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EC number: 204-000-3
CAS number: 112-72-1
a lipophilic, white, waxy solid that is practically insoluble in water.
Aliphatic alcohols are expected to be
absorbed by all common routes of exposure (dermal, oral and inhalation)
The extent of absorption of aliphatic
alcohols varies with chain length. For example, in rats, the extent of
dermal penetration increases up to C7 (heptan-1-ol) and thereafter
declines with longer carbon chain lengths (Valette and Cavier, 1954).
Based on comparative in vitro skin permeation data and dermal absorption
studies in hairless mice, aliphatic alcohols show an inverse
relationship between absorption potential and chain length with the
shorter chain alcohols having a significant absorption potential.
Approximately 50% of a dose of radiolabelled [1-14C]octan-1-ol
was absorbed upon skin application to mice for 24 hours, a figure that
decreased with increasing chain length to about 7% for similarly
labelled decan-1-ol (C10) and 3% for dodecan-1-ol (C12) (Iwata et al.,
1987). The absorption of decan-1-ol has been confirmed in a reliable in
vitro study, where the percutaneous absorption rate of a 10% (w/w)
FRM in 9:1 (v/v) ethanol: water mixture using unoccluded porcine skin
was ca.8% (Berthauld et al., 2011).
Data are available from a well conducted in
vitro study using human skin in which myristyl alcohol (C14-alcohol,
tetradecan-1-ol) gave a percutaneous absorption rate of 1.2% at 6 hours
and 6.3% at 24 hours (P&G, 2008). This confirms the findings of the
Valette and Cavier and Iwata papers that aliphatic alcohols show an
inverse relationship between absorption potential and chain length. A
reliable study which investigated the in vitro percutaneous absorption
of decan-1-ol using human skin over an 8 hour exposure and occluded
conditions reported a potential absorption of 66%. However it is
considered that the occluded conditions of the experiment were the
likely factor for such a high percutaneous absorption rate (Buist et
The dermal absorption of tetradecan-1-ol is
between 2 and 3%, interpolated from dodecan-1-ol and hexadecan-1 -ol
(Iwata et al., 1987), supported by the in vitro
percutaneous absorption study (P&G, 2008).
Similar to the dermal absorption potential,
it is expected that orally administered aliphatic alcohols also show a
chain-length dependant potential for gastro-intestinal absorption, with
shorter chain aliphatic alcohols having a higher absorption potential
than longer chain alcohols.With regards to the blood-brain barrier
chain-length dependant absorption potential exists with the lower
aliphatic alcohols and acids more readily being taken up than aliphatic
alcohols/acids of longer chain-length (Gelman and Gilbertson, 1975).
Taking into account the efficient biotransformation of the alcohols and
the physicochemical properties of the corresponding carboxylic acids the
potential for elimination into breast milk is considered to be low.
Short-chain aliphatic alcohols are known to
be rapidly and extensively absorbed from the gastrointestinal tract
(Aaes-Jorgensen et al. 1959; Bandi et al. 1971a, 1971b), whereas
long-chain saturated alcohols (e.g. C18) are said to be poorly absorbed
(CIR, 1985). The presence of only <0.5% of an oral dose of octan-1-ol
in the faeces of rats (Miyazaki, 1955) supports the view that absorption
of shorter chain-length alcohols is likely to be extensive following
The uptake of substances into the
lungs requires that the substance should be sufficiently water soluble
to dissolve in the mucous of the respiratory tract lining. In addition,
the substance needs to have a log Kow which is favourable to absorption,
i.e. between -1 and 4. For lower carbon numbers in the Alcohols
Category, the absorption can be estimated using a Quantitative
Structure-Property Relationship (QSPR) to estimate the blood:air
partition coefficient for human subjects as published by Meulenberg and
Vijverberg (2000). The resulting algorithm uses the dimensionless Henry
coefficient and the octanol:air partition coefficient (Koct:air) as
There is a Quantitative
Structure-Property Relationship (QSPR) to estimate the blood:air
partition coefficient for human subjects as published by Meulenberg and
Vijverberg (2000). The resulting algorithm uses the dimensionless Henry
coefficient and the octanol:air partition coefficient (Koct:air) as
The higher carbon number alcohols,
from C9 upwards, are of low water solubility and have a partition
coefficient which is greater than 4, so little systemic exposure would
be expected following inhalation exposure.
Absorbed aliphatic alcohols potentially
could be widely distributed within the body (OECD, 2006). However, as a
result of the rapid and efficient metabolism, it is not anticipated that
aliphatic alcohols wouldremain in the body for any significant
length of time. Evidence of this was presented in a paper describing
oral (gavage) administration of (Z)-octadec-9-enol and
(Z,Z)-octadec-9,12-enol to rats (Bandi et al., 1971b). The distribution
of major lipid classes in the heart, brain, kidneys, liver, testes,
adipose tissue and blood was unaffected by treatment and it was
concluded that long chain alcohols did not accumulate in these tissues.
Long chain fatty alcohols are
synthesised within cells and are therefore found within organisms and
occur naturally in the environment. Endogenous and exogenous long chain
alcohols are metabolised in catabolic (breakdown) and anabolic
(synthesis) pathways. Cellular metabolism can cycle between long chain
alcohols and their corresponding acids. Alcohols are used as building
blocks in the synthesis of lipids for energy storage. Pathways exist for
the conversion of alcohols to acids. It is therefore concluded that,
should systemic exposure occur to anthropogenic long chain alcohols,
mammals including test species and humans share common pathways for
their metabolism and the products of metabolism are naturally-occurring
Formation of fatty alcohols
It is well-known that
naturally-occurring fatty alcohols are to be found in cells of
microorganisms, plants, and animals (Weber and Mangold, 1982;
Fatty alcohols are formed from fatty acids
as initial steps in the synthesis of lipids (involving formation of
esters by reaction of acids with glycerol); they are also part of the
pathways of the catabolism of alcohols to produce energy. The
interconversion of fatty alcohols and fatty acids is described in detail
below, and has been described as the fatty alcohol cycle (Rizzo et
al., 1987; Figure 1 attached). Rizzo et al.
demonstrated that both synthesis and oxidation of fatty alcohols takes
place within cultured skin fibroblasts. Fatty alcohol is oxidised to the
corresponding aldehyde, which is followed by further oxidation to fatty
acid, via an enzyme complex (see below). In turn, fatty acids can be
converted via the corresponding aldehyde to fatty alcohol. Cells
incubated in radioactive palmitate(salts
or esters of hexadecanoic acid, C16) showed increased levels of labelled
hexadecanol. In the presence of non-labelled hexadecanol, and labelled
palmitate, cellular levels of labelled hexadecanol increased up to
10-fold, which suggests that rapid metabolism of palmitate to
hexadecanol is occurring.
When incubated in the absence of fatty acid
and the presence of labelled hexadecanol, cells rapidly oxidised
hexadecanol to palmitic acid (hexadecanoic acid) (Rizzo et al.,
1987). Double labelling demonstrated simultaneous interconversion of
hexadecanol and palmitic acid. Shorter and longer alcohols are also
oxidised by fatty alcohol: NAD oxidoreductase (FAD). In living organisms
products from the pathway would be incorporated into other molecules and
transported from the cells. More recently, understanding of the fatty
acid cycle has helped in the understanding of metabolic disease (Rizzo
W. B., 2011; James, P. F., 1990). Cells from individuals lacking an
effective part of the enzyme complex accumulate long chain fatty
The mammalian alcohol dehydrogenase system
is a group of pathways which catalyse the conversion of alcohols and
aldehydes, which includes different forms of the enzymes which vary in
substrate specificity. The alcohol dehydrogenases (ADHs) are divided
into six classes, denoted by ADH1-ADH6. Five of the six classes of
alcohol dehydrogenase have been identified in humans. One of the
classes, ADH3, is the ancestral form of all mammalian ADHs, and has been
traced in all living species investigated. The alcohol dehydrogenase
system is considered to be able to detoxify a wide range of alcohols and
aldehydes without the generation of toxic radicals (Höög, J-O.et
Long chain alcohols are also able to be used
as substrates in the synthesis of wax esters and of ether glycerolipids
(Rizzo W. B., 2011; Shuobo et al.,2012).
A study with long-chain saturated and unsaturated alcohols indicates
that formation of wax esters occurs within the small intestine (Bandi et
al., 1971b). Synthesis of wax esters has been demonstrated by
incorporating genes from a number of bacterial and mammalian organisms
into yeast and measuring the transformation of long chain alcohols to
waxes (Shuobo et al.,2012). Most of the enzymes were more
active in using longer chain alcohols (C12-C20),
though the mouse enzyme also used decanol as a substrate. Long chain
alcohols are also precursors of lipids in animal tissues (Weber and
Mangold, 1982). However, synthesis of complex lipids is less important
than metabolism to the corresponding acid via the (fatty) alcohol
dehydrogenase system; in the study by Rizzo the majority of [1-14C]hexadecanol
was converted to hexadecanoic acid (Rizzo W. B., 1987).
Data on intracellular concentrations
of individual alcohols is not easy to find, though it is probably low.
The cellular concentration of hexadecanol is reported to be 137 ± 58
pmol/mg protein (Rizzo, 1987). Protein was total cell protein. The low
intracellular concentrations is considered to reflect the conversion of
long chain alcohols to other substances via catabolic and anabolic
pathways. It is not easy to convert such a concentration into mass
alcohol per total mass of an organism, since it would depend upon cell
type, but reasonable assumptions would convert this into concentrations
Long chain alcohols are used in
pharmaceutical formulations, and their role in promotion of skin
penetration has been studied (Kanikkannan N, 2002; Raut et al.,2014).
Deuterated alcohols including hexan-1-ol, octan-1ol and decan-1-ol have
been investigatedin vivo(in humans) to determine the effect
of dermal application on skin lipid content (Dias, M.et al.,2008).
It was reported that decanol did not change skin lipid content, though
hexanol and octanol reduced stratum corneaum lipid content.
Intracellular concentrations of dodecanol
have been assessed in a study on Chinese hamster ovary cells. Strain
CHO-K1 (wild-type for fatty alcohol: NAD+oxidoreductase
activity), were reported to have lower intracellular concentrations than
a mutant strain FAA.1 which was deficient in FA: NAD+oxidoreductase
activity. The cell had been incubated in serum-supplemented medium.
See Table below for data presented in this publication.
TableFatty alcohol levels in CHO-K1
Fatty alcohol level, μg/mg protein
Long chain aliphatic alcohols are
metabolised by a pathway that also acts on alkanes and fatty acids
(Mudge, 2008; Veenstra et al., 2009). Alkanes may be
oxidised to alcohols and alcohols converted via short-lived aldehydes to
fatty acids. It is notable that fatty acids obtained from natural
sources are exempt from REACH, due to inclusion in REACH Annex V
paragraph 8. The fatty acids produced by the action of alcohol
dehydrogenase followed by aldehyde dehydrogenation enter the β-oxidation
cycle producing acetyl-CoA products (and a propionyl‑CoA from odd
chain-length molecules) and ATP. These enzymes are found in the soluble
fraction of various tissues, and are relatively non-specific, accepting
a wide variety of substrates (de Wolf and Parkerton, 1999). The products
enter into the metabolic processes of the cells. Both alcohol (FAD) and
aldehyde dehydrogenase (FALDH) enzymes (used in conversion to fatty
acids) are ubiquitous in the plant and animal kingdoms but the location
of the relevant enzyme system, the chemical specificity and the rate at
which the reaction occurs differ between phyla and species. There are
many publications in the public domain which describe the cellular
metabolism of alcohols and the ubiquity of the enzymes involved (Höög,
J-O et al., 2001; Duester, G et al.,
1999; Menzel et al., 2001).
An in vitro study of the
biotransformation of linear and multiple-branched fatty alcohols (C12,
C14) has been conducted (Menzel et al., 2001), with
the intention to examine the pathway and relative rate of metabolism of
linear compared to branched alcohol structures. Thein vitrotest
system used either pig liver or fish (rainbow trout) liver homogenate as
the source of the metabolic enzymes, and substance-specific GC analysis
to follow the conversion of the alcohols into the corresponding fatty
acids over a ten day period. The results demonstrated that in pig liver
homogenate an intensive metabolism of the alcohols to the corresponding
fatty acids takes place, with half-lives 3.8 d for C12, 6.7 d for C14
and 8 d for C12 branched alcohols. Photometric measurements of the
esterase activity indicated that the fish liver homogenate was at least
approximately ten times less active; this was ascribed to the overall
lower metabolic activity of cold-blooded animals though the possible
role of method of sample preparation is noted, though the exploration of
these matters was not the objective of this study. The conclusion of
this study was that linear C12 alcohol was degraded more rapidly than
the C12 multiply-branched equivalent, by a factor of approximately 2.5.
Mammalian synthesis of alcohols begins
with formation of fatty acids, formed by Type I synthesis in mammals.
Type I synthesis is a series of reactions in a single complex produces
hexadecanoic acid (C16), occasionally C18 is formed. In addition,
subsequent reactions can produce longer chains, and unsaturation of the
C9-C10 bond. Some essential fatty acids cannot be synthesised because
they have an unsaturated bond at a different position in the molecule.
Fatty acids can be elongated or shortened by addition or removal of
two-carbon units in normal metabolic processes (Mudge, 2005; Mudge,
2008; Lehninger, 1993). Fatty alcohols are formed from fatty acids
through the two step fatty acid reductase (FAR) process, involving fatty
acyl-CoA dehydrogenase which converts a fatty acyl-CoA into a fatty
alcohol and CoASH.
Metabolic degradation of long chain
The initial step in the mammalian metabolism
of primary alcohols is the oxidation to the corresponding carboxylic
acid, with the corresponding aldehyde being a transient intermediate.
These carboxylic acids are susceptible to further degradation via
acyl-CoA intermediates by the mitochondrialb-oxidation
process. This mechanism removes C2 units in a stepwise process and
linear acids are more efficient in this process than the corresponding
branched acids. In the case of unsaturated carboxylic acids, cleavage of
C2-units continues until a double bond is reached. Since double bonds in
unsaturated fatty acids are in the cis-configuration, whereas the
unsaturated acyl-CoA intermediates in theb-oxidation cycle
are trans, an auxiliary enzyme, enoyl-CoA isomerase catalyses the shift
from cis to trans. Thereafter,β-oxidation
continues as with saturated carboxylic acids (WHO, 1999).
An alternative metabolic pathway for
aliphatic acids exists through microsomal degradation via omega-or
omega-1 oxidation followed by β-oxidation. This mechanism provides an
efficient stepwise chain-shortening pathway for branched aliphatic acids (Verhoeven,
et al., 1998).
The acids formed from the longer chained
aliphatic alcohols can also enter the lipid biosynthesis and may be
incorporated in phospholipids and neutral lipids (Bandi et al, 1971a and
b and Mukherjee et al. 1980). A small fraction of the aliphatic alcohols
may be eliminated unchanged or as the glucuronide conjugate (Kamil et
Studies using labelled hexadecan-1-ol found
up to 23% free phospholipid in the blood. Phospholipid, triglyceride and
diacyl glyceryl ether were found to have taken up significant
radiolabel. This indicates that this substance is incorporated into
normal lipid metabolism pathways (Friedberg, 1976). It is considered
that other aliphatic alcohols would also be incorporated into lipid
metabolic pathways. Saturated linear primary alcohols have been
evaluated by JECFA who concluded that “Hexyl alcohol is oxidised to
hexanal which is rapidly oxidised to hexanoic acid; hexanoic acid is
metabolised via the fatty acid and tricarboxylic acid pathways. ” (WHO,
1999). Other saturated linear primary alcohols with different chain
lengths (C4-C16 inclusive) are metabolised in a similar way (WHO, 1999).
Longer chained aliphatic alcohols within this category may enter common
lipid biosynthesis pathways and will be indistinguishable from the
lipids derived from other sources (including dietary glycerides) (Kabir,
comparison of the linear and branched aliphatic alcohols shows a high
degree of similarity in biotransformation. For both sub-categories the
first step of the biotransformation consists of an oxidation of the
alcohol to the corresponding carboxylic acids, followed by a stepwise
elimination of C2 units in the mitochondrial β-oxidation process. The
metabolic breakdown for both the linear and mono-branched alcohols is
highly efficient and involves processes for both sub-groups of alcohols.
The presence of a side chain does not terminate the β-oxidation process,
however in some cases a single Carbon unit is removed before the C2
elimination can proceed. ELIMINATIONThe
long chain aliphatic carboxylic acids are efficiently eliminated and
aliphatic alcohols are therefore not expected to have a tissue retention
or bioaccumulation potential (Bevan, 2001).
When rats were given an oral dose of
octan-1-ol, only trace amounts (<0.5%) of unchanged alcohol were
detected in the faeces (Miyazaki, 1955). Oral administration of the
long-chain unsaturated alcohols (Z)-octadec-9-enol and
(Z,Z)-octadec-9,12-enol led to an increase in the unsaturated C18 in
lipids isolated from the feces (Bandi et al., 1971b). Faecal
recoveries of unchanged alcohol were 20 and 50%, respectively, when rats
were given an oral dose of the higher alcohols hexadecan-1-ol and
octadecan-1-ol (McIsaac and Williams, 1958; Miyazaki, 1955).
Following the 24-hour application of the
analogue dodecan-1-ol (radiolabelled with14C) to skin of
hairless mice, more than 90% of the absorbed dose was excreted in
expired air and 3.5% was eliminated in the faeces and urine after 24
hours; only 4.6% of the absorbed dose [representing 0.13% of the applied
dose] remained in the body (Iwataet al. 1987). A similar
general pattern of extensive and rapid excretion would also be expected
for other aliphatic alcohols.
The glucuronic acid conjugates formed during
the metabolism of most aliphatic alcohols are excreted in the urine
(Wasti, 1978; Williams, 1959). For 1-octanol, 9.5% of an oral dose was
excreted by rabbits in urine as glucuronide (Kamilet al.
1953). Although lipophilic alcohols have the physiochemical potential to
accumulate in breast milk, rapid metabolism to the corresponding
carboxylic acid followed by further degradation suggests that breast
milk can only be, at most, a minor route of elimination from the body
In summary, long chained alcohols are
generally highly efficiently metabolised and there is limited potential
for retention or bioaccumulation for the parent alcohols and their
acid is the common name for hexadecanoic acid. Radiolabelled
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serum albumen in a 1:1 ratio, The protocol used for extraction of
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