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Description of key information

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential
Absorption rate - dermal (%):

Additional information


Tetradecan-1-ol is 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) (OECD, 2006).


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 al., 2010).

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 ingestion.


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 independent variables.

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 independent variables.

  • Using these values for hexan-1-ol predicts a blood:air partition coefficient of approximately 40:1 meaning that, if lung exposure occurred, there would be some systemic exposure. This is supported by the effects observed in the acute inhalation study.
  • Using these values for octan-1-ol predicts a blood:air partition coefficient of approximately 13:1 meaning that, if inhalation exposure occurred, there would be some systemic exposure.

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 metabolites.

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; Kolattukudy, 1976).

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[1](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 alcohols.

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, al., 2001). 

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 approaching µg/g.

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, 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[2]. See Table below for data presented in this publication.

TableFatty alcohol levels in CHO-K1 cells

Cell line

Fatty alcohol level, μg/mg protein

Fatty alcohol level, μg/mg protein

Fatty alcohol level, μg/mg protein

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 alcohols

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 al., 1953).

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, 1993; 1995a,b).

A 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 (OECD, 2006).  

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 biotransformation products.

[1]Palmitic acid is the common name for hexadecanoic acid. Radiolabelled palmitic acid (1-14C or 9,10-3H) was bound to fatty acid-free bovine serum albumen in a 1:1 ratio, The protocol used for extraction of fatty acid and fatty alcohol enabled both free and esterified fatty acids and alcohols to be measured.

[2]Ham’s F-12 medium containing 10% (vol/vol) foetal bovine serum supplemented with 1 mM glutamine.


Alves, Célia et al. (2012). Organic compounds in aerosols from selected European sites – Biogenic versus anthropogenic sources. Atmospheric Environment. 59, 243–255.


Bandi ZL, Mangold HK, Holmer G and Aaes-Jorgensen E (1971a). The alkyl and alk-1-enyl glycerols in the liver of rats fed long chain alcohols or alkyl glycerols. FEBS Letters 12, 217-220.


Bandi ZL, Aaes-Jorgensen E and Mangold HK (1971b). Metabolism of unusual lipids in the rat. 1. Formation of unsaturated alkyl and alk-1-enyl chains from orally administered alcohols. Biochimica et Biophysica Acta 239, 357-367.

Dias M, Naik A, Guy RH, Hadgraft J, Lane ME. (2008). In vivo infrared spectroscopy studies of alkanol effects on human skin. Eur J Pharm Biopharm. 69(3):1171-5.

Duester, G et al., (1999). Recommended nomenclature for the vertebrate alcohol dehydrogenase gene family. Biochemical Pharmacology, Volume 58, Issue 3, 1 August 1999, Pages 389–395.

Friedberg, S J., (1976). Plasma transport forms of ingested fatty alcohols in the rat. Lipids 11(8):587-93.


Gelman RA and Gilbertson JA (1975). Permeability of the blood-brain barrier to long-chain alcohols from plasma. Nutrition and Metabolism 18, 169-175.

Höög, J-O, Hedberg, J. J., Strömberg, P., Svensson, S. (2001). Mammalian alcohol dehydrogenase - Functional and structural implications. Journal of Biomedical Science Volume 8, Issue 1, pp 71-76.

James, P. F., Rizzo, W. B., Lee J., Zoeller, R. A., (1990). Isolation and characterization of a Chinese hamster ovary cell line deficient in fatty alcohol:NAD+ oxidoreductase activity. Proc. Natl. Acad. Sci 87, 6102-6106.

JECFA (1999). Evaluation of certain food additives and contaminants. 49th Report of the Joint FAO/WHO Expert Committee on Food Additives. WHO Tech Rep Series No 884. WHO, Geneva.

Kamil, I.A. et al, (1953_ Studies in detoxication 46. The metabolism of aliphatic alcohols. The glucuronic acid conjugation of acyclic aliphatic alcohols. Biochem 53:129-136.

Keller et al., 2012). Studying fatty aldehyde metabolism in living cells with pyrene-labeled compounds. Lipid research 53, 7, 1410-1416.

Kanikkannan N1, Singh M., (2002). Skin permeation enhancement effect and skin irritation of saturated fatty alcohols. Int J Pharm. 6;248(1-2):219-28.

Kolattukudy, P.E., (1975). Biochemistry of cutin, suberin and waxes, the lipid barriers on plants. In: Recent advances in the chemistry and biochemistry of plant lipids, pp. 203–246, Galliard, T., Mercer, E.I., eds. Academic Press, New York London as cited in Weber and Mangold (1982).

Kolattukudy, P.E. (1976) Introduction to natural waxes. In: Chemistry and biochemistry of natural waxes, pp. 1–15, Kolattukudy, P.E., ed. Elsevier, Amsterdam New York London as cited in Weber and Mangold (1982).

Lehninger, A. L., Nelson, D. L. and Cox, M. M. (1993). Principles of Biochemistry. New York, Worth Publishers.

McIsaac WM and Williams RT (1958). The metabolism of spermaceti. West African Journal of Biological Chemistry 2, 42-44.

Menzel M., Wind T., Steber J. (2001). Evaluation of the biotransformation behaviour of unbranched and branched fatty alcohols by an in vitro assay with liver homogenate.

Meulenberg, C.J. and H.P. Vijverberg, Empirical relations predicting human and rat tissue:air partition coefficients of volatile organic compounds. Toxicol Appl Pharmacol, 2000. 165(3): p. 206-16.

MiyazakiM (1955). Nutritive value of aliphatic alcohols II. The nutritive value and toxicity of saturated alcohols of six to eighteen carbon atoms. Journal of the Agricultural and Chemical Society of Japan 29, 501-505 (cited in FDA, 1978).


Mudge, S. M. (2005). Fatty alcohols – a review of their natural synthesis and environmental distribution. Report to ERASM (European Risk Assessment and Management) and the SDA (Soap and Detergent Association). November 2005. 151 p. (available online at

Mudge, S.M., Belanger, S.E., Nielsen, A.M., (2008). Fatty Alcohols — Anthropogenic and Natural Occurrence in the Environment. Royal Society of Chemistry, London, UK. ISBN 978-0-85404-152-7.

Mukherjee KD, Weber N, Mangold HK et al. (1980). Competing pathways in the formation of alkyl, alk-1-enyl and acyl moieties in the lipids of mammalian tissues. European Journal of Biochemistry 107, 289-294.


OECD (2006). Long Chain Alcohols. SIDS Initial Assessment Report for SIAM 22.

Raut, S V, Nemade, L S, Desai, M T, Bonde, S D, Dongare, S U, (2014). Chemical penetration enhancers: for transdermal drug delivery systems. International Journal of Pharmacy Review & Research Vol 4 Issue 1 33 – 40.

Rizzo WB, Craft DA, Dammann AL, Phillips MW. (1987). Fatty alcohol metabolism in cultured human fibroblasts. Evidence for a fatty alcohol cycle. J Biol Chem. 262:17412–17419.

Rizzo W.B., 2011. The role of fatty aldehyde dehydrogenase in epidermal structure and function. Dermatoendocrinol. Apr;3(2):91-9.

Sanderson, H., van Compernolle, R., Dyer, S. D., Price, B. B., Nielsen, A. M., Martin Selby, Ferrer, D., Stanton, K. (2013). Occurrence and risk screening of alcohol ethoxylate surfactants in three U.S. river sediments associated with wastewater treatment plants, Science of The Total Environment, Volumes 463–464, 1 October, Pages 600-610.

Shuobo Shi, Juan Octavio Valle-Rodríguez, Sakda Khoomrung, Verena Siewers and Jens Nielsen (2012). Functional expression and characterization of five wax ester synthases in Saccharomyces cerevisiae and their utility for biodiesel production. Biotechnology for Biofuels, 5:7

Veenstra G, Webb C, Sanderson H, Belanger S.E, Fisk P, Nielsen A, Kasai Y, Willing A, Dyer S, Penney D, Certa H, Stanton K, Sedlak R (2009). Human Health Risk Assessment of Long chain aliphatic alcohols. Ecotoxicology and Environmental Safety, 72, 4 1016-1030.

Verhoeven, N.M et al, (1998). The metabolism of phytanic acid and pristanic acid in man. J. Inherit. Metab. Dis. 21:697-728.


Wasti K (1978). A literature review - problem definition studies on selected toxic chemicals. Environmental Protection Research Division, US Army Medical Research and Development Command, Maryland USA (cited in CIR, 1988).


Weber N and Mangold, HK, (1982) Metabolism of long chain alcohols in cell suspension cultures of soya and rape. Planta 155:225-230.

Williams RT (1959). Detoxification Mechanisms. 2nd Edition, Chapman and Hall,London.


WHO (1999). Evaluation of Certain Food Additives and Contaminants, WHO technical Report Series 884.

de Wolf W., Parkerton T. (1999), Higher alcohols bioconcentration: influence of bio-transformation, Symposium 'Persistent, bioaccumulative, toxic chemicals' at the 217th ACS National Meeting, Anaheim (CA), March 21 – 25, 1999.