Dihydroxyacetone

Drugs, Cosmetics -> FDA Regulatory Status of Color Additives

FLAVORING AGENT OR ADJUVANT -> FDA Substance added to food

Crystalline powder

Colorless, crystalline solid

In water, 9.3X10+5 mg/L at 25 dege C

Soluble in ethanol, ethyl ether, acetone; insoluble in ligroin

Slowly soluble in 1 part water, 15 parts alcohol

90 °C

90 °C

0.02 [mmHg]

4.35X10-5 mm Hg at 25 °C

This chemical does not meet GHS hazard criteria for 12.9% (201 of 1563) of reports.

Warning

H315 (86.9%): Causes skin irritation [Warning Skin corrosion/irritation]

P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P351+P338, P319, P321, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 1563 reports by companies from 10 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Chemical: 2-Propanone, 1,3-dihydroxy-

2-Propanone, 1,3-dihydroxy- is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of 2-Propanone, 1,3-dihydroxy- are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 28-03-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/1158

2-Propanone, 1,3-dihydroxy-: Does not have an individual approval but may be used under an appropriate group standard

Certification of this color additive when used as in drugs is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act. Dihydroxyacetone may be safely used in amounts consistent with good manufacturing practice in externally applied drugs intended solely or in part to impart a color to the human body.

Certification of this color additive when used in cosmetics is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act. Dihydroxyacetone may be safely used in amounts consistent with good manufacturing practice in externally applied cosmetics intended solely or in part to impart a color to the human body.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

... Consumption of dihydroxyacetone and pyruvate (DHP) increases muscle extraction of glucose in normal men. To test the hypothesis that these three-carbon compounds would improve glycemic control in diabetes the effect of DHP on plasma glucose concentration, turnover, recycling, and tolerance in 7 women with noninsulin-dependent diabetes /was evaluated/. The subjects consumed a 1,500-calorie diet (55% carbohydrate, 30% fat, 15% protein), randomly containing 13% of the calories as DHP (1/1) or Polycose (placebo; PL), as a drink three times daily for 7 days. On the 8th day, primed continuous infusions of [6-(3)H]-glucose and U-(14)C-glucose were begun at 05.00 hr, and at 09.00 hr a 3-hr glucose tolerance test (75 g glucola) was performed. Two weeks later the subjects repeated the study with the other diet. The fasting plasma glucose level decreased by 14% with DHP (DHP = 8.0 + or - 0.9 mmol/L; PL = 9.3 + or - 1.0 mmol/L, p less than 0.05) which accounted for lower postoral glucose glycemia (DHP = 13.1 + or - 0.8 mmol/L, PL = 14.7 + or - 0.8 mmol/L, p< 0.05). 6-(3)H-glucose turnover (DHP = 1.50 + or - 0.19 mg/kg-L/min, PL = 1.77 + or - 0.21 mmg/kg-L/min, p less than 0.05) and glucose recycling, the difference in 6-(3)H-glucose and U-(14)C-glucose turnover rates, decreased with DHP (DHP = 0.25 + or - 0.07 mg/kg-L/min, PL = 0.54 + or - 0.10 mg/kg-L/min, p< 0.05). Fasting and postoral glucose, plasma insulin, glucagon, and C peptide levels were unaffected by DHP. /Mixture of dihydroxyacetone and pyruvate/.

Dihydroxyacetone (DHA) effectively antagonized the lethal effect of cyanide in mice and rabbits, particularly if administered in combination with thiosulfate. Oral DHA (2 and 4 g/kg) given to mice 10 min before injection (ip) of cyanide increased the LD50 values of cyanide from 5.7 mg/kg to 12 and 17.6 mg/kg, respectively. DHA prevented cyanide-induced lethality most effectively, if given orally 10-15 min before injection of cyanide. A combination of pretreatment with oral DHA (4 g/kg) and post-treatment with sodium thiosulfate (1 g/kg) increased the LD50 of cyanide by a factor of 9.9. Furthermore, DHA given intravenously to rabbits 5 min after subcutaneous injection of cyanide increased the LD50 of cyanide from 6 mg/kg to more than 11 mg/kg, while thiosulfate (1 g/kg) given intravenously 5 min after cyanide injection increased the LD50 of cyanide only to 8.5 mg/kg. DHA also prevented the convulsions that occurred after cyanide intoxication.

Potassium cyanide (CN) intoxication in mice was found to be effectively antagonized by dihydroxyacetone (DHA), particularly if administered in combination with another CN antidote, sodium thiosulfate. Cyanide-induced convulsions were also prevented by DHA treatment, either alone or in combination with thiosulfate. Injection (ip) of DHA (2 g/kg) 2 min after or 10 min before CN (sc) increased LD50 values of CN (8.7 mg/kg) by factors of 2.1 and 3.0, respectively. Treatment with a combination of DHA and thiosulfate after CN increased the LD50 by a factor of 2.4. Pretreatment with a combination of DHA and thiosulfate (1 g/kg) increased the LD50 of CN to 83 mg/kg. Administration of alpha-ketoglutarate (2.0 g/kg), but not pyruvate, 2 min after CN increased the LD50 of CN by a factor of 1.6. Brain, heart and liver cytochrome oxidase activities were also measured following in vivo CN treatment with and without DHA. Pretreatment with DHA prevented the inhibition of cytochrome oxidase activity by CN and treatment with DHA after CN accelerated the recovery of cytochrome oxidase activity, especially in brain and heart homogenates ...

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 23(SRC), determined from a log Kow of -1.95(2), and a regression-derived equation(3) indicates that dihydroxyacetone is expected to have very high mobility in soil(SRC). Volatilization of dihydroxyacetone from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.5X10-12 atm-cu m/mole(SRC), derived from its vapor pressure, 4.35X10-5 mm Hg(2), and water solubility, 9.3X10+5 mg/L(2). Dihydroxyacetone is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(2). Biodegradation data in soil were not available(SRC, 2012).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 23(SRC), determined from a log Kow of -1.95(2) and a regression derived equation(3), indicates that dihydroxyacetone is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 5.5X10-12 atm-cu m/mole(SRC), derived from its vapor pressure, 4.35X10-5 mm Hg(2), and water solubility, 9.3X10+5 mg/L(2). According to a classification scheme(5), an estimated BCF of 9(SRC), from its log Kow(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2012).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dihydroxyacetone, which has a vapor pressure of 4.35X10-5 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase dihydroxyacetone is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 2 days(SRC), calculated from its rate constant of 5.2X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Dihydroxyacetone does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from, as of October 25, 2012: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=96-26-4]

The Koc of dihydroxyacetone is estimated as 9(SRC), using a log Kow of -1.95(1) and a regression-derived equation(2). According to a classification scheme(2), this estimated Koc value suggests that dihydroxyacetone is expected to have very high mobility in soil. [

/HUMAN EXPOSURE STUDIES/ ... Consumption of dihydroxyacetone and pyruvate (DHP) increases muscle extraction of glucose in normal men. To test the hypothesis that these three-carbon compounds would improve glycemic control in diabetes the effect of DHP on plasma glucose concentration, turnover, recycling, and tolerance in 7 women with noninsulin-dependent diabetes /was evaluated/. The subjects consumed a 1,500-calorie diet (55% carbohydrate, 30% fat, 15% protein), randomly containing 13% of the calories as DHP (1/1) or Polycose (placebo; PL), as a drink three times daily for 7 days. On the 8th day, primed continuous infusions of [6-(3)H]-glucose and U-(14)C-glucose were begun at 05.00 hr, and at 09.00 hr a 3-hr glucose tolerance test (75 g glucola) was performed. Two weeks later the subjects repeated the study with the other diet. The fasting plasma glucose level decreased by 14% with DHP (DHP = 8.0 + or - 0.9 mmol/L; PL = 9.3 + or - 1.0 mmol/L, p less than 0.05) which accounted for lower postoral glucose glycemia (DHP = 13.1 + or - 0.8 mmol/L, PL = 14.7 + or - 0.8 mmol/L, p< 0.05). 6-(3)H-glucose turnover (DHP = 1.50 + or - 0.19 mg/kg-L/min, PL = 1.77 + or - 0.21 mmg/kg-L/min, p less than 0.05) and glucose recycling, the difference in 6-(3)H-glucose and U-(14)C-glucose turnover rates, decreased with DHP (DHP = 0.25 + or - 0.07 mg/kg-L/min, PL = 0.54 + or - 0.10 mg/kg-L/min, p< 0.05). Fasting and postoral glucose, plasma insulin, glucagon, and C peptide levels were unaffected by DHP. /Mixture of dihydroxyacetone and pyruvate/.

/ALTERNATIVE and IN VITRO TESTS/ ... The effects of dihydroxyacetone (DHA) on cell survival and proliferation of a human keratinocyte cell line, HaCaT /were investigated/. Dose- and time-dependent morphological changes, chromatin condensation, cytoplasmic budding and cell detachment were seen in cells treated with DHA. Several dead cells were observed after long-time (24 hr) incubation with 25 mM DHA or more. Furthermore, an extensive decline in proliferation was observed 1 day after DHA exposure for 24 hr. When applied in different concentrations (5-50 mM) and for different time periods (1, 3 or 24 hr) DHA caused a G(2)/M block after the cyclin B(1) restriction point. Exit from this cell-cycle block was associated with massive apoptosis, as revealed by a clonogenic assay, TUNEL staining and electron microscopy. Furthermore, DHA caused DNA damage as revealed by the alkaline comet assay.

An estimated BCF of 9 was calculated in fish for dihydroxyacetone(SRC), using a log Kow of -1.95(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for dihydrocyacetone is estimated as 5.5X10-12 atm-cu m/mole(SRC) derived from its vapor pressure, 4.35X10-5 mm Hg(1), and water solubility, 9.3X10+5 mg/L(1). This Henry's Law constant indicates that dihydrocyacetone is expected to be essentially nonvolatile from water surfaces(2). Dihydroxyacetone's Henry's Law constant indicates that volatilization from moist soil surfaces not may occur(SRC). Dihydroxyacetone is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Dihydroxyacetone (DHAT) is a color additive that is added to sunless tanning products to produce an artificial tan. Although this agent has been used extensively as safe sunless tanning, no published data are available to judge whether the abuse of DHAT causes a potential hazard to the human skin. The purpose of this study was to clarify whether frequent treatment with DHAT solutions had a deleterious effect on the wide skin surface of hairless descendants of Mexican hairless dogs. The skin reactions to the DHAT-treatment were investigated by daily clinical observations and histopathological examinations (21 and 42 days after the beginning of the DHAT-treatment). Clinical observations showed that skin color changes were apparent within 6 hr after the first treatment with 5% DHAT solutions, with maximal darkening between 12 and 24 hr. Twenty-one days after the beginning of the treatment with 5% DHAT solutions, the skin developed irritant dermatitis, and then the skin lesions gradually became severe during this study. Histopathological examinations showed entire epidermal thickening, 21 days after the beginning of the treatment with 5% DHAT solutions. Forty-two days after the beginning of the treatment with 5% DHAT solutions, the skin exhibited remarkable epidermal degeneration (hyperplastic and dyskeratotic changes) and moderate inflammatory reactions in the dermis. In severe dermatitic sites, found focal epidermal necrosis or interepidermal blister formation beneath the thickened parakeatotic corneum. Throughout this study, there were no clinical and histopathological changes in the sites treated with vehicle alone. These results revealed that the skin coloring generated by frequent wide treatments with DHAT caused severe contact dermatitis which was associated with the damaged stratum corneum.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ To assess the effects of oral intake of pyruvate and dihydroxyacetone on body composition and metabolism, rats were divided into two groups and pair-fed one of the following isocaloric diets for 112 days. The control diet was a liquid diet with the following caloric composition: 14% protein, 28% fat, and 58% carbohydrate. The experimental diet was the same as the control diet except for the partial substitution of carbohydrate content with pyruvate and dihydroxyacetone. Rats receiving the experimental diet gained less weight than rats receiving the control diet. This reduction in body weight appeared to be largely the result of inhibition of lipid accumulation. The experimental diet reduced body fat content by 32% without any significant effect on either protein or water content. Rats receiving the experimental diet did not have increased loss of calories in the stool, but had greater rates of heat production and energy expenditure, which was accompanied by an elevated plasma level of thyroxine. Furthermore, rats receiving the experimental diet had a smaller rate of lipid synthesis in their adipose tissue, and a reduced plasma insulin level. The data suggest that inhibition of gain in weight with the addition of pyruvate and dihydroxyacetone to the diet is the result of an increased loss of calories as heat at the expense of storage as lipid. /DHA and pyruvate mixture/

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... Supplements of glutamine, with and without dihydroxyacetone (DHA), which have previously been shown to stimulate hepatic glycogen synthesis, were administered in the diet of obese Zucker rats for periods of 1 and 3 wk. ...Dietary glutamine had no effect on food intake, weight gain, or body composition. Addition of DHA caused a reduction in food intake and weight gain and a stimulation of in vivo hepatic glycogen synthesis after 1 wk, but these changes were abolished by the end of 3 wk. Hepatic lipogenesis in vivo was increased by DHA treatment for 1 and 3 wk.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Once a week for 80 weeks, 0.1 mL of 5% or 40% dihydroxyacetone (DHA) in aqueous solution was placed on the clipped backs of Swiss-Webster mice, 100 animals per group, equally divided by sex. Fresh DHA solutions were prepared for each application. All mice that died and those killed in moribund condition were examined for tumors and other abnormalities. Tissues examined included skin, liver, spleen, stomach, small and large intestines, kidney, bladder, adrenals, gonads, uterus, pituitary, thyroid, thymus, salivary glands, axillary lymph nodes, lung, and brain. Grossly observable tumors were fixed for microscopic examination. The authors did not provide details regarding the disposition of animals still surviving after the final compound administration at 80 weeks. The authors reported that no significant differences were seen between control mice dosed with distilled water and those treated with DHA. Except for the brown color on the DHA-treated mice, no differences in physical appearance, behavior, weight gains, or survival were observed. The number of tumors identified in male mice were 22, 16, and 16, respectively, in the 0, 5%, and 40% DHA groups. Corresponding figures for the female mice were 26, 27, and 26 tumors in the 0, 5%, and 40% DHA groups, respectively. Microscopic findings were also reported, with no significant differences observed between treated animals and controls. The number of mice examined microscopically were 26 males and 30 females in the control group, 26 males and 26 females in the 5% DHA group, and 18 males and 25 females in the 40% DHA group.

For more Non-Human Toxicity Excerpts (Complete) data for DIHYDROXYACETONE (10 total), please visit the HSDB record page.

The rate constant for the vapor-phase reaction of dihydroxyacetone with photochemically-produced hydroxyl radicals has been estimated as 5.2X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 2 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Dihydroxyacetone is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Dihydroxyacetone contains does not contain chromophores that absorb at wavelengths >290 nm(2) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

Occupational exposure to dihydroxyacetone may occur through inhalation and dermal contact with this compound at workplaces where dihydroxyacetone is produced or used. Use data indicate that the general population may be exposed to dihydroxyacetone via dermal contact with consumer products containing dihydroxyacetone. (SRC)

Certification of this color additive when used as in drugs is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act. Dihydroxyacetone may be safely used in amounts consistent with good manufacturing practice in externally applied drugs intended solely or in part to impart a color to the human body.

Certification of this color additive when used in cosmetics is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act. Dihydroxyacetone may be safely used in amounts consistent with good manufacturing practice in externally applied cosmetics intended solely or in part to impart a color to the human body.

...The toxicity of dihydroxyacetone appears to be due to its intracellular conversion to an aldehyde compound, presumably methylglyoxal, since the glyoxalase mutant becomes sensitive to dihydroxyacetone. Based on information that gldA is preceded in an operon by the ptsA homolog and talC gene encoding fructose 6-phosphate aldolase, this study proposes that the primary role of gldA is to remove toxic dihydroxyacetone by converting it into glycerol.

Several bacteria use glycerol dehydrogenase to transform glycerol into dihydroxyacetone (DHA). DHA is subsequently converted into DHA phosphate (DHA-P) by an ATP- or phosphoenolpyruvate (PEP)-dependent DHA kinase. Listeria innocua possesses two potential PEP-dependent Dha kinases. One is encoded by 3 of the 11 genes forming the glycerol (gol) operon. This operon also contains golD (lin0362), which codes for a new type of DHA-forming NAD(+)-dependent glycerol dehydrogenase. The subsequent metabolism of DHA requires its phosphorylation via the PEP:sugar phosphotransferase system components enzyme I, HPr, and EIIA(DHA)-2 (Lin0369). P-EIIA(DHA)-2 transfers its phosphoryl group to DhaL-2, which phosphorylates DHA bound to DhaK-2. The resulting Dha-P is probably metabolized mainly via the pentose phosphate pathway, because two genes of the gol operon encode proteins resembling transketolases and transaldolases. In addition, purified Lin0363 and Lin0364 exhibit ribose-5-P isomerase (RipB) and triosephosphate isomerase activities, respectively. The latter enzyme converts part of the DHA-P into glyceraldehyde-3-P, which, together with DHA-P, is metabolized via gluconeogenesis to form fructose-6-P. Together with another glyceraldehyde-3-P molecule, the transketolase transforms fructose-6-P into intermediates of the pentose phosphate pathway. The gol operon is preceded by golR, transcribed in the opposite orientation and encoding a DeoR-type repressor. Its inactivation causes the constitutive but glucose-repressible expression of the entire gol operon, including the last gene, encoding a pediocin immunity-like (PedB-like) protein. Its elevated level of synthesis in the golR mutant causes slightly increased immunity against pediocin PA-1 compared to the wild-type strain or a pedB-like deletion mutant.

The present study investigated the fate of dihydroxyacetone (DHA) in an in vitro absorption study. In these studies, human ... skin penetration and absorption were determined over 24 or 72 hr in flow-through diffusion cells. ... For DHA, penetration studies found approximately 22% of the applied dose remaining in the skin (in both the stratum corneum and viable tissue) as a reservoir after 24 hr. Little of the DHA that penetrates into skin is actually available to become systemically absorbed.

Used as an emulsifier and in humectants, plasticizers, fungicides, and cosmetics (for synthetic suntan); [Hawley]

Farming (Pesticides) [Category: Industry]

Intermediate, emulsifier, humectant, plasticizers, fungicides, cosmetics (creates synthetic suntan)

Artificial tanning agent

2023: 20,338 lb

Production volumes for non-confidential chemicals reported under the Inventory Update Rule.[Table#7194]

Man-Tan, Oxatone, Tanorama, Q.T (Quick Tan); Tan Tone; Magic Tan

Otan, Soleal

All Other Chemical Product and Preparation Manufacturing

2-Propanone, 1,3-dihydroxy-: ACTIVE