Glyoxal

58.03610

58.04

203-474-9

50NP6JJ975

1162

262684

2810

DTXSID5025364

Yellow prisms or irregular pieces turning white on cooling; opaque at 10 °C; vapors are green|Yellow crystals or light yellow liquid

2912190001

34.14000

-0.61580

Glyoxal appears as yellow crystals melting at15°C. Hence often encountered as a light yellow liquid with a weak sour odor. Vapor has a green color and burns with a violet flame.

1.14 g/cm³ @ Temp: 20 °C

15 °C

51 °C @ Press: 776 Torr

285ºC

n20/D 1.409

Micible with water.

2-8ºC

18 mm Hg ( 20 °C)

>1 (vs air)

LD50 in rats, guinea pigs (mg/kg): 2020, 760 orally (Smyth)

Mixing glyoxal and /chlorosulfonic acid, ethyleneimine, oleum, nitric acid, or sodium hydroxide/...in a closed container caused temperature and pressure to increase.

Mild odor

pH of 40% aqueous solution = 2.1 to 2.7

1.14e-11 cm3/molecule*sec

3.33e-09 atm-m3/mole|Henry's Law constant = 3.33X10-9 atm-cu-m/mol at 25 °C

10.0 lb/gallon at 20 °C; burns with violet flame; aqueous solution contains monomolecular glyoxal and reacts weakly with acid; glyoxal VP resists discoloration; undergoes many addition & condensation reactions with amines, amides, aldehydes & hydroxyl-containing materials.|Glyoxal is oxidized by dilute nitric acid to glyoxyl acid, & by concentrated nitric acid to oxalic acid|Anhydrous polymer changes to monomer on heating; non-hygroscopic; crystalline powder; more soluble in hot water than in cold water /Dihydrate/|Conversion factors: 1 mg/L= 422 ppm; 1 ppm= 2.4 mg/cu m|Hydroxyl radical reaction rate constant = 1.14X10-11 cu cm/molec-sec at 25 °C

Mixtures with air may explode. Polymerizes quickly on standing, or on contact with a trace of water (possibly a violent reaction), or when dissolved in solvents containing water, [Merck, 502(1968)]. Soluble in water. An aqueous solution contains mono molecular glyoxal. [Hawley]

Aldehydes

Polymerizable

GLYOXAL reacts vigorously with strong oxidizing agents such as nitric acid. Polymerizes rapidly even at low temperature if anhydrous [Noller]. Aqueous solutions are more stable but also polymerize on standing. Reacts with itself in the presence of base to give glyconates. Undergoes addition and condensation reactions that may be exothermic with amines, amides, aldehydes, and hydroxide-containing materials. Mixing in equal molar portions with any of the following substances in a closed container caused the temperature and pressure to increase: chlorosulfonic acid, oleum, ethyleneimine, nitric acid, sodium hydroxide [NFPA 1991].

545 °F (NTP, 1992)|285 °C

Critical temperature = 495 K; critical pressure = 5.88X10+6 Pa

UN 1760

1

R20; R36/38; R43; R68

S36/37

MD2700000

Xn

Well closed.

Stability Combustible. Incompatible with strong oxidizing agents. Strong reducing agent. May polyermize exothermically.

P280-P305 + P351 + P338

H315-H317-H319-H341

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.

Mixture of vapor and air may explode.|Reacts violently with chlorosulfonic acid; ethylene imine; oleum; sodium hydroxide; nitric acid.|An aqueous solution monomolecular glyoxal and reacts weakly to acid.|Mixtures with air may explode, and contact with water causes violent polymerization. Like formaldehyde, pure glyoxal may polymerize exothermically and ignite in storage.

Glyoxal is an indirect food additive for use only as a component of adhesives.

Behavior in Fire: Heat may cause polymerization to a combustible, viscous material. (USCG, 1999)|Combustible.

|Warning|H315: Causes skin irritation [Warning Skin corrosion/irritation]|P201, P202, P261, P264, P271, P272, P280, P281, P302+P352, P304+P312, P304+P340, P305+P351+P338, P308+P313, P312, P321, P332+P313, P333+P313, P337+P313, P362, P363, P405, and P501|Danger|H302+H332 (30.27%): Harmful if swallowed or if inhaled [Warning Acute toxicity, oral; acute toxicity, inhalation]|P201, P202, P261, P264, P270, P271, P272, P280, P281, P285, P301+P312, P302+P352, P304+P312, P304+P340, P304+P341, P305+P351+P338, P308+P313, P312, P321, P330, P332+P313, P333+P313, P337+P313, P342+P311, P362, P363, P403+P233, P405, and P501|Aggregated GHS information provided by 1458 companies from 28 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P280, P301+P312, P302+P352, P305+P351+P338, P310, P321, P330, P332+P313, P362, and P501|Aggregated GHS information provided by 38 companies from 1 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P261, P264, P270, P271, P272, P280, P281, P301+P312, P302+P352, P304+P312, P304+P340, P305+P351+P338, P308+P313, P312, P321, P330, P332+P313, P333+P313, P337+P313, P362, P363, P405, and P501|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P260, P261, P264, P270, P271, P272, P280, P301+P310, P302+P352, P304+P312, P304+P340, P305+P351+P338, P309+P311, P312, P314, P321, P330, P332+P313, P333+P313, P337+P313, P362, P363, P405, and P501|P260, P261, P264, P270, P272, P280, P301+P310, P302+P352, P305+P351+P338, P309+P311, P314, P321, P330, P332+P313, P333+P313, P337+P313, P362, P363, P405, and P501

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)|Use carbon dioxide, foam, powder.

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

SMALL SPILLS AND LEAKAGE: If you should spill this chemical, use absorbent paper to pick up all liquid spill material. Seal the absorbent paper, as well as any of your clothing which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Wash any surfaces you may have contaminated with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should keep this material in a tightly closed container under an inert atmosphere, and store it at ambient temperatures. (NTP, 1992)

Goggles or face shield,40% solution; rubber gloves (USCG, 1999)|Wear protective clothing and self contained breathing apparatus.|/If contact with skin is anticipated/: /Wear/ protective gloves, protective clothing. /If contact with eyes is anticipated/: Safety goggles, or eye protection in combination with breathing protection. /If ingestion is anticipated/: Do not eat, drink, or smoke during work.

Mixtures with air may explode.|Mixing glyoxal and /chlorosulfonic acid, ethyleneimine, oleum, nitric acid, or sodium hydroxide/...in a closed container caused temperature and pressure to increase.

Collect leaking and spilled liquid in sealable containers as far as possible. Use face shield. (Extra personal protection: filter respirator for organic gases and vapours.)|Waste glyoxal resins from textile treatment are biodegraded by pseudomonas using the aqueous resin solution as a substrate.

While extent of precautions needed under various types of industrial use is not known with certainty, it would appear reasonable to handle these dialdehydes with certain precautions as used for formaldehyde and other lower molecular weight monoaldehydes. /Dialdehydes/|/If ingested/: /Get/ fresh air, rest. /If contacted with eyes/: Remove contaminated clothes, rinse skin with plenty of water or shower. /If contacted with skin/: Remove contaminated clothes, rinse skin with plenty of water or shower. /If contacted with eyes/: First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then take to a doctor. /If ingested/: Rinse mouth, refer for medical attention.|SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Liquid /is/ irritating to skin and eyes.|Inhalation causes some irritation of nose and, 40% solution throat.

Personal protection: face shield and filter respirator for organic gases and vapours adapted to the airborne concentration of the substance. Collect leaking and spilled liquid in sealable containers as far as possible.

Well closed.

A harmful contamination of the air can be reached very quickly on evaporation of this substance at 20 °C.

The substance is irritating to the eyes and skin.

Repeated or prolonged contact may cause skin sensitization.

NO open flames.

AVOID ALL CONTACT!

Use local exhaust or breathing protection.

Protective gloves. Protective clothing.

Wear safety goggles or eye protection in combination with breathing protection.

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Glyoxal is produced, as an intermediate or a final product, by process units covered under this subpart.

Glyoxal was detected in the Tuscarora Mountain Tunnel, PA at average levels of 0.3 ug/cu m (tunnel inlet) and 93 ug/cu m (tunnel outlet)(1). The average emission factor of glyoxal in the tunnel from vehicles was estimated as 0.184 mg/km(1). Glyoxal was emitted from the tailpipe of diesel operated trucks at a rate of 2,100 ug/km(2). Glyoxal was detected in the emissions of combusted wood at levels of 670, 439 and 616 mg/kg for pine, oak and eucalyptus, respectively(3). Glyoxal was emitted from the tailpipe of light duty gasoline powered vehicles at rates of 170 ug/km (vehicles equipped with catalytic converters) and 28,000 ug/km (vehicles not equipped with catalytic converters)(4).

URBAN/SUBURBAN: Glyoxal was detected in the ambient air of Rio de Janeiro, Brazil at levels of 0.011-0.649 ug/cu m from samples obtained from October 1999-November 2000(1). Glyoxal was detected in the ambient air of Long Beach, Azusa, Claremont, and Los Angeles, CA at levels of 0-4 ppb in September 1993(2). Highest levels were observed during mid afternoon of a two day smog episode, indicating photochemical formation of glyoxal from other hydrocarbons(2). Glyoxal was detected at levels of 0.20 and 0.41 ug/cu m in the ambient air of a city residential site and city street site in Berlin, Germany, respectively(3). Glyoxal was detected in aerosol samples from Tokyo, Japan in 1992 at levels ranging from 0.038-0.046 ug/cu m(4). The average concentration of glyoxal measured in ambient air in the vicinity of Los Angeles, CA was reported as 2.4 ug/cu m(5).|RURAL/REMOTE: Glyoxal was detected at a level of 0.16 ug/cu m in the ambient air of a rural residential site in Berlin, Germany(1).

IDENTIFICATION: Glyoxal is generally available as an aqueous solution, typically containing 30-50% glyoxal in which hydrated oligomers are present. This chemical is used as a chemical intermediate in the production of pharmaceuticals and dyestuffs, as a cross-linking agent in the production of polymers, as a biocide, and as a disinfecting agent. Due to microbial activity as well as non-enzymatic autoxidation of oil or browning reactions of saccharides, glyoxal is frequently detected in fermented food and beverages. It is found in beer, wine and tea. HUMAN EXPOSURE: The main routes of occupational exposure to glyoxal during use as a disinfectant are via inhalation and dermal absorption. The general population is exposed mainly through ingestion of glyoxal containing food, but could be exposed through polluted air in urban areas and traces of glyoxal found in drinking water. Glyoxal is endogenously produced during normal cellular metabolism by a multitude of enzyme independent pathways. Glyoxal is found in human blood and individuals with diabetes or renal failure have higher concentrations. Glyoxal is irritating to mucous membranes and acts as a skin sensitizing agent. ANIMAL/PLANT STUDIES: The acute toxicity of glyoxal in experimental animals is low to moderate, depending upon the concentration of the chemical. After inhalation exposure, local irritations of the eyes and respiratory tract as well as hyperemia and foamy secretion in the lungs predominate. After oral exposure to glyoxal, macroscopic observations include irritations to the gastrointestinal tract and congestion in the gastrointestinal tract, lung, kidney and adrenal glands. In the prominent target organs, pancreas and kidney, the toxic action of glyoxal leads to severe degenerative changes resembling those induced during diabetes. A 28 day study at high dosages of glyoxal administered to rats effects included reduced water and food intake and retardation of body weight gain. A 90 day feeding study in dogs failed to reveal any treatment related effects. Glyoxal is irritating to mucous membranes and acts as a sensitizing agent in experimental animals. Fetotoxic effects occurred only with doses of glyoxal that induced maternal toxicity. Glyoxal is directly genotoxic in vitro in bacterial and mammalian cells inducing DNA adducts, mutations, chromosomal aberrations, DNA repair, sister chromatid exchanges and DNA single strand breaks. In vivo, a genotoxic activity of glyoxal was established at the site of application in the pyloric mucosa of rats by demonstration of unscheduled DNA synthesis and DNA simple strand breaks were further observed in the rat liver. Glyoxal showed tumor promoting activity in a two stage glandular stomach carcinogenesis study in male Wistar rats, where it was inactive in a short-term liver foci assay. In an assay for tumor initiating activity of glyoxal in skin and in cell transformation assays, glyoxal yielded negative results. Exposure to glyoxal has shown to inhibit activities of aerobic and anerobic bacteria , green algae and invertebrates.

LD50 Rabbit dermal 10 g/kg|LD50 Rat oral 7070 mg/kg|LC50 Rat (female) inhalation 2410 mg/cu m/4 hr /40% glyoxal/|LC50 Rat (male) inhalation 2470 mg/cu m/4 hr /40% glyoxal/|For more Non-Human Toxicity Values (Complete) data for GLYOXAL (18 total), please visit the HSDB record page.

/OTHER TERRESTRIAL SPECIES/ ... Glyoxal induced meiotic abnormalities on microsporocytes of corn (Zea mats). For topinambur (Helianthus tuberosus), approx. 100 mg glyoxal/L /caused/ toxic concerning the proliferation of the rhizome fragments in an in vitro tissue culture. The NOEC (no-observedeffect concentration) was 68 mg glyoxal/L, and the EC30 value (30 % inhibition of proliferation) was 136 mg glyoxal/L.

During certain pathological conditions (e.g., diabetes mellitus, uraemia), raised concentrations of glyoxal have been measured. The concentration of glyoxal in blood samples from normal human subjects (n = 19) was 0.21 +/- 0.14 umol/kg. For blood plasma, a value of approximately 0.1 umol/liter estimated for normal healthy subjects, which can double in diabetics.

Glyoxal is endogenously produced during normal cellular metabolism by a multitude of enzyme-independent pathways, such as the spontaneous reaction of amino groups in proteins with reducing sugars (Maillard reaction), sugar autoxidation, DNA oxidation, peroxidation of polyunsaturated fatty acids, and UV photodamage, and in conditions of oxidative stress and depletion of GSH(1).|Glyoxal is a combustion product of burned wood(1), and may be released to the environment from forest fires(SRC).

Glyoxal's production and use as a croslinking agent in permanent-press fabrics, textiles, organic synthesis, glues, and biocides(1,2), may result in its release to the environment through various waste streams(SRC).|Glyoxal is a photochemical degradation product of aromatic and olefinic hydrocarbons(1). The reaction of cyclopentene with ozone in the atmosphere leads to the formation of glyoxal(2). Glyoxal has been identified as a disinfection byproduct in drinking water treated with chlorine dioxide and ozone(3,4).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1(SRC), determined from a structure estimation method(2), indicates that glyoxal is expected to have very high mobility in soil(SRC). Volatilization from moist soil surfaces is not expected to be an important environmental fate process given a Henry's law constant of 3.33X10-9 atm-cu m/mol(3). The potential for volatilization of glyoxal from dry soil surfaces may exist(SRC) based upon an extrapolated vapor pressure of 255 mm Hg at 25 °C(4). Screening studies using sewage seed have indicated that glyoxal is readily biodegradable(5,6).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1(SRC), determined from a structure estimation method(2), indicates that glyoxal is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected to be an important environmental fate process(3), based on a Henry's law constant of 3.33X10-9 atm cu m/mol(4). According to a classification scheme(5), an estimated BCF of 3(SRC), from an estimated log Kow of -1.66(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Glyoxal undergoes direct photolysis with an estimated atmospheric lifetime of 5 hours(8), suggesting that photolysis in sunlit surface waters may be an important environmental fate process(SRC). Glyoxal is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups. Screening studies using sewage seed have indicated that glyoxal is readily biodegradable(9,10).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), glyoxal, which has an extrapolated vapor pressure of 255 mm Hg at 25 °C(2), is expected to exist solely in the vapor phase in the ambient atmosphere. Vapor-phase glyoxal 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 34 hours(SRC), calculated from its rate constant of 1.14X10-11 cu cm/molecule-sec at 25 °C(3). Glyoxal also undergoes direct photolysis in the environment, with an estimated atmospheric lifetime of 5 hours(4). Glyoxal also reacts with ozone(4); however, the rate is significantly slower than the rate of direct photolysis and reaction with hydroxyl radicals and not considered an important atmospheric degradation mechanism(4).

The rate constant for the vapor-phase reaction of glyoxal with photochemically-produced hydroxyl radicals has been measured as 1.14X10-11 cu cm/molecule-sec at 25 °C (1). This corresponds to an atmospheric half-life of about 34 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Glyoxal absorbs light greater than 290 nm and undergoes direct photolysis(2). The estimated photolysis lifetime of glyoxal in the atmosphere has been estimated as 5 hours(2). Glyoxal also reacts with ozone(2); however, the rate is significantly slower than the rate of direct photolysis and reaction with hydroxyl radicals and not considered an important atmospheric degradation mechanism(2). Glyoxal is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(3).

An estimated BCF of 3 was calculated for glyoxal(SRC), using an estimated log Kow of -1.66(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).

Using a structure estimation method based on molecular connectivity indices(1), the Koc for glyoxal can be estimated to be 1(SRC). According to a classification scheme(2), this estimated Koc value suggests that glyoxal is expected to have very high mobility in soil(SRC).

The Henry's Law constant for glyoxal is 3.33X10-9 atm-cu m/mol(1). This Henry's Law constant indicates that glyoxal is expected to be essentially nonvolatile from water and moist soil surfaces(2). The potential for volatilization of glyoxal from dry soil surfaces may exist(SRC) based upon an extrapolated vapor pressure of 255 mm Hg at 25 °C(3).

DRINKING WATER: Glyoxal was identified as a disinfection byproduct in treated water at levels of 0.23-173 ug/L, depending upon the disinfection process(1). Glyoxal was identified as a byproduct produced by the disinfection of drinking water (treatment method used chlorine dioxide), and was detected at levels of 3.5-4.9 ug/L in drinking water samples from Israel(2).|RAIN/SNOW: Glyoxal was detected in snow/sleet (2.62-5.53 ug/L) and rain (0.05-53.2 ug/L) from Tokyo, Japan in 1992(1). Glyoxal was detected in rain (13-231 ug/L), fog (824-1,978 ug/L), and mist (1,206-1717 ug/L), in Los Angeles, CA(2).

Glyoxal was detected in auto-oxidized edible oils (sesame, safflower and sardine oils) at levels of <1 to 5 ug/g(1). Glyoxal was identified, not quantified, as a volatile component of roasted coffee beans(2). Glyoxal is frequently detected in fermented foods and beverages(3).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 50,395 workers (9,890 of these are female) are potentially exposed to glyoxal in the US(1). Occupational exposure to glyoxal may occur through inhalation and dermal contact with this compound at workplaces where glyoxal is produced or used(SRC). The general population is exposed to glyoxal via dermal exposure from permanent press fabrics, through the inhalation of ambient air, ingestion of food, and the ingestion of drinking water where it may be produced as a disinfection byproduct(SRC).

Glyoxal has been detected in human blood(1).

In biological materials, less than 10% of the glyoxal present is in unbound forms in aqueous solution (free glyoxal and hydrates), as most of the reactive carbonyl groups are reversibly bound to cysteinyl, lysyl, and arginyl residues of proteins.|The endogenous concentrations of glyoxal in human tissues and body fluids, as with other alpha-oxoaldehydes, are limited by the high catalytic efficiency of the glyoxalase system as well as by the rapid reaction of glyoxal with proteins.|After acute and chronic oral administration, there is evidence of systemic absorption, with distribution to erythrocytes, liver, lung, kidney, pancreas, and adrenal glands. There is some qualitative evidence that glyoxal is absorbed after dermal exposure. Granular and vacuole degeneration in liver, kidney, and pancreas have been observed along with a distinct increase in blood glucose levels following dermal application.

/In lab animals/...urine contained oxalic acid the day following oral administration but disappeared during the two next weeks.|The cytosolic GSH-dependent glyoxalase system is the major pathway for the detoxification of glyoxal ... Glyoxal reacts non-enzymatically with GSH with formation of a hemithioacetal, which is subsequently converted to S-glycolylglutathione by glyoxalase I. Glyoxalase II catalyses the hydrolysis of S-glycolylglutathione to glycolate, re-forming the GSH from the first reaction. The activity of glyoxalase I in situ is approximately proportional to the cytosolic concentration of GSH. When GSH is severely depleted (eg, under conditions of oxidative stress), however, 2-oxoaldehyde dehydrogenase and aldose reductase may also metabolize glyoxal. Imbalances in intracellular redox systems may impair these detoxification mechanisms, resulting in higher levels of glyoxal. A further GSH-independent route of detoxification via glyoxalase III exists.|Glyoxal is metabolized in vitro by the rat liver to oxalic acid via glycolic acid and glyoxylic acid.

Glyoxal attacks the amino groups of proteins, nucleotides, and lipids with its highly reactive carbonyl groups. A sequence of non-enzymatic reactions, called glycation, yields stable advanced glycation end-products (AGEs) with a background extent of 0.1-1% of lysine and arginine residues in proteins and 1 in 1.0 X 10-7 nucleotides in DNA. ... Glyoxal forms stable adducts with guanosine by reaction with the N-1 as well as with the exocyclic nitrogen of guanine. The rate of glyoxal-guanine adduct formation is rapid under physiological conditions. A stable tricyclic glyoxal-DNA adduct is formed by covalent binding to two nitrogens of guanine under physiological conditions in vitro. Besides 8-hydroxy-deoxyguanosine, the glyoxal-deoxyguanosine (dG) adduct is one of the major deoxyguanosine oxidation products, being formed by oxygen radicals, lipid peroxidation systems, various types of oxidative stress, and UV irradiation and after in vivo exposure to beta-hydroxy-substituted N-nitrosamines.|Glyoxal ... is considered an important intermediate in the formation of advanced glycation end-products (AGEs). AGE modification alters protein function and inactivates enzymes, resulting in disturbance of cellular metabolism, impaired proteolysis, and inhibition of cell proliferation and protein synthesis. The extent of AGE modification increases with the increasing life span of proteins. Consequently, AGEs are especially associated with long-lived proteins, such as collagens, lens crystallins, and neurofilaments, but also have been identified in shorter-lived proteins, including hemoglobin, plasma proteins, lipoproteins, and intracellular proteins.|Inhibition studies in bacterial mutagenicity tests demonstrated the production of the reactive oxygen species superoxide, hydrogen peroxide, and singlet oxygen from glyoxal. The mutagenic activity of glyoxal is related to singlet oxygen, as well as to the intracellular GSH level. The hydroxyl radical plays a prominent role in glyoxal-induced DNA cleavage.|... Isolated rat hepatocytes were incubated with different concentrations of glyoxal. Glyoxal by itself was cytotoxic at 5mM, depleted GSH, formed reactive oxygen species (ROS) and collapsed the mitochondrial membrane potential. Glyoxal also induced lipid peroxidation and formaldehyde formation. Glycolytic substrates, eg fructose, sorbitol and xylitol inhibited glyoxal-induced cytotoxicity and prevented the decrease in mitochondrial membrane potential suggesting that mitochondrial toxicity contributed to the cytotoxic mechanism. Glyoxal cytotoxicity was prevented by the glyoxal traps d-penicillamine or aminoguanidine or ROS scavengers were also cytoprotective even when added some time after glyoxal suggesting that oxidative stress contributed to the glyoxal cytotoxic mechanism.

Inhalation causes some irritation of nose and,40% solution throat. Contact with liquid,40% solution irritates eyes and causes mild irritation of skin; stains skin yellow. (No information available on symptoms of ingestion.) (USCG, 1999)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. Volatile chemicals have a high risk of being aspirated into the victim's lungs during vomiting which increases the medical problems. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. IMMEDIATELY transport the victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

Fresh air, rest.

Remove contaminated clothes. Rinse skin with plenty of water or shower.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

...Remove contaminated clothing and shoes. Flush affected areas with plenty of water. If in eyes, hold eyelids open, and flush with plenty of water. If swallowed and victim is conscious, have victim drink water, or milk.

/HUMAN EXPOSURE STUDIES/ ... Glyoxal was not an initiator. A repeated insult patch test conducted in 155 human volunteers indicated that glyoxal was not a sensitizer.|/HUMAN EXPOSURE STUDIES/ Of 14 workers who had contact with 40% glyoxal, 9 exhibited a contact dermatitis with localizations mainly on the lower arms and fingers. Patch tests with a 20% glyoxal solution produced a positive reaction in 7 of 9 workers.|/SIGNS AND SYMPTOMS/ Moderately irritating to skin and mucous membranes.|/SIGNS AND SYMPTOMS/ In the 1940s to 1960s, histopathological findings in studies with acute application of glyoxal pointed to a connection between effects induced by glyoxal and those induced in the course of diabetes; this has been confirmed by recent intensive studies on the mechanism of action of endogenous glyoxal and its involvement in the development of diabetic complications.|For more Human Toxicity Excerpts (Complete) data for GLYOXAL (9 total), please visit the HSDB record page.

Ethanedial

The substance can be absorbed into the body by inhalation of its aerosol or vapour and by ingestion.

Redness.

Redness. Pain.

80% as a chemical intermediate for dihydroxydimethylol ethylene urea for post-curing of permanent-press fabrics, 12% as a cross-linking agent in the paper industry, 8% in the manufacture of homogenized tobacco to wrap cigars, & in numerous miscellaneous applications (1972)

Commercially available in anhydrous form as crystalline dihydrate, or as a 40% aqueous solution which may contain polymerization inhibitors. /Dihydrate/|GRADES: 40% solution; pure, solid; VP.|Glyoxal is a dialdehyde supplied commercially as 30% aqueous solution, consisting of mixture of monomeric & polymeric hydrates along with small amounts of impurities which render the solution acid.|Glyoxal can undertake rotational isomerization between the planar cis and trans conformations, with trans-glyoxal being the more stable isomer.|...It is generally employed as an aqueous solution... in which hydrated oligomers are present due to nucleophilic addition. ...Some of the most important hydrated derivatives of glyoxal formed by nucleophilic addition in aqueous solution... include the monomer ethane-1,1,2,2-tetraol (I), the dimer 2-dihydroxymethyl-(1,3)dioxolane-4,5-transdiol (II), and the trimer bis(dioxolane) (i.e., 2,2'-bi-1,3-dioxolanyl-4,4',5,5'-tetraol) (III) - both cis and trans configurations. However, the proportion of the different structures varies with concentration and pH.

Adhesive manufacturing|Ethanedial: ACTIVE|Ethanedial, trimer: INACTIVE

Method: EPA-OGWDW/TSC 556.1; Procedure: Gas chromatography/electron capture detection; Analyte: glyoxal; Matrix: finished drinking water and raw source water; Detection Limit: 0.39 ug/L.|Method: EPA-TSC/NERL 556; Procedure: Pentafluorbenzylhydroxylamine derivatization and capillary gas chromatography with electron capture detection; Analyte: glyoxal; Matrix: finished drinking water and raw source water; Detection Limit: 0.59 ug/L.

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