Malonic acid

104.06100

104.06

205-503-0

9KX7ZMG0MK

1085

8124

DTXSID7021659

White crystals|Crystalline powder|Colorless hygroscopic solid which sublimes in vacuum

2917190090

74.60000

-0.8

Malonic acid appears as white crystals or crystalline powder. Sublimes in vacuum. (NTP, 1992)

1.6 g/cm³

135 °C (decomp)

215 °C @ Press: 14 Torr

201.9ºC

1.479

H2O: 1400 g/L (20 ºC)

Store at RT.

4.66E-07mmHg at 25°C

2.85(at 25 °C)

2.85 (at 25 °C)|pKa1 = 2.8, pKa2 = 5.7 at 25 °C

Enthalpy of Sublimation: 72.7 kJ/mol at 306 deg K, 108.0 kJ/mol at 348 deg K|Henry's Law constant = 4.8X10-13 atm-cu m/mole at 23 °C (estimated from vapor pressure and water solubility)|Hydroxyl radical reaction rate constant = 1.6X10-12 cu-cm/molc sec at 25 °C (est)

Water soluble.

Acids, Carboxylic

MALONIC ACID is a carboxylic acid. Carboxylic acids donate hydrogen ions if a base is present to accept them. They react in this way with all bases, both organic (for example, the amines) and inorganic. Their reactions with bases, called "neutralizations", are accompanied by the evolution of substantial amounts of heat. Neutralization between an acid and a base produces water plus a salt. Carboxylic acids with six or fewer carbon atoms are freely or moderately soluble in water; those with more than six carbons are slightly soluble in water. Soluble carboxylic acid dissociate to an extent in water to yield hydrogen ions. The pH of solutions of carboxylic acids is therefore less than 7.0. Many insoluble carboxylic acids react rapidly with aqueous solutions containing a chemical base and dissolve as the neutralization generates a soluble salt. Carboxylic acids in aqueous solution and liquid or molten carboxylic acids can react with active metals to form gaseous hydrogen and a metal salt. Such reactions occur in principle for solid carboxylic acids as well, but are slow if the solid acid remains dry. Even "insoluble" carboxylic acids may absorb enough water from the air and dissolve sufficiently in it to corrode or dissolve iron, steel, and aluminum parts and containers. Carboxylic acids, like other acids, react with cyanide salts to generate gaseous hydrogen cyanide. The reaction is slower for dry, solid carboxylic acids. Insoluble carboxylic acids react with solutions of cyanides to cause the release of gaseous hydrogen cyanide. Flammable and/or toxic gases and heat are generated by the reaction of carboxylic acids with diazo compounds, dithiocarbamates, isocyanates, mercaptans, nitrides, and sulfides. Carboxylic acids, especially in aqueous solution, also react with sulfites, nitrites, thiosulfates (to give H2S and SO3), dithionites (SO2), to generate flammable and/or toxic gases and heat. Their reaction with carbonates and bicarbonates generates a harmless gas (carbon dioxide) but still heat. Like other organic compounds, carboxylic acids can be oxidized by strong oxidizing agents and reduced by strong reducing agents. These reactions generate heat. A wide variety of products is possible. Like other acids, carboxylic acids may initiate polymerization reactions; like other acids, they often catalyze (increase the rate of) chemical reactions This chemical is incompatible with strong oxidizers. It is also incompatible with bases and reducing agents. (NTP, 1992)

Molar heat of combustion: 864 kJ/mol

92 kJ/mol

Critical temperature: 805 K (estimated); critical pressure: 5640 kPa (estimated)

III

UN 3261

1

R22; R36/37/38

S26-S37/39

OO0175000

Xn

Separated from bases and strong oxidants.

Stable. Incompatible with oxidizing agents, reducing agents, bases.

P280-P305 + P351 + P338

H302-H318

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.|Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Contaminated packaging: Dispose of as unused product.

Incompatible materials: Bases, Oxidizing agents, Reducing agents

UN 3261

P280; P305 + P351 + P338

Flash point data for this chemical are not available; however, it is probably combustible. (NTP, 1992)|Combustible.

|Danger|H302 (81.68%): Harmful if swallowed [Warning Acute toxicity, oral]|P261, P264, P270, P271, P280, P301+P312, P302+P352, P304+P340, P305+P351+P338, P310, P312, P321, P330, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 279 companies from 17 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P280, P301+P312, P305+P351+P338, P310, P330, and P501|Warning|P264, P270, P301+P312, P330, and P501

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces 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 store this chemical under ambient temperatures, and keep it away from oxidizing materials. (NTP, 1992)

MINIMUM PROTECTIVE CLOTHING: If Tyvek-type disposable protective clothing is not worn during handling of this chemical, wear disposable Tyvek-type sleeves taped to your gloves. RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. Splash proof safety goggles should be worn while handling this chemical. Alternatively, a full face respirator, equipped as above, may be used to provide simultaneous eye and respiratory protection. (NTP, 1992)|Eye/face protection: Face shield and safety glasses. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Skin protection: Handle with gloves.|Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

ACCIDENTAL RELEASE MEASURES; Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.|Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.|ACCIDENTAL RELEASE MEASURES; Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Do not let product enter drains.|Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.|For more Preventive Measures (Complete) data for Malonic acid (6 total), please visit the HSDB record page.

A skin and severe eye irritant.

Sweep spilled substance into covered containers. Then wash away with plenty of water.

Separated from bases and strong oxidants.

Evaporation at 20 °C is negligible; a harmful concentration of airborne particles can, however, be reached quickly when dispersed.

The substance is severely irritating to the eyes and respiratory tract. The substance is irritating to the skin.

NO open flames.

Use local exhaust or breathing protection.

Protective gloves.

Wear safety goggles.

Based on monitoring at a Los Angeles roadway tunnel, the emission rate malonic acid was 14.0 ug/L of gasoline-equivalent burned(1). Malonic acid was detected in effluents from a kraft pulp mill bleach factory(2) and at a concentration of 8.1 mg/L in shale oil process retort water(3).

SEDIMENT: A sediment sample collected at a bog in the foothills of the Sierra Nevada Mountains in 1984 had a malonic acid concentration of 225 nmol/g(1). [(1) Kawamura K, Kaplan IR Environ Sci Technol 21: 105-110 (1987)|SOIL: A soil sample collected at the north campus of UCLA (Los Angeles, CA) in 1984 had a malonic acid concentration of 5.93 nmol/g(1).

URBAN/SUBURBAN: Monitoring conducted in Los Angeles, CA in 1984 detected malonic acid concentrations of 0.14-1.58 nmol/cu m(1). Aerosol samples (PM2.5) collected at 8 sites in the southeastern US in 1999-2000 monitoring detected malonic acid concentrations of 1.82-4.30 ng/cu m(2). Air monitoring conducted at five sites in southern CA in Sept 1993 detected malonic acid at an average particulate concentration of 38.6 ng/cu m (range of 0.3-473.5 ng/cu m)(3). An average malonic acid concentration of 55 ng/cu m (range of 6.4-190 ng/cu m) was detected in air samples collected in Tokyo, Japan in 1988-1989(4). Atmospheric aerosol samples taken from a semi-urban site in Schenectady, NY in 1991 had a malonic acid concentration range of 43-107 ng/cu m(5). Ambient aerosol samples collected at seven locations in Hong Kong during Oct-Dec 2003 had a mean malonic acid concentration of 142 ng/cu m (range of 38-324 ng/cu m)(6). Atmospheric particulate samples collected from 12 sites in southern California in 1995 as part of the Southern California Children's Health Study detected average annual malonic acid concentrations ranging from 0.76 to 8.02 ng/cu m(7).|RURAL/REMOTE: Air monitoring at mountainous inland sites in Japan in July 1986 (Takasaki and Karuizawa) detected malonic acid concentrations of 12.0 and 11.1 ng/cu m respectively(1). Arctic aerosol sampling conducted in Alert, Canada during 1987-1988 detected malonic acid concentration range of 0.05-19 ng/cu m (average of 2.5 ng/cu m)(2). A background level of malonic acid in aerosol from the Antarctic is reported as 0.4 ng/cu m(3). Aerosol collected from the Great Smoky Mountain National Park, TN in the summer of 1995 had a day-time malonic acid concentration of 4.4-28.6 ng/cu m(4).

Dust samples collected from outside locations at UCLA and downtown Los Angeles, CA in 1984 had malonic acid concentrations of 22.3 and 56.7 nmol/g respectively(1). The emission rate of malonic acid from the combustion of pine wood was 38.35 mg/kg log burned(2). Malonic acid has been identified as a constituent of tobacco smoke(3).

IDENTIFICATION AND USE: Malonic acid is used in biochemical and cell studies, as well as in chemical synthesis. This acid is well known as a competitive inhibitor of succinic dehydrogenase, and has been used extensively in investigations of the tricarboxylic acid cycle. It can be used in veterinary medicine to prevent resorption of bone tissue in broiler chicks caused by disturbance of photoperiodism. HUMAN STUDIES: The influence of malonic acid on the proliferation rate of cultured human fetal skin fibroblasts was investigated. Addition of malonate stimulated fibroblast proliferation. The maximum stimulation occurred in the medium at the 0.01 mM concentration of malonic acid. When the cells were cultured in the medium with serum, the influence of malonate on the cells proliferation increased. ANIMAL STUDIES: Malonic acid (MA) is a reversible inhibitor of succinate dehydrogenase (SDH) which induces mitochondrial dysfunction followed by secondary excitotoxicity and apoptosis due to generation of reactive oxygen species. Intrastriatal injection of malonate results in both chemically induced hypoxia and striatal lesions that are similar to those seen in Huntington's disease and cerebral ischemia. Malonic acid was mildly irritating to skin in rats. In an in vitro eye irritation test, malonic acid was considered to be irritating. The behavioral effects of unilateral intrastriatal administration of malonate (0.6, 1.8 or 6 umol) in adult male rats have been reported. Low doses of malonate (1.8 umol) decreased exploratory activity and caused ipsiversive rotational behavior. High doses of malonate (6 umol) induced contralateral rotational behavior and convulsive episodes. Malonate-induced striatal toxicity was significantly reduced following lesions of either the glutamatergic or dopaminergic afferents to the striatum. Intrastriatal injection of malonate produced age-dependent striatal lesions, which were significantly greater in 4- and 12-month-old animals than in 1-month-old animals. Malonic acid was negative for mutagenicity in a bacterial reverse mutation assay.

The present experiments were carried out to provide direct in vivo evidence for the involvement of c-Jun N-terminal kinase (JNK) in the induction of ischemic brain injury. Malonate, which produces lesions similar to those of focal ischemia-reperfusion by a reversible inhibition of succinate dehydrogenase in mitochondria, was injected into the left striatum in the rat brain without or with the simultaneous injection of a cell permeable peptidic JNK inhibitor, (L)-HIV-TAT48-57-PP-JBD20. Two regions of malonate-induced brain injury were visualized as a hyperintense region with surrounding hypointense regions by apparent diffusion coefficient mapping magnetic resonance imaging. The JNK inhibitor significantly counteracted both hyper- and hypointense regions at the early stage of brain injury. Histological examination clarified that the inhibitor suppressed the induction of coagulation necrosis and spongy degeneration at early and late stages. /Malonate/|The acute and long-term effects of the local perfusion of 3,4-methylenedioxymethamphetamine (MDMA) and the interaction with the mitochondrial inhibitor malonate (MAL) were examined in the rat striatum. MDMA, MAL or the combination of MAL with MDMA was reverse dialyzed into the striatum for 8 h via a microdialysis probe while extracellular dopamine (DA) and serotonin (5-HT) were measured. One week later, tissue immediately surrounding the probe was assayed for DA and 5-HT tissue content. Local perfusion of MDMA increased DA and 5-HT release but did not produce long-term depletion of DA or 5-HT in tissue. Malonate also increased both DA and 5-HT release but, in contrast to MDMA, produced only long-term depletion of DA. The combined perfusion of MDMA/MAL synergistically increased the release of DA and 5-HT and produced long-term depletion of both DA and 5-HT in tissue. These results support the conclusion that DA, compared with 5-HT, neurons are more susceptible to mitochondrial inhibition. Moreover, MDMA, which does not normally produce DA depletion in the rat, exacerbated MAL-induced DA depletions. The effect of MDMA in combination with MAL to produce 5-HT depletion suggests a role for bio-energetic stress in MDMA-induced toxicity to 5-HT neurons. Overall, these results highlight the importance of energy balance to the function of DA and 5-HT neurons and to the toxic effects of MDMA. /Malonate/|We examined whether creatine administration could exert neuroprotective effects against excitotoxicity mediated by N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid. Oral administration of 1% creatine significantly attenuated striatal excitotoxic lesions produced by NMDA, but had no effect on lesions produced by AMPA or kainic acid. Both creatine and nicotinamide can exert significant protective effects against malonate-induced striatal lesions. We, therefore, examined whether nicotinamide could exert additive neuroprotective effects with creatine against malonate-induced lesions. Nicotinamide with creatine produced significantly better neuroprotection than creatine alone against malonate-induced lesions. Creatine can, therefore, produce significant neuroprotective effects against NMDA mediated excitotoxic lesions in vivo and the combination of nicotinamide with creatine exerts additive neuroprotective effects. /Malonate/|The mitochondrial inhibitors malonate and 3-nitropropionic (3NP) acid are potent neurotoxins in vivo. Administration of these compounds results in neuronal loss similar to that seen in Huntington's disease. Although the mechanism of cell death produced by these compounds likely involves activation of N-methyl-D-aspartate receptors, it remains unclear why the striatum demonstrates regional susceptibility to the toxicity of these and other mitochondrial poisons. We hypothesized that dopamine, a weak neurotoxin that occurs in high concentrations in the striatum, may contribute to the neuronal damage caused by mitochondrial inhibition. We investigated whether depletion of striatal dopamine using the catecholaminergic toxin 6-hydroxydopamine would attenuate lesions induced by mitochondrial inhibition. We found that dopamine depletion reduced significantly the extent of histological damage in the striatum elicited by both intraparenchymal injections of 0.8 micromol malonate and 20 mg/kg systemic administration of 3NP. These data suggest that dopamine or one of its metabolites may contribute to mitochondrial toxin-induced cell death. /Malonate/|For more Interactions (Complete) data for Malonic acid (7 total), please visit the HSDB record page.

LD50 Rats female oral 2750 mg/kg bw|LD50 Rats male oral 3250 mg/kg bw|LD50 Rat oral 1310 mg/kg|LD50 Rat ip 1500 mg/kg|For more Non-Human Toxicity Values (Complete) data for Malonic acid (6 total), please visit the HSDB record page.

Malonic acid is found in small amounts in sugar beet and green wheat, being formed by oxidative degradation of malic acid(1). Malonic acid has been identified in celery, parsnip, green pepper, tangerine, beet, oats, tabasco, chili, orange, grapefruit, lime, melon, cantaloupe, sunflower, barley, prickly pear, Indian fig, ginseng, black bean, kidney bean, green bean, peach, corn, Scotch pine, alfalfa, banana, tobacco plant, and juniper(2).

Malonic acid's production and use as an intermediate in manufacture of barbituates and pharmaceuticals(1) may result in its release to the environment through various waste streams(SRC). Malonic acid is emitted to the atmosphere in gasoline engine emissions(2), tobacco smoke(3) and combustion of wood(4). Malonic acid and other short-chain dicarboxylic acids can be formed in the atmosphere via photochemical reactions of cyclic olefins and other hydrocarbons emitted to air by both biogenic and anthropogenic sources(5). Hydrolysis of dimethyl and diethyl malonates in the environment produces malonic acid(6,7).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 4(SRC), determined from a structure estimation method(2), indicates that malonic acid is expected to have very high mobility in soil(SRC). Respective pKa1 and pKa2 values of 2.8 and 5.7(3), indicate this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of malonic acid from moist soil surfaces is not expected to be an important fate process(SRC) due to ionization. Based on biodegradation screening results of analogous dicarboxylic acids (succinic acid and oxalic acid), malonic acid is expected to be readily biodegradable(3). In two 5-day BOD studies, malonic acid achieved 38 to 76.6% theoretical BODs(5,6).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 4(SRC), determined from a structure estimation method(2), indicates that malonic acid is not expected to adsorb to suspended solids and sediment(SRC). Respective pKa1 and pKa2 values of 2.8 and 5.7(3), indicate this compound will exist almost entirely in the anion form in the environment and therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from its log Kow of -0.81(5) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Based on biodegradation screening results of analogous dicarboxylic acids (succinic acid and oxalic acid), malonic acid is expected to be readily biodegradable(3). In two 5-day BOD studies, malonic acid achieved 38 to 76.6% theoretical BODs(6,7). Malonic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(8).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), malonic acid, which has a vapor pressure of 2.7X10-6 mm Hg at 23 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase malonic acid 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 10 days(SRC), calculated from its rate constant of 1.6X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase malonic acid may be removed from the air by wet and dry deposition(SRC). Malonic acid absorbs weakly at wavelengths >290 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of malonic acid with photochemically-produced hydroxyl radicals has been estimated as 1.6X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 10 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Malonic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Malonic acid absorbs weakly at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). The rate constant for the OH radical reaction of malonic acid with hydroxyl radicals in aqueous solutions at pH 1-2.2 is 2.7X10+7 L/mol-sec(4); this corresponds to an aquatic half-life of 81 years at an aquatic concentration of 1X10-17 hydroxyl radicals per liter(5).

An estimated BCF of 3 was calculated in fish for malonic acid(SRC), using a log Kow of -0.81(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 of malonic acid can be estimated to be 4(SRC). According to a classification scheme(2), this estimated Koc value suggests that malonic acid is expected to have very high mobility in soil. Respective pKa1 and pKa2 values of 2.8 and 5.7(3), indicate this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

Respective pKa1 and pKa2 values of 2.8 and 5.7(1) indicate malonic acid will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). Ionization indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Malonic acid is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 2.7X10-6 mm Hg(2).

DRINKING WATER: Malonic was identified as a byproduct formed in drinking water as the result of ozone disinfection(1).|RAIN/SNOW: Rain and snow samples (19 total samples) collected at 14 sites in California during 1982-1984 contained malonic acid concentrations ranging from 0.015 to 2.42 uM(1). Malonic acid was detected in cloud water samples collected at Whiteface Mountain, NY in the summer of 1987(2). Snow, sleet and rain samples collected in Tokyo, Japan in 1992 had malonic acid levels 0.78 to 76.5 ug/L(3).

Malonic acid has been identified in celery, parsnip, green pepper, tangerine, beet, oats, tabasco, chili, orange, grapefruit, lime, melon, cantaloupe, sunflower, barley, prickly pear, Indian fig, ginseng, black bean, kidney bean, green bean, peach, corn, and banana(1).

According to the 2016 TSCA Inventory Update Reporting data, 2 reporting facilities estimate the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of malonic acid in the United States may be as low as <10 workers and as high as 10-25; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 1913 workers (272 of these are female) were potentially exposed to malonic acid in the US(1). Occupational exposure to malonic acid may occur through inhalation and dermal contact with this compound at workplaces where malonic acid is produced or used. Monitoring data indicate that the general population may be exposed to malonic acid via inhalation of ambient air and tobacco smoke, and ingestion of food(SRC).

/VET/ It is established that resorption of bone tissue in broiler chicks caused by disturbance of photoperiodism can be prevented by adding malonic acid to feed. The data obtained are discussed within the scope of the concept of free-radical pathology of connective tissue in connection with the antioxidant properties of malonate.

Malonic acid injected into rats or rabbits is excreted largely unchanged, but also causes increased excretion of citric and alpha-ketoglutaric acids.

Some malonate may be metabilized through the tricarboxylic acid cycle, with decarboxylation to acetate followed by transformation to succinate, which has been detected in rat urine. /Malonate/

SYMPTOMS: Symptoms of exposure to this compound include irritation of the skin, eyes, mucous membranes and upper respiratory tract. It can damage the skin and mucous membranes. ACUTE/CHRONIC HAZARDS: This compound may be harmful by inhalation, ingestion or skin absorption. It is a strong irritant. It can damage the skin and mucous membranes. When heated to decomposition it emits acrid smoke, irritating fumes and toxic fumes of carbon monoxide and carbon dioxide. (NTP, 1992)

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. IMMEDIATELY call a hospital or poison control center even if no symptoms (such as redness or irritation) develop. IMMEDIATELY transport the victim to a hospital for treatment after washing the affected areas. 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. Corrosive chemicals will destroy the membranes of the mouth, throat, and esophagus and, in addition, 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. Transport the victim IMMEDIATELY to a hospital. (NTP, 1992)

Fresh air, rest. Refer for medical attention.

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.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Organic acids and related compounds/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist respirations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Activated charcoal is not effective ... . Do not attempt to neutralize, because of exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Organic acids and related compounds/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Early intubation, at the first sign of upper airway obstruction, may be necessary. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Organic acids and related compounds/

/ALTERNATIVE and IN VITRO TESTS/ The influence of malonic acid on the proliferation rate of cultured human fetal [correction of embryo] skin fibroblasts was investigated. Addition of malonate to the serum-less incubation mixture stimulated fibroblast proliferation. The maximum stimulation occurred in the medium at the 0.01 mM concentration of malonic acid. When the cells were cultured in the medium with serum, the influence of malonate on the cells proliferation increased.|/ALTERNATIVE and IN VITRO TESTS/ Formaldehyde fixation is the main method for crosslinking cellular proteins prior to their usage in immunocytochemistry. In order to create these links, formaldehyde undergoes a Mannich reaction in which the formaldehyde forms a methylene bridge between the aminogroup of two amino acids. Crosslinking increases protein stability allowing for more accurate preservation of in vivo conformations which in turn increases binding affinity of fluorochrome conjugated antibodies for fluorescent imaging. Formaldehyde is also a known carcinogen as classified by the National Cancer Institute. Malonic acid, a green, plant-based, water-soluble, and relatively inexpensive polycarboxylic acid has been shown to undergo crosslinking of proteins through an unknown mechanism. To test whether malonic acid can crosslink proteins within cells we fixed SH-5YSY cells with either malonic acid or formaldehyde and then stained with a fluorochrome conjugated antibody for the cytoskeletal protein a-tubulin. The cells were then imaged 72 hours after fixation. We observed a non-significant difference in the fluorescence of immunostained SH-5YSY cells fixed with malonic acid as compared to paraformaldehyde (p-value = 0.2469, ANOVA). In addition, we have created a theoretical mechanism showing malonic acid forming a propyl bridge for crosslinking proteins in a similar mechanism to that of formaldehyde. Here, we show that malonic acid is able to fix cells and retain fluorescence just as well as paraformaldehyde up to 72 hours after fixation and present several possible mechanisms for this chemical process.

dithallium malonate

The substance can be absorbed into the body by inhalation and by ingestion.

Cough. Sore throat.

Redness. Pain.

Redness. Pain.

All other chemical product and preparation manufacturing|Propanedioic acid: ACTIVE|The occurrence of malonic acid has been reported in the leaves of lucerne and in green wheat plants. This acid is well known as a competitive inhibitor of succinic dehydrogenase, and has been used extensively in investigations of the tricarboxylic acid cycle.

Food additives -> Flavoring Agents|Fatty Acyls [FA] -> Fatty Acids and Conjugates [FA01] -> Dicarboxylic acids [FA0117]|Cosmetics -> Buffering

Flavoring Agents