Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 293-917-2
CAS number: 91648-55-4
Table 1: Data availability for toxicokinetics, metabolism and
C11ASO4KCAS not available
Table 2: Metabolites formed from alkyl sulfates with even chain
4-butyrolactone (ring structure)
Glycolic acid sulfate
Major MetaboliteFound in rats, dogs, humans
Minor metaboliteFound in rats, dogs, humans
Minor metaboliteFound in dogs (and humans)
* investigated substances were potassium
salts of C10, C12, C14& C18alkyl
Table 3: Influence of chain length on elimination of alkyl sulfates
Number of animals, sex*
Recovery from urine at 48 h (% of dose)*
Recovery from feces at 48 h (% of dose)*
Recovery from carcass at 48 h (% of dose)*
* mean number of number of animals indicated, all values are mean
values; ** n.a. = not available; 5 mg/kg bw of the35S labeled
compounds was applied i.p. to MRC rats
behaviour of alkyl sulfates was assessed. Alkyl
well absorbed after ingestion. After absorption, these chemicals are
distributed mainly to the liver. Alkyl sulfates are metabolized by
cytochrome P450-dependent w-oxidation
and subsequent beta-oxidation of the aliphatic fatty acids. End products
of the oxidation are a C4sulfate and a C3or C5sulfate.
In addition, for the alkyl sulfates, sulfate is formed as a metabolite.
The metabolites are rapidly excreted in urine. Due
to the low concentrations of the substances in consumer products and the
limited uptake after dermal exposure which is the main route for
consumers, significant exposure of the developing foetus via the
placenta or the neonate via the breast milk is not likely. Therefore a bioaccumulation
of alkyl sulfates is not expected.
Absorption: 100% via oral route, 1% via dermal route
Distribution: Unquantified amounts of three different alkyl sulfates
were found only in the kidney and the liver.
Metabolism: Alkylsulfates have a common metabolic fate that involves
omega- and beta-oxidation to the respective C2 and C4 (even numbered AS)
and the C3 and C5 (odd numbered AS). The oxidation products are mainly
sulfated and excreted. C2-fragments may enter the C2 pool of the body
and are either oxidized to CO2 or found in the body. Hydrolysis of the
ether bond between the fatty alcohol and the sulfate chain may occur to
a small degree. About 10 to 20% of the dose usually is eliminated as
Excretion: The majority was excreted via urine. Only smaller amounts are
excreted via the faeces. Elimination is fastest for C12 (complete within
approx. 6 h) but decreases for other chain length.
To draw a coherent picture of the toxicokinetic, metabolism and
distribution of the various members of the alkyl sulfates this endpoint
is covered by read across to structurally related alkyl sulfates (AS).The
possibility of a read-across to other alkyl sulfates in accordance with
Regulation (EC) No 1907/2006 Annex XI 1.5. Grouping of substances and
read-across approach was assessed. In Annex XI 1.5 it is given that a
read-across approach is possible for substances, whose physicochemical,
toxicological and ecotoxicological properties are likely to be similar
or follow a regular pattern as a result of structural similarity. The AS
reported within the AS category show structural similarity. The alkyl
chain length in the alkyl sulfate category varies from C8 to C18. In
addition most chemicals of this category are not defined substances, but
mixtures of homologues with different alkyl chain lengths (UVCBs). The
most important common structural feature of the category members is the
presence of a predominantly linear aliphatic hydrocarbon chain with a
polar sulfate group, neutralized with a counter ion. This structural
feature confers the surfactant properties of the alkyl sulfates. The
surfactant property of the members of the AS category in turn represent
the predominant attribute in mediating effects on mammalian health. Due
to the structural similarities also the disposition within the body is
comparable throughout the category. The AS of the AS category also have
similar physico-chemical, environmental and toxicological properties,
validating the read across approach within the category. The approach of
grouping different AS for the evaluation of their toxicokinetics,
metabolism and distribution as well as their effects on human health and
the environment was also made by the OECD in the SIDS initial assessment
profile  and by a voluntary industry programme carrying out Human and
Environmental Risk Assessments (HERA [2). Data reported within the
discussion below summarize the information of the SIDS and HERA reports.
After oral administration, alkyl sulfates are well absorbed in rats,
dogs and humans (SIDS, 2007). This was indicated by excretion of up to
98% of the dose administered (maximum for C12 AS Na) in the urine and by
comparison of excretion after oral and i.v. or i.p. application for
several alkyl sulfates. Hence, oral absorption is assumed to be 100%.
Absorption by the percutaneous route is limited, since anionic
surfactants tend to bind to the skin surface (SIDS, 2007). Early studies
with isolated human skin were unable to detect penetration of a
homologous series of AS, ranging from C8 to C18 carbon chain lengths.
Animal studies confirmed a low level of percutaneous absorption of AS.
Less than 0.4% of a 3 μmol dose of 35S-labeled C12 AS Na was
percutaneously absorbed in guinea pigs, based on recovery of the
radiolabel in urine, faeces and expired air. Studies with rats indicated
that pre-washing of the skin with surfactant enhanced AS skin
penetration. Early studies with isolated human skin (not specified
further) were unable to detect dermal penetration of C12 AS Na.
Based on experimental data on animals and humans, a default assumption
of 1% dermal absorption was taken for deriving the DNEL. Since dermal
absorption decreases with increasing concentration of a solution, this
percentage can be used for workers as a worst case approach.
After oral administration of 14.4 mg/kg bw of the erythromycin salt of
C16 AS to dogs or 250 mg/person to humans, radioactivity in plasma was
maximal within 30 minutes to 2 hours of exposure in both species
indicating rapid absorption (SIDS, 2007). The plasma concentration
declined rapidly afterwards and reached 10 % of the maximum
concentration after 6 hours, indicating rapid elimination.
Whole body autoradiography has been performed to follow the distribution
of 35S-C10 AS K, C12 AS K and C18 AS K or their metabolites within the
body with time in experiments with rats after i.p. injection. For all
compounds the only organs, where radioactivity was detected were liver
and kidney. The levels (not quantified) were highest 1 h after
application. C10AS K was cleared from tissues more rapidly than C18 AS
K. After 6 hours, only traces of the C10 AS K salt remained in the
kidney, whereas it took 12 hours for the C18 AS K salt to be cleared
from the kidney.
Alkyl sulfates are extensively metabolized in rats, dogs and humans.
This was tested with radiolabeled C10, C11, C12, C16 and C18 alkyl
sulfates, potassium salts (SIDS, 2007).
The postulated mechanism is degradation involving omega-oxidation,
followed by beta-oxidation, to yield metabolites with chain lengths of
C2 and C4 for even-chain carbon alkyl sulfates. The major metabolite for
even-chained alkyl sulfates was identified as the 4-carbon compound,
butyric acid 4-sulfate. The 4-butyrolactone has been found as a minor
metabolite which is also formed after application of butyric acid
4-sulfate. Dog and human urine also contained one other minor
metabolite, glycolic acid sulfate.
Metabolism of odd numbered chains (specifically, C11) in rats was
postulated to follow a similar omega-, beta-degradation pathway:
propionic acid-3-sulfate was the major urinary metabolite and pentanoic
acid-5-sulfate and inorganic sulfate were minor metabolites.
The C2 fragments enter the C2 pool of the body and are either oxidized
to CO2 or found in the body. About 10 to 20% of the dose usually is
eliminated as inorganic sulfate.
The major path of excretion of the alkyl sulfates is the urine. The data
show, that there are only minor differences for the alkyl sulfates of
different chain lengths in the overall excretion after i.p. application.
There are also no major differences in overall excretion between male
and female rats or after oral, intraperitoneal or intravenous
application. The rate of excretion in the urine, however, is somewhat
different. After oral as well as i.p. application, excretion of the C12
compound is complete within 6 hours. In contrast the excretion amounts
only to about 60% (C10), 40% (C11), 15% (C18) after i.p. application,
and to 25% for C11 or C18 6 hours after oral application. This indicates
faster metabolism of the C12 compound than for the other chain lengths.
Lower amounts of the alkyl sulfates are excreted via the faeces within
48 hours after oral application for the C12, C16 and C18 compounds. The
lowest value was obtained for the C12, while the highest values with
considerable variation of 2.5 - 19.9% (2 m, 2f) were found for C11. In
the bile from <1 to 7.7% (highest amount with C11) of the dose applied
was found up to 6 hours after i.v. application, indicating, that the
amounts in faeces are mainly due to metabolism and not to unabsorbed
compound. In addition the distribution of label in urine and faeces from
orally administered potassium dodecyl-35S-sulfate (C12 A35S K) was
similar in both antibiotic-treated and untreated rats, indicating that
the intestinal flora does not play a significant role in the metabolism
of this compound.
Based on the above mentioned data, tissue accumulation can be excluded.
Influence of counter ions on ADME
Due to dissociation, there is no effect of the counter ion on
absorption, distribution, metabolism and excretion of the alkyl sulfate
moiety expected (Hera, 2002). This is supported by comparable results
achieved with alkyl sulfates having different counter ions reported
within this section.
Discussion on absorption rate
Absorption by the percutaneous route is limited, since anionic
surfactants tend to bind to the skin surface (SIDS, 2007). Both, studies
with isolated human skin and animal tests confirmed a low level of
percutaneous absorption. Based on experimental data on animals and
humans, a default assumption of 1% dermal absorption was taken for
deriving the DNEL. Since the dermal absorption decreases with increasing
concentration of a solution this percentage can be used for workers as a
worst case approach.
 SIDS initial assessment profile, (2007);
 (HERA Draft report, 2002);
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
Ce site web utilise des cookies afin de vous garantir la meilleure expérience possible sur nos sites web.
Welcome to the ECHA website. This site is not fully supported in Internet Explorer 7 (and earlier versions). Please upgrade your Internet Explorer to a newer version.
Do not show this message again