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d-Glucitol d-Sorbitol Glucitol Hexanehexol Hydrogenated glucose syrup Sorbit


SYNONYMS SORBITOL d-Glucitol d-Sorbitol Glucitol Hexanehexol Hydrogenated glucose syrup Sorbit CHEMICAL STRUCTURE CHEMICAL FORMULA C 6


  • C 6 H 14 O 6


CAS Number



CoE Number









E Number




Melting Point: 11 o C

Boiling point: 295 o C


Flavouring substance.



CoE limits:


Food (mg/kg)

Exceptions (mg/kg)






Acceptable Daily Intake:


ADI (mg/kg)

ADI Set by

Date Set


Not specified




FDA Status:[CFR21]

Section Number



Direct food substance recognised as safe [12.0%-99.0%]


Natural Occurrence: Sorbitol is reportedly found in cherries, plums, pears, apples, seaweed and algae [Fenaroli, 1995]. Sorbitol is on of the most widely found sugar alcohols in nature with relatively high concentrations occurring in apples, pears, plums, peaches and apricots. Also reported found in several varieties of berries, seaweed and algae [Fenaroli, 2005].

Reported Uses: Sorbitol is reportedly used (maximum levels) in baked goods at 153.5 ppm; fats and oils 2.29 ppm; milk products 56.27 ppm; frozen dairy 71.71 ppm; fruit juice 10.00 ppm; Meat products 27.66 ppm; poultry 55 ppm; soft candy 421.9 ppm; confectionery & frosting 17.38 ppm; sweet sauce 0.04 ppm; gelatins & puddings 1.00 ppm; snack foods 15.00 ppm; non- alcoholic beverages 34.44ppm; alcoholic beverages 0.06 ppm; nut products 6.00 ppm; hard candy 935.8 ppm ad chewing gum 491.5 ppm [Fenaroli, 2005]. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications [Fenaroli, 2005].


In Vivo Toxicity Status








Test Type














Reported Dosage













[Lewis, 2000].

Inhalation toxicity

A total of 31 ingredients were tested in 90-day nose-only rat inhalation studies using mainstream cigarette smoke. Studies were designed following conventional toxicity testing methods employed for food additives and other consumer products. The authors concluded that these ingredients, which included D-sorbitol applied at levels up to 100,000 ppm on cigarettes produced minimal changes in the overall toxicity profile of mainstream cigarette smoke, and in some cases, the addition of high levels of an ingredient caused a small reduction in toxicity findings, probably due to displacement of burning tobacco [Gaworski et al., 2011].

Reproductive and Developmental Toxicity

A three-generation study was conducted in Sprague-Dawley [CD] rats with 20 males and 20 females per group. Each group received the test material by dietary administration. A control group received 20 % rice starch. One group received 20 % sorbitol and another group received 20 % sucrose ad libitum. The pups of the F 1a , F 2a , and F 3a generations were weighed and killed at four days and examined for sex determination of abnormalities. The F 1b , F 2b , and F 3b pups were weighed, sexed, and litters culled to eight per dam. Marked inhibition of food consumption occurred. Suppression of weight gain was noted. Mating performance and the pregnancy rates were not affected. Gestation period was increased [23 - 24 days] in 36 % of litters of the first mating versus 16.1 % of controls and 23.2 % of second mating versus 7.3 % of controls. At terminal necropsy caecal enlargement was noted [Palmer et al.,


Fifteen weanling male Wistar rats were administered sorbitol at levels of 10 % or 15 % in the diet for 17 months showed no evidence of deleterious effect on weight gain, reproduction, lactation or histopathological appearances of the main organs. The only difference with the controls was slight diarrhoea and, consequently, a retardation in growth, with rapid return to the normal. In supplement, a reproduction study made on 30 rats [equally divided by sex] and extended over four generations di d not reveal any abnormalities [Le Breton, 1956].

In another three generation reproduction study, Charles river CD [SD] Rats were fed a sucrose based cereal diet with 0, 2.5, 5 or 10% of sorbitol included at the expense of sucrose. There was found to be no effect of treatment upon any of the reproductive parameters measured and no abnormal pups were observed in any generation. Enlargement of the caecum was found at the necropsy of all sorbitol treated rats of all generations. Increases in serum calcium were noted in F 0 males and females exposed to 10% sorbitol and F1b males exposed to either 5 or 10% sorbitol. Microscopic examinations revealed no treatment-related changes [MacKenzie et al., 1986].

Groups of 31-33 CFT female weanling rats received test diets containing either/or 20% rice starch [control], 20% sorbitol or 20% sucrose for comparison. The test diets were administered for five weeks prior to mating.

There were no treatment related effects upon implantation, pre-implantation rates or post-implantation loss, litter and mean foetal weights, with no major malformations or minor abnormalities, and skeletal variants. There was a low overall pregnancy rate [approximately 50%] for all groups. No skeletal variations were attributable to treatment. Other parameters were reported to be within normal back ground limits [Palmer et al., 1977].

Litter size was decreased [total and viable pups] as was litter weight, but with increased mean pup weight. No terata were observed grossly. There was a marked reduction in food consumption. Statistically significant decreased absolute thyroid weight and lower adjusted heart weight and higher adjusted ovary weight were noted. Distension of the caecum was observed in the F 3b generation. Two males and one female showed an absence of extramedullary haematopoiesis in the liver [Palmer et al., 1978].

Groups of 20 yellow-silver does, of an outbred rabbit strain, aged three to four months [2.7 - 3.0 kg] received test diets ad libitum containing 20 % sorbitol or 20 % sucrose baked into the food pellets. Males were untreated. The test

diets were administered from days 7 - 19 of gestation

The incidence of

.. skeletal malformations was similar in treatment and control [sucrose] groups. No major visceral abnormalities were noted. The food intake was decreased during the period of sorbitol administration. No other treatment effects were noted [Hummler, 1978].

Inhalation toxicity

The addition of sorbitol at 35,300 ppm to reference cigarettes, used in a 90 day-sub-chronic inhalation exposure in rats, led to a series of pathological changes to smoke exposure that were indistinguishable from those changes caused by the control cigarettes. This indicated that addition of sorbitol to a reference cigarette had no discernable effect upon the type or severity of the treatment related pathological changes associated with tobacco smoke exposure [Baker et al., 2004].

Other relevant studies

The absorption of sorbitol is reported to be much slower than that of glucose or fructose. Both normal and diabetic human subjects who consumed an oral dose of 35 g of sorbitol excreted less than 3 % in the urine. No sorbitol was detected in the faeces. In experiments with uniformly labelled 14 C-sorbitol [sorbitol-U- 14 C], at least 75 % of the dose given orally was metabolised to CO 2 . In normal subjects, there was no significant increase in the blood sugar levels; in diabetic subjects the blood sugar was reported to be increased slightly. The concentration of sorbitol in the blood was reported to be immeasurably small [Adcock et al., 1957].

In experiments with rats given sorbitol-U- 14 C by intraperitoneal injection,

57.4 % of the activity was reportedly excreted as CO 2 , 17.3 % in the urine,

and 4.2 % was found as liver

glycogen with 0.6 % as liver fatty acids. In

diabetic rats, a smaller proportion was oxidized and the major portion was

excreted in the urine [Stetten et al., 1951]. Sorbitol has a strong glycogenic effect in the fasted diabetic rat [Stetten et al., 1951]. Sorbitol has a more efficient antiketogenic effect in liver slices of fasted rats than glucose or fructose [Blakley, 1952], and behaved similarly in the intact rat [JECFA 1973]. Sorbitol is oxidized to fructose by a DPN-linked polyol dehydrogenase [McCorkindale et al., 1954].

The intravenous infusion of sorbitol in rabbits caused a prompt fructosaemia and a variable secondary glucosaemia occurred later [Seeberg et al., 1955]. Experiments in rats [Wick et al., 1951] given sorbitol-U- 14 C support the view that at least two pathways exist for the oxidation of sorbitol in the body: (a) oxidation after conversion to glucose, and (b) the direct oxidation of the primarily formed fructose [JECFA, 1973]. Sorbitol was demonstrated not to be metabolized by hepatectomized animals [Wick et al., 1951].

Rats fed sorbitol, at a level of 16% in their diet for three months showed persistently high calcium absorption and retention with heavy citric acid excretion. Thickening of the rat’s skeleton was reported [Founier et al., 1967]. These effects are similar to those reportedly produced by lactose in the same conditions. In feeding experiments on rats, sorbitol showed the same calorific value as glucose [Morgan et al., 1961].

In humans sorbitol has been shown to improve the iron absorption efficiency in 10/12 human subjects [Loria et al., 1962]. Activated charcoal in 70 % sorbitol is used often in the management of acute poisoning episode. The authors tested the effects of 30 g of activated charcoal in 150 ml of 70 % sorbitol administered to healthy human subjects. There was found to be no effect on any serum parameters measured and they concluded that it mad an attractive gastrointestinal decontaminant due to its palatability, rapid onset and long duration of action [Minocha et al., 1984].

The threshold of the laxative effect sorbitol is reported to be 0.5 g/kg in children, with abominable cramping occurring with as little as 0.3 mg/kg. In a reported small study, human adults were able to tolerate 110 grams of sorbitol per day. In amounts of 40 g daily, spread throughout the day's intake of food, sorbitol was reportedly well tolerated by human subjects for a long period

[Treon, 1963]. A total of 25 g daily in two doses caused no laxative effect in

  • 86 human subjects. In about 5 % of these subjects, there was a somewhat

increased amount of gas appeared in the bowel [Peters et al., 1958]. Quantities of sorbitol greater than 50 g daily were laxative. This effect was presumably due to the relatively slow rate at of absorption of sorbitol from the small bowel [Tacquet, 1957].

A total of 75 male and 75 female Sprague- Dawley rats of the CD strain were included in each dosage group were exposed to diets containing 0 [control],

  • 20 % sorbitol, or 20 % sucrose. Each group consisted of 50 male and

  • 50 female rats for tumorigenic evaluation, 15 male and 15 female rats for

laboratory investigation, and 10 males and 10 females for interim sacrifice at

  • 26 and 52 weeks. All animals were derived from parents exposed to the

respective test diets. The diet of all groups was maintained at 20 %

carbohydrate supplementation through the use of rice starch in the 0 % groups. Protein was maintained constant in all groups through the addition of casein. For the 20 % sucrose groups, the carbohydrate was increased 5 % per week until the desired level was attained. An increase in water consumption was noted or both male and female fed 20% sorbitol in the diet rats and was associated with increased urine excretion. No other treatment related effects were observed [Hunter et al., 1978].

At autopsy reduced absolute and relative group mean thyroid weights were recorded for males and females in both the 20 % sorbitol and 20 % sucrose groups. Histological examination of the animals indicated no microscopic treatment-related effects on the major organ systems. However, the incidence of both unilateral and bilateral hyperplasia of the adrenal medulla was increased significantly for both males and females in the 20 % sorbitol group. Only unilateral hyperplasia was seen in the controls. Macroscopic examination indicated that 20 % sorbitol caused caecal enlargement in both males and females. No other treatment-related gross pathological changes were noted [Hunter et al., 1978].

Sorbitol 0 or 20% was administered in the diet of pure-bred beagle dogs [eight male and eight female animals per group]. An additional group received 20 % sucrose for comparative purposes. Rice starch was included in the diets of the controls so that the diet consisted of 80% normal diet and 20 % carbohydrate. The study was terminated at 104 weeks. There was an increase in total serum protein, body weight, and organ weight in the 20 % sorbitol groups when compared to the control group. There was a slight increase in the utilization of food in the 20 % sorbitol group. There were no other significant findings [Heywood et al., 1977].

Behavioural data

No data identified

In Vitro Toxicity Status

A total of 95 ingredients were tested individually through addition at different concentrations to the tobacco of experimental cigarettes. Mainstream cigarette smoke chemistry analysis, bacterial mutagenicity testing, and cytotoxicity testing were conducted. The authors concluded that these added ingredients, which included D-sorbitol at levels up to 100,000 ppm produced minimal changes in the overall toxicity profile of mainstream cigarette smoke, and in some cases, the addition of high levels of an ingredient caused a small reduction in toxicity findings, probably due to displacement of burning tobacco [Gaworski et al., 2011].

Carcinogenicity and mutagenicity

Baker et al., [2004]; examined the effects of the addition of 482 tobacco ingredients upon the biological activity and chemistry of mainstream smoke. The ingredients, essentially different groups of flavourings and casings, were

added in different combinations to reference cigarettes. The addition of sorbitol at 35,300 ppm was determined not to have affected the mutagenicity of the total particulate matter (TPM) of the smoke in either the Ames, in vitro micronucleus assay or the neutral red assay when compared with that of the control cigarettes [Baker et al., 2004].

The mutagenicity of the smoke condensate was assayed in the Salmonella plate incorporation [Ames] assay with the tester strain TA98 in the presence of an S9 metabolic activation system. The cytotoxicity of the cigarette condensate was determined in the neutral red uptake assay and the (3-(4,5-


tetrazolium, inner salt assay (MTS assay) with the human hepatocellular liver carcinoma cell line, HEP-G2. It was concluded that the in vitro mutagenicity and cytotoxicity of the cigarette smoke was not increased by the addition of the ingredients, which included sorbitol at levels up to 50000 ppm [In vitro toxicity testing of tobacco ingredients in burnt form (Internal document R-


Sorbitol has been found to be negative in the Ames mutagenicity assay with the following strains of Salmonella typhimurium TA97A and TA102 both with and without metabolic activation, at 0.5-50 mg/plate [Fujita et al., 1986].

The potential effects of the sorbitol pathway (involving the conversion of glucose to fructose via sorbitol as an intermediate) were investigated in diabetic mouse oocytes. Increasing concentrations of sorbitol suppressed FSH-induced maturation in oocytes of control mice. Oocytes from diabetic mice cultured in the presence of aldose reductase inhibitors (aldose reductase is produced in the presence of excess glucose under diabetic conditions converting glucose to sorbitol) reversed suppression of FSH-induced meiotic maturation. Contol mice cultured with activators of aldose reductase showed compromised FSH maturation. Additional experiments indicated that treatment with sorbitol or activators of the polyol pathway resulted in reduced cell-cell communication (between oocyte and cumulas cell) and compromised FSH mediated cAMP production and de novo purine synthesis. The author concluded that suppression of FSH-induced meiotic maturation in diabetic mouse oocytes may result from glucose shunting through the polyol pathway [Colton & Downs, 2004].

Chinese hamster ovary cells were found to be positive for structural changes associated with genotoxicity, after exposure to media made hyperosmotic with sorbitol (300, 350, 400 and 450mM). Cells were treated for 4h, with a 16 or 24-26h recovery period (from the beginning of treatment) prior to analysis. Increased chromosomal aberrations corresponded with a decrease in cell survival. However the authors state that the compounds tested may have had a direct effect on DNA and toxicity in addition to the effect on osmotic pressure [Galloway et al., 1987].

Additional information concerning the in vitro mutagenicity of this material may be found in “An Interim report on data originating from Imperial Tobacco Limited’s Genotoxicity testing programme September 2003” or “An updated

report on data originating from Imperial Tobacco Limited’s external Genotoxicity testing programme – Round 2 August 2007”.


Information relating to the pyrolysis and/or transfer of sorbitol is detailed in the Report on Thermochemical Properties of Ingredients document. In the aforementioned document, the term ‘pyrolysis’ means the heating of an ingredient in isolation under controlled conditions in an analytical device to examine its degradation potential. The expression ‘transfer data’ on the other hand is used to describe the fate of an ingredient in qualitative and quantitative terms following the smoking of a tobacco product to which it has been applied.


Adcock, et al., (1957) The metabolism of Sorbitol in the human subject. Biochemical Journal. 65: 554-560.

Baker RR, et al., (2004) An overview of the effects of tobacco ingredients on smoke chemistry and toxicity. Food Chem Toxicol. 42 Suppl: S53-83.

Blakley, (1952) Biochemical Journal 52: 269 [As cited in JECFA 1973].

Colton SA & Downs SM (2004). Potential role for the sorbitol pathway in meiotic dysfunction exhibited by oocytes from diabetic mice. Journal of Experimental Zoology. Part A Comparative Experimental Biology. 301(5):


Fenaroli’s Handbook of Flavor Ingredients, Volume 2, 1995.

Fenaroli’s Handbook of Flavor Ingredients (2005). Fifth Edition. CRC Press. ISBN: 0-8493-3034-3.

Founier, et al., (1967) Effects d’une ingestion prolongee de sorbitol sur l’utilisation du calcium et sur l’ossification du rat. C.r.hebd. Séanc. Acad. Sci., Paris 264: 1301.

Fujita et al., (1986) Mutagenicity test of food additives with Salmonella typhimurium TA97 and TA102. Kenkyu Nenpo Tokyo Toritsu Eisei Kenkyusho 37: 447-452.

Galloway et al., (1987). Effects of high osmotic strength on chromosome aberrations, sister-chromatid exchanges and DNA strand breaks, and the relation to toxicity. Mutat Res 189(1):15-25.

Gaworski et al., (2011). An evaluation of the toxicity of 95 ingredients added individually to experimental cigarettes: approach and methods. Inhalation Toxicology, 23(51) 1-12.

Heywood et al., (1977) Xylitol toxicity studies in the beagle dog. Unpublished report from Huntingdon Research Centre, submitted to World Health Organization by F. Hoffman La Roche Co., Ltd., Basle, Switzerland, as cited in JECFA 1978.

Hummler, H. (1978) Reproduction study in rabbits in oral administration of Ro 06-7045-Xylitol, Phase II - Teratology study. Unpublished company report submitted to the World Health Organization by F. Hoffman La Roche Co., Ltd., Basle, Switzerland, as cited in JECFA 1978.

Hunter et al., (1978) Xylitol tumorigenicity and toxicity study in long-term dietary administration to rats. Unpublished report from Huntingdon Research Centre, submitted to World Health Organization by F. Hoffman La Roche Co., Ltd., Basle, Switzerland as cited in JECFA 1978.

In vitro toxicity testing of tobacco ingredients in burnt form (Internal document


JECFA (1973). 17th report of the Joint FAO/WHO Expert Committee on Food Additives. WHO Food Additives Series 5.

JECFA (1978). 22nd report of the Joint FAO/WHO Expert Committee on Food Additives. WHO Food Additives Series 13.

Le Breton, E. (1956) Unpublished report as cited in JECFA 1973.

Lewis (2000) Sax’s dangerous properties of industrial materials Vol 3. Tenth Edition John Wiley & Sons New York.

Loria et al., (1962) Effect of sorbitol on iron absorption in man. American Journal of Clinical Nutrition. 10: 124 -127.

McCorkindale et al., (1954) Biochemical Journal 57: 518 [As cited in JECFA,


McKenzie et al., (1986) Three-generation reproduction study of rats ingesting up to 10% sorbitol in the diet and a brief review of the toxicological status of sorbitol. Food & Chemical Toxicology. 24(3): 191-200.

Minocha et al., (1984) Effect of activated charcoal in 70% sorbitol in healthy individuals. Journal of Toxicology & Clinical Toxicology. 22(6): 529-536.

Morgan et al., (1961) Proceedings of the Nutrition JECFA 1973].




cited in

Palmer et al., (1977) Effect of xylitol during a modified teratology study in rats. Final report. Unpublished report from Huntingdon Research Centre, Huntingdon, Cambridgeshire, England; submitted to the World Health Organization by Hoffman La Roche Co., Ltd., Basle Switzerland [As cited in JECFA 1978].

Palmer et al., (1978) Effect of xylitol on reproductive functions of multiple generations in the rat. Final report. Unpublished report from Huntingdon Research Centre, Huntingdon, Cambridgeshire, England; submitted to the World Health Organization by F. Hoffman La Roche Co., Ltd., Basle, Switzerland [As cited in JECFA 1978].

Seeberg et al., (1955) Metabolism of intravenously infused sorbitol. Proceeding of the Society of Experimental Biology. (N.Y.) 89: 303.

Stetten et al., (1951) Metabolism of sorbitol and glucose compared in normal and alloxan diabetic rats. Journal of Biological Chemistry. 193: 157.

Tacquet (1957) Unpublished report [As cited in JECFA 1973].

Treon (1963) Unpublished report [As cited in JECFA 1973].

Wick et al., (1951) Action of insulin on the permeability of cells to sorbitol. American Journal of Physiology 166: 421.