicity or lack of appreciable dermal transfer. Corroboration for lack of systemic toxicity is partially supported by a corresponding repeat oral dose study (28 day) in rats using 115733-09-0 in which a similarly low toxicity outcome (NOAEL=150mg/kg for females; 1,000 mg/kg for males was noted).

Three metabolism studies in rhesus monkeys by Cresswell et al. (1978) were reported in WHO (1996). After a single oral administration of radiolabelled ABS with a mean molecular weight of 349 (150 mg/kg bw), plasma concentrations peaked at 41.2 μg/mL at 4 hours. Concentrations declined during the period 6-24 hours with a biological half-life reported to be approximately 6.5 hours. Concentrations were below the limit of detection at 48 hours.

Similar results for peak plasma levels and half-life were found following 7 consecutive daily oral doses of ABS at 30 mg/kg bw. In the monkeys, the highest concentration of radiolabelled ABS 2 hours after the last dose was found in the stomach (239 μg/g). At this time, high concentrations were found also in the intestinal tract, kidney and liver. Moderate levels were seen in the lungs, pancreas, adrenal and pituitary glands. At 24 hours, high levels seen in the intestinal tract (256 μg/g) and liver were the only levels that exceeded that of plasma. Levels in other tissues lower than plasma indicated no specific tissue-specific accumulation or localisation of ABS and/or metabolites (Cresswell et al, 1978).

After 7 subcutaneous doses of radiolabelled ABS (1 mg/kg bw/day) highest levels were seen at injection sites (114 μg/g) after 2 hours. At this time, levels between 1 and 2.45 μg/g were seen in the lungs, intestinal tract, spleen, kidney, thyroid and pituitary gland. At 4 hours, tissue levels were generally lower than at 2 hours except for the intestinal tract, kidney and liver, these latter two organs associated with biotransformation and excretion. Levels in the intestinal tract were attributable to biliary excretion. At 24 hours, skin injection sites were the only tissue sites for which levels exceeded that of plasma (Cresswell et al, 1978).

A study of the excretion of single oral or subcutaneous doses of radiolabelled ABS in the rhesus monkey showed almost all but approximately 6% of the oral ABS and around 25% of the subcutaneous ABS excreted via urine or faeces within 120 hours. In both instances, excretion occurred predominantly (up to 74%) via the urine (Cresswell et al, 1978).


For three additional metabolism studies identified in the open literature, a five week oral study using 14C labeled dodecylbenzene sulfonate (DoDBS) in rats is also relevant to assess the potential ADME characteristics of ABS. In this study, 81.8% of administered DoDBS was excreted during the dosing period; 52.4 and 29.4 % in the faeces and urine respectively. Low levels of DoDBS were detected in all tissues on termination of the study. A tangential study using a single i.p. injection resulted in the total elimination of 94.5% within 10 days with 84.7% being eliminated in the first 24 hours.

According to Michael (1968), the main metabolites from an orally administered radiolabelled mixture of C10-14 ABS in rats were sulfophenyl butanoic acid and sulfophenyl pentanoic acid, formed via ω-oxidation and ß-oxidation of the parent ABS molecules. From thin layer chromatography, these two molecules were also claimed to be the two metabolites found in urine and two of the four metabolites found in faeces in a subsequent test of oral administration of radiolabelled calcium or sodium salts of ABS in rats (Sunakawa et al, 1979, as cited in WHO, 1996).

In rhesus monkeys, thin layer chromatography of urine samples following oral (30 mg/kg bw) or subcutaneous (1 mg/kg bw) administration of radiolabelled ABS showed 5 metabolites (unidentified) and only trace quantities of the original parent compound (Cresswell et al, 1978).

Overall, given the relatively increased hydrophobicity of the higher chain commercial ABS substances, expected low transdermal penetration based on low dermal subchronic toxicity and high levels of metabolism followed by excretion of metabolites, there is little support for significant systemic bioaccumulation of this substance within the body.

[1]             ISBN 9241571691, Linear Alkylbenzene Sulfonates and Related Compounds