Fatty alcohol

Most fatty alcohols in nature are found as waxes, which are esters of fatty acids and fatty alcohols.[1] They are produced by bacteria, plants and animals for purposes of buoyancy, as source of metabolic water and energy, biosonar lenses (marine mammals) and for thermal insulation in the form of waxes (in plants and insects).[3] The traditional sources of fatty alcohols have largely been various vegetable oils, which remain a large-scale feedstock. Animal fats (tallow) were of historic importance, particularly whale oil, however they are no longer used on a large scale. Tallows produce a fairly narrow range of alcohols, predominantly C₁₆–C₁₈, while plant sources produce a wider range of alcohols from (C₆–C₂₄), making them the preferred source. The alcohols are obtained from the triglycerides (fatty acid triesters), which form the bulk of the oil. The process involves the transesterification of the triglycerides to give methyl esters which are then hydrogenated to produce the fatty alcohols.[4] Higher alcohols (C₂₀–C₂₂) can be obtained from rapeseed oil or mustard seed oil. Midcut alcohols are obtained from coconut oil (C₁₂–C₁₄) or palm kernel oil (C₁₆–C₁₈).

Fatty alcohols are also prepared from petrochemical sources. In the Ziegler process, ethylene is oligomerized using triethylaluminium followed by air oxidation. This process affords even-numbered alcohols:

Al(C₂H₅)₃ + 18 C₂H₄ → Al(C₁₄H₂₉)₃

Al(C₁₄H₂₉)₃ + 3⁄2 O₂ + 3⁄2 H₂O → 3 HOC₁₄H₂₉ + 1⁄2 Al₂O₃

Alternatively ethylene can be oligomerized to give mixtures of alkenes, which are subjected to hydroformylation, this process affording odd-numbered aldehyde, which is subsequently hydrogenated. For example, from 1-decene, hydroformylation gives the C₁₁ alcohol:

C₈H₁₇CH=CH₂ + H₂ + CO → C₈H₁₇CH₂CH₂CHO

C₈H₁₇CH₂CH₂CHO + H₂ → C₈H₁₇CH₂CH₂CH₂OH

In the Shell higher olefin process, the chain-length distribution in the initial mixture of alkene oligomers is adjusted so as to more closely match market demand. Shell does this by means of an intermediate metathesis reaction.[5] The resultant mixture is fractionated and hydroformylated/hydrogenated in a subsequent step.

Very long-chain fatty alcohols (VLCFA), obtained from plant waxes and beeswax have been reported to lower plasma cholesterol in humans. They can be found in unrefined cereal grains, beeswax, and many plant-derived foods. Reports suggest that 5–20 mg per day of mixed C₂₄–C₃₄ alcohols, including octacosanol and triacontanol, lower low-density lipoprotein (LDL) cholesterol by 21%–29% and raise high-density lipoprotein cholesterol by 8%–15%. Wax esters are hydrolyzed by a bile salt–dependent pancreatic esterase, releasing long-chain alcohols and fatty acids that are absorbed in the gastrointestinal tract. Studies of fatty alcohol metabolism in fibroblasts suggest that very long-chain fatty alcohols, fatty aldehydes, and fatty acids are reversibly inter-converted in a fatty alcohol cycle. The metabolism of these compounds is impaired in several inherited human peroxisomal disorders, including adrenoleukodystrophy and Sjögren–Larsson syndrome.[6]

Fatty alcohols are relatively benign materials, with LD₅₀ (oral, rat) ranging from 3.1–4 g/kg for hexanol to 6–8 g/kg for octadecanol.[1] For a 50 kg person, these values translate to more than 100 g. Tests of acute and repeated exposures have revealed a low level of toxicity from inhalation, oral or dermal exposure of fatty alcohols. Fatty alcohols are not very volatile and the acute lethal concentration is greater than the saturated vapor pressure. Longer-chain (C₁₂–C₁₆) fatty alcohols produce fewer health effects than short-chain (smaller than C₁₂). Short-chain fatty alcohols are considered eye irritants, while long chain alcohols are not.[7] Fatty alcohols exhibit no skin sensitization.[8]

Repeated exposure to fatty alcohols produce low-level toxicity and certain compounds in this category can cause local irritation on contact or low-grade liver effects (essentially linear alcohols have a slightly higher rate of occurrence of these effects). No effects on the central nervous system have been seen with inhalation and oral exposure. Tests of repeated bolus dosages of 1-hexanol and 1-octanol showed potential for CNS depression and induced respiratory distress. No potential for peripheral neuropathy has been found. In rats, the no observable adverse effect level (NOAEL) ranges from 200 mg/kg/day to 1000 mg/kg/day by ingestion. There has been no evidence that fatty alcohols are mutagenic or cause reproductive toxicity or infertility. Fatty alcohols are effectively eliminated from the body when exposed, limiting possibility of retention or bioaccumulation.[8]

Margins of exposure resulting from consumer uses of these chemicals are adequate for the protection of human health as determined by the Organisation for Economic Co-operation and Development (OECD) high production volume chemicals program.[7][9]

Fatty alcohols up to chain length C₁₈ are biodegradable, with length up to C₁₆ biodegrading within 10 days completely. Chains C₁₆ to C₁₈ were found to biodegrade from 62% to 76% in 10 days. Chains greater than C₁₈ were found to degrade by 37% in 10 days. Field studies at wastewater treatment plants have shown that 99% of fatty alcohols lengths C₁₂–C₁₈ are removed.[8]

Fate prediction using fugacity modeling has shown that fatty alcohols with chain lengths of C₁₀ and greater in water partition into sediment. Lengths C₁₄ and above are predicted to stay in the air upon release. Modeling shows that each type of fatty alcohol will respond independently upon environmental release.[8]

Fish, invertebrates and algae experience similar levels of toxicity with fatty alcohols although it is dependent on chain length with the shorter chain having greater toxicity potential. Longer chain lengths show no toxicity to aquatic organisms.[8]

This category of chemicals was evaluated under the Organisation for Economic Co-operation and Development (OECD) high production volume chemicals program. No unacceptable environmental risks were identified.[9]