Oxalic acid

90.034

90.03

208-932-1

9E7R5L6H31

0529

62774

3261|1759

DTXSID0025816

ANHYDROUS OXALIC ACID, CRYSTALLIZED FROM GLACIAL ACETIC ACID IS ORTHORHOMBIC, CRYSTALS BEING PYRAMIDAL OR ELONGATED OCTAHEDRA|Colorless powder or granular solid [Note: The anhydrous form (COOH)2 is a white powder].

2917111000

74.6

-0.3

Oxalic acid is an odorless white solid. Sinks and mixes with water. (USCG, 1999)

1.9 g/cm³

189.5 °C (decomp)

200 °C @ Press: 0.1 Torr

188.8±19.7 °C

1.480

14%

STORE IN COOL, DRY, WELL-VENTILATED LOCATION. /OXALIC ACID DIHYDRATE/

<0.001 mmHg

4.3

Combustible Solid

Odorless.

1.43e-10 atm-m3/mole|Henry's Law constant: 1.4X10-10 atm-cu m/mole at 25 °C (experimental)

pKa 1: 1.46; pKa 2: 4.40

MP: 101-102 °C GIVING OFF WATER OF CRYSTALLIZATION & STARTING TO SUBLIME; K1= 5.36X10-2; K2= 5.3X10-5; DENSITY: 1.653 @ 18.5 °C/4 °C; DENSITY OF 1% (WT/WT) AQ SOLN: 1.0035 @ 17.5 °C/4 °C; DENSITY OF 3% (WT/WT) AQ SOLN: 1.0105 @ 17.5 °C/4 °C; DENSITY OF 5% (WT/WT) AQ SOLN: 1.0175 @ 17.5 °C/4 °C; DENSITY OF 10% (WT/WT) AQ SOLN: 1.0350 @ 17.5 °C/4 °C; DENSITY OF 13% (WT/WT) AQ SOLN: 1.0455 @ 17.5 °C/4 °C /OXALIC ACID DIHYDRATE/|DISSOCIATION CONSTANT: 6.5X10-2 /OXALIC ACID DIHYDRATE/|SUBLIMES BEST @ 157 °C; @ HIGHER TEMP DECOMP INTO CO2, CARBON MONOXIDE, FORMIC ACID, & WATER; HYGROSCOPIC|MONOCLINIC TABLETS, PRISMS, OR GRANULES; 1 G DISSOLVES IN 7 ML WATER; 1 G DISSOLVES IN 2 ML BOILING WATER; 1 G DISSOLVES IN 2.5 ML ALCOHOL; 1 G DISSOLVES IN 1.8 ML BOILING ALCOHOL; 1 G DISSOLVES IN 100 ML ETHER; 1 G DISSOLVES IN 5.5 ML GLYCEROL /OXALIC ACID DIHYDRATE/|Transparent, colorless crystals or white powder /Oxalic acid dihydrate/|Odorless /Oxalic acid dihydrate/|For more Other Experimental Properties (Complete) data for OXALIC ACID (6 total), please visit the HSDB record page.

Water soluble. Hygroscopic

Acids, Carboxylic

OXALIC ACID is hygroscopic and sensitive to heat. This compound may react violently with furfuryl alcohol, silver, sodium, perchlorate, sodium hypochlorite, strong oxidizers, sodium chlorite, acid chlorides, metals and alkali metals. (NTP, 1992). The heating of mixtures of Oxalic acid and urea has lead to explosions. This is due to the rapid generation of the gases CO2, CO, and NH3 [Praxis Naturwiss. Chem., 1987, 36(8), 41-42]. Oxalic acid and urea react at high temperatures to form toxic and flammable ammonia and carbon monoxide gases, and inert CO2 gas [Von Bentzinger, R. et al., Praxis Naturwiss. Chem., 1987, 36(8), 41-42].

Not flammable (USCG, 1999)

-245.61 KJ/mol

Combustible Solid

III

8

UN 3261 8/PG 3

1

R21/22

S24/25-S23-S36/37/39-S27-S26

RO2450000

Xn:Harmful

Separated from strong oxidants and food and feedstuffs. Dry. Well closed.

OXALIC ACID CAN BE DEHYDRATED BY CAREFUL DRYING @ 100 DEG C, BUT LOSSES OCCUR THROUGH SUBLIMATION /OXALIC ACID DIHYDRATE/

P280-P305 + P351 + P338

H302 + H312-H318

Oxalic acid is a waste chemical stream constituent which may be subjected to ultimate disposal by controlled incineration. Pretreatment involves chemical reaction with limestone or calcium oxide forming calcium oxalate. This may then be incinerated utilizing particulate collection equipment to collect calcium oxide for recycling.

Reacts with strong alkalies, strong oxidizing materials, chlorites, and hypochlorites. /Oxalic acid dihydrate/|Strong oxidizers, silver compounds, strong alkalis, chlorites [Note: Gives off water of crystallization at 215 degrees F and begins to sublime].

UN 3261

P280; P301 + P312 + P330; P305 + P351 + P338 + P310

Special Hazards of Combustion Products: Generates poisonous gases (USCG, 1999)|Combustible. Gives off irritating or toxic fumes (or gases) in a fire.

|Warning|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P280, P301+P312, P302+P352, P312, P322, P330, P363, and P501|Danger|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P280, P301+P312, P302+P352, P305+P351+P338, P310, P312, P322, P330, P363, and P501|Aggregated GHS information provided by 1220 companies from 17 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|P260, P264, P270, P280, P301+P312, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P310, P312, P314, P321, P322, P330, P363, P405, and P501|P201, P202, P260, P261, P264, P270, P271, P273, P280, P281, P301+P312, P302+P352, P304+P340, P305+P351+P338, P307+P311, P308+P313, P310, P312, P314, P321, P330, P332+P313, P362, P403+P233, P405, and P501|P201, P202, P260, P264, P270, P280, P281, P301+P312, P301+P330+P331, P303+P361+P353, P304+P340, P305+P351+P338, P308+P313, P309+P311, P310, P314, P321, P330, P363, P405, and P501

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-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)

Neutralizing Agents for Acids and Caustics: Lime or soda ash (USCG, 1999)

Skin: Wear appropriate personal protective clothing to prevent skin contact. Eyes: Wear appropriate eye protection to prevent eye contact. Wash skin: The worker should immediately wash the skin when it becomes contaminated. Remove: Work clothing that becomes wet or significantly contaminated should be removed and replaced. Change: Workers whose clothing may have become contaminated should change into uncontaminated clothing before leaving the work premise. Provide: Eyewash fountains should be provided in areas where there is any possibility that workers could be exposed to the substance; this is irrespective of the recommendation involving the wearing of eye protection. (NIOSH, 2016)|... EYE & SKIN PROTECTION /MUST/ BE PROVIDED FOR PERSONS WORKING WITH OXALIC ACID.|Wear special protective clothing and positive pressure self-contained breathing apparatus. /Oxalic acid dihydrate/|If mists of oxalic acid should be encountered from hot solutions ... adequate ventilation should be provided or proper respiratory protective devices worn.|Respirator for dust or mist protection; rubber, neoprene, or vinyl gloves; chemical safety glasses; rubbers, over leather or rubber safety shoes; apron or impervious clothing for splash protection.|For more Personal Protective Equipment (PPE) (Complete) data for OXALIC ACID (12 total), please visit the HSDB record page.|(See protection codes)

USE WATER SPRAY, DRY CHEM, "ALC RESISTANT" FOAM, OR CARBON DIOXIDE. DUST MAY BE REDUCED WITH WATER SPRAY. AQUEOUS SOLUTION MUST BE CONTAINED FOR DISPOSAL. USE WATER TO KEEP FIRE-EXPOSED CONTAINERS COOL. WATER MAY CAUSE FOAMING OF MOLTEN MATERIAL. /OXALIC ACID DIHYDRATE/

Cover with soda ash or sodium bicarbonate. Mix and add water. Neutralize and drain into a drain with sufficient water.

Adequate ventilation.|The worker should immediately wash the skin when it becomes contaminated.|Work clothing that becomes wet or significantly contaminated should be removed and replaced.|Workers whose clothing may have become contaminated should change into uncontaminated clothing before leaving the work premises.|For more Preventive Measures (Complete) data for OXALIC ACID (6 total), please visit the HSDB record page.

The chief effects of inhalation of the dust or vapor are irritation of the eyes and upper respiratory tract.

Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 1 mg/cu m.|Vacated 1989 OSHA PEL TWA 1 mg/cu m; STEL 2 mg/cu m is still enforced in some states.

Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 1 mg/cu m.|Recommended Exposure Limit: 15 Min Short-Term Exposure Limit: 2 mg/cu m.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance, protective gloves and safety goggles. Sweep spilled substance into covered plastic containers. If appropriate, moisten first to prevent dusting. Wash away remainder with plenty of water.

Separated from strong oxidants and food and feedstuffs. Dry. Well closed.

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

The substance is corrosive to the eyes, skin and respiratory tract. Corrosive on ingestion. The substance may cause effects on the calcium balance after ingestion. Exposure at high levels could cause death.

Repeated or prolonged contact with skin may cause dermatitis. Exposure may result in kidney stones, slow-healing ulcers and black finger nails.

NO open flames.

PREVENT DISPERSION OF DUST!

Use ventilation (not if powder), local exhaust or breathing protection.

Protective gloves. Protective clothing.

Wear face shield or eye protection in combination with breathing protection.

| 3 - Materials that, under emergency conditions, can cause serious or permanent injury.| 1 - Materials that must be preheated before ignition can occur. Materials require considerable preheating, under all ambient temperature conditions, before ignition and combustion can occur.| 0 - Materials that in themselves are normally stable, even under fire conditions.

Oxalic acid has been qualitatively detected in pulp mill effluents(1). Oxalic acid was identified in two prebleaching spent liquors of kraft pulp mill effluents at concns of 0.5 and 6 g/ton of pulp(2). It was detected during kraft pulp bleaching at a concn of 130 g/ton in a spent chlorination liquor and 590 g/ton in a spent alkali extraction liquor(3). Oxalic acid was identified in the automobile exhaust of a 1982 Toyota Corolla at a concn of 182 nmole/cu-m(4). It was also identified at a concn of 482 nmole/cu-m in automobile exhaust from a 1971 Mercedes Benz(4).

Oxalic acid was detected at concns ranging from 30 to 6 mg/kg in soil 0 to 540 cm, respectively, below the surface at a site in Germany(1). Oxalic acid was identified in 2 soil samples taken from the UCLA campus (Los Angeles, CA) at concns of 166 and 156 nmol/g(2). Oxalic acid was detected in 2 fractions of bog sediment from the Los Angeles, CA area at concns of 1,410 (humic acid fraction) and 3,350 (fulvic acid fraction) nmol/g(2). Significant concns of oxylate (dissolved plus particulate) were present in sediments taken from a diversity of aquatic environments, ranging from 0.1 to 0.7 mmol/l of sediment(3). These included pelagic and littoral sediments from two freshwater lakes (Searsville Lake, CA and Lake Tahoe, CA), a hypersaline, meromictic, alkaline lake (Big Soda Lake, NV), and a south San Francisco Bay mud flat and salt marsh(3).

URBAN/SUBURBAN: Oxalic acid was the dominant species of dicarboxylic acids in the range C2-C10 identified in the Los Angeles, CA ambient atmosphere(1). In June, 1984, oxalic acid was detected in west Los Angeles air at concns of 6.38 and 2.12 nmol/cu-m(1). Oxalic acid was detected in west Los Angeles ambient air in 6 samples at a concn range of 3.40 to 8.65 nmol/cu-m and an average concn of 5.4 nmol/cu-m in October, 1984(1). In the same study during October of 1984, it was detected in 2 samples taken from downtown Los Angeles at concns of 6.60 and 8.31 nmol/cu-m(1). Oxalic acid was also detected in greenhouse air at UCLA (Los Angeles, CA) in December of 1984 at concns of 1.31 and 2.83 nmol/cu-m(1). Oxalic acid was detected in airborne aerosols above Takasaki and Karuizawa, Japan at average concns of 5.1 and 3.8 ng/cu-m, respectively, during July of 1986(2). Oxalic acid was detected at a concn of approximately 3 ng/cu-m in airborne particulate matter in a suburban area in Japan(3). In September of 1985, oxalic acid was detected in the ambient atmosphere of Claremont, CA in 12 of 12 samples taken at a concn range of <0.12 to 0.94 ug/cu-m(4).

Oxalic acid was identified in greenhouse dust and dust from downtown Los Angeles, CA at a concns of 2,330 and 2,510 nmol/g, respectively(1).

A number of sulfhydryl compounds were shown to inhibit CO2 and oxalate formation from glyoxylate by rat liver homogenates and hepatocytes. The most significant inhibition occurred with cysteine and this inhibition was concentration dependent. In rats made hyperoxaluric by administering ethylene glycol in their drinking water, daily intraperitoneal injections of cysteine caused a rapid and marked decrease in urinary oxalate excretion which was maintained over the duration of the treatment (28 days). Over this time period, the level of urinary oxalate excretion inthese ethylene glycol treated rats was reduced to that of the controls.It is postulated that the decrease is due to the formation of acysteine-glyoxylate adduct, 2-carboxy-4-thiazolidine carboxylate, which prevents glyoxylate being further oxidized to oxalate. Cysteine or similar sulphydryl compounds may therefore have potential as therapeutic agents in the prevention of renal stones.|The study was conducted to investigate the effect of vitamin A, B1 and B6 deficiency on oxalate metabolism in rats. A significant hyperoxaluria was the common observation in all the three vitamin deficiencies (vitamin B6 greater than vitamin A greater than vitamin B1). The activities of hepatic glycolate oxidase and glycolate dehydrogenase were markedly enhanced in vitamin A and vitamin B6 deficient rats. However, lactate dehydrogenase levels remained unaltered in these deficiencies as compared to their respective pair fed controls. Vitamin B1 deficiency of 4 weeks duration could augment the activity of glycolate oxidase only, with no alterations in the glycolate dehydrogenase and lactate dehydrogenase levels. Intestinal oxalate uptake studies revealed increased bioavailability of oxalate from the gut in vitamin A and vitamin B6 deficient rats. Thus, the results suggest the relative contribution of both exogenous as well as endogenous oxalate in the process of calculogenesis under various nutritional stress conditions in rat.|Hyperoxalemia can be aggravated by vitamin C supplementation in regular hemodialysis patients. The present study was undertaken to examine the validity of this observation in an experimental setting. Fifty five-sixths nephrectomized rats were divided into two groups: 30 rats were allowed free access to water containing 8 mg/ml of vitamin C (100-160 mg/100 g/24 hr) and the remainder given tap water without vitamin C. The serum creatinine increased and the hematocrit decreased gradually; however, there was no difference between the two groups. Plasma vitamin C, oxalate and urinary oxalate levels were higher in the vitamin treated group than the nontreated rats. Histological examination revealed glomerular and interstitial fibrosis and round cell infiltration as well as tubular cyst formation. Oxalate deposits in renal tubules were found only in vitamin C-treated rats with advanced renal failure. Nontreated animals with equally advanced renal impairment showed no oxalate deposits. These results confirm previous clinical findings that vitamin C supplementation aggravates the secondary oxalosis of chronic renal failure.|Male Wistar strain rats which had been fed a glycolic acid diet developed severe nephrocalcinosis with urinary calculi within 4 weeks. Rats fed the same diet with citrate salts added had, however, either slight or no nephrocalcinosis without any stones in the urinary system. Nephrocalcinosis intermediate between those in the citrate groups and the glycolic acid group, with some urinary calculi, was observed in the citric acid group. During the experiment, the urinary oxalate concentration increased markedly and was higher in the citrate and citric acid than in the glycolic acid group. The urinary citrate concentration was significantly higher in the citrate groups and lower in the citric acid and glycolic acid groups. Therefore, citrate salts can be concluded to inhibit nephrocalcinosis and calculi formation as a result of decreased urinary saturation by means of increase in urinary citrate, in spite of a slight increase in the urinary oxalate.|For more Interactions (Complete) data for OXALIC ACID (6 total), please visit the HSDB record page.

LDLo Dog oral 1000 mg/kg

Oxalic acid (OA) a metabolite of ethylene glycol, was selected for testing in the RACB protocol based on the biological activity of the parent compound. ... Data collected on body weights, clinical signs, & food/water consumption during the dose-range-finding segment (Task 1) were used to set concns for the main study (Task 2) at 0.05%, 0.10%, & 0.2% OA in drinking water. These concns reduced water consumption in the middle & high dose groups by approx 25%, & yielded calculated consumption estimates of nearly =89, 162, & 275 mg OA/kg/day. There were no adverse clinical signs. One female died in both the low & middle dose groups. At 0.2% OA, the number of litters/pair was reduced by 5% & the pup weight adjusted for litter size was reduced by nearly =4%; sire & dam weights were not affected during Task 2. For the last litter born in Task 2, body weights & pup number were recorded for the controls & 0.1 & 0.2% OA groups; there were no treatment-related changes in pup survival or weight gain to postnatal day 14. Because a modest degree of effect seen at the top dose group in Task 2 was identified only after summing all the Task 2 litter data, it was predicted that the single litter produced in Task 3 would be insufficient to help determine the affected sex. Thus, the last litter from the control & high dose animals were reared for testing in Task 4, & Task 3 was not conducted. After the Task 4 mice were weaned, 10 F0 mice from the control & 0.2% groups were killed & necropsied. No changes were seen in body or organ weights from females. For males, the only significant effect was a 19% decr in prostate weight at 0.2% OA. Total calcium levels in blood were measured for 10 mice of each sex in the control & 0.2% OA groups; the control level of 9.4 mg/dl was unchanged by OA consumption. In the Task 4 one-wk mating trial, there was a 20% reduction in the number of live pups/litter delivered by the 0.2% OA group. No other differences were observed. After 7 days of vaginal lavage, the F1 mice were killed & necropsied. While terminal body weight was unchanged in either sex, female kidney weight (adjusted for body weight) was increased by 10% in the OA-treated females. There were no other changes in organ weights. The % of abnormal sperm forms increased from 2.2% in controls to 4.0% in the 0.2% OA group. Serum calcium levels in either sex were unchanged from control levels of 7.9 mg/dl. In summary, in the F0 mice, OA at these levels reduced water consumption, & reduced the number of litters/pair, adjusted pup weight, & prostate weight in the absence of detected somatic organ changes. In F1 mice, an incr in kidney weight occurred concomitant with a reduction in the number of live pups/litter, & increased abnormal sperm forms. If the kidney weight effect is the result of reduced water consumption, then it can be concluded that Oxalic Acid is a reproductive toxicant in Swiss mice at concns that reduce parental water consumption, but that cause few other somatic effects.

MANY PLANTS CONTAIN OXALATE, NOTABLY RHUBARB LEAVES, DIEFFENBACHIA OR DUMBCANE, BEETS, SPINACH, MANGOLD, HALOGETON, SORREL, PURSLANE, DOCK, GREASEWOOD & RUSSIAN THISTLE. /OXALATES/|PLANTS CONTAINING OXALATES: ATRIPLEX SPECIES, BETA VULGARIS, CALANDRINIA SPECIES, EMEX AUSTRALIS, ENCHYLAENA TOMENTOSA, HALOGETON GLOMERATUS, OXALIS SPECIES, PORTULACA SPECIES, RHEUM RHAPONTICUM, RUMEX SPECIES, SALSOLA KALI, SARCOBATUS VERMICULATUS, THRELKELDIA PROCERIFLORA, TRIANTHEMA SPECIES. /FROM TABLE; OXALATES/|Oxalic acid is present in many plants and vegetables, notably in those of the Oxalis and Rumex families, where it occurs in the leaves, roots, rhizomes, and sap of the plant as the potassium or calcium salt(1-2). For example, waterlilies and duckweed are oxylate-containing plants(3) and these frequently colonize lakes and other aquatic environments. Furthermore, oxylate may constitute as much as 50% of the dry weight of some plant organs, serving both an excretory and a storage function by chelating and precipitating excess calcium ions(3). It is the product of the metabolism of many molds(1). Several species of Penicillium and Aspergillus convert sugar into calcium oxylate with 90% yields under optimum conditions(1). It also occurs in human and animal urine and the calcium salt is a major constituent of kidney stones(2).

Oxalic acid may be released to the environment as emissions from rendering, tobacco smoke(1), and automobile exhaust(2). Oxalic acid may be produced in the atmosphere by photochemical oxidations of anthropogenic compounds during long range transport(3). Oxalic acid has been identified in pulp kraft mill effluents(4-6); therefore, it may be released to the environment in waste streams resulting from pulp bleaching(SRC). The estimated emission rate of oxalic acid in the South East Air Basin, CA is 87 kg/day(7).

TERRESTRIAL FATE: An estimated Koc value of 5(1,SRC) for oxalic acid indicates high mobility in soil(2) and oxalic acid has been detected in groundwater(3). Volatilization from moist soils is not expected to be rapid based upon a low Henry's Law constant. Several screening studies indicate rapid biodegradation of oxalic acid(4-8). Although these studies are not specific to soil media, they suggest that oxalic acid will readily biodegrade in soil. The oxalic acid concn in another study was determined to decrease from 30 mg/kg on a soil surface to about 6 mg/kg 540 cm below the soil surface(3) which suggests that biodegradation may have occurred(SRC). Photolysis is expected to be an important terrestrial fate process; the daytime persistence of oxalic acid on soil surfaces is not expected to exceed a few hours(9).|AQUATIC FATE: Several screening studies(4-8) and grab sample tests(9) indicate that under aerobic and anaerobic conditions, oxalic acid will readily biodegrade in aquatic ecosystems. Based on an experimental Henry's Law constant of 1.4X10-10 atm-cu m/mole at 25 °C(2), oxalic acid is expected to be essentially nonvolatile from water(1). Adsorption to sediment and bioconcentration in aquatic organisms may not be important fate processes for oxalic acid in water systems. Based on pKa1 and pKa2 values of 1.25 and 4.28(3), respectively, oxalic acid will exist primarily as the oxalate ion under environmental conditions (pH 5-9,SRC). Aquatic oxidation is not likely to be an important fate process based on a half-life of 285 yrs in water under continuous sunlight(3,SRC). Oxalic acid may react slowly in water with photochemically produced OH radicals, but it is expected to be removed rapidly from surface water by direct photolysis; the daytime persistence of oxalic acid is not expected to exceed a few hours(10).|ATMOSPHERIC FATE: Based on a measured vapor pressure of 2.3410-4 mm Hg at 25 °C(2), oxalic acid is expected to exist almost entirely in the vapor phase in the ambient atmosphere(3). In the vapor phase, oxalic acid in the ambient atmosphere is very slowly degraded by reaction with photochemically formed hydroxyl radicals; the half-life for this reaction in air can be estimated to be about 223 days(1). Oxalic acid in the ambient atmosphere may react slowly with OH radicals, but it is removed rapidly by photolysis; the daytime persistence of oxalic acid is not expected to exceed a few hours(4). Based on its high water solubility, removal from air via wet deposition is likely to occur(4,SRC). Oxalic acid may also be removed from air via dry deposition with 11% of the total deposition being dry deposition(4).

The rate constant for the vapor-phase reaction of oxalic acid with photochemically produced hydroxyl radicals can be estimated to be 7.2X10-14 cu cm/molecule-sec at 25 °C which corresponds to an atmospheric half-life of about 223 days at an atmospheric concn of 5X10+5 hydroxyl radicals per cu cm(1,SRC). Acids are generally resistent to hydrolysis(4); therefore, oxalic acid is not expected to hydrolyze in aquatic environments. Based on dissociation constant values pKa1 and pKa2 of 1.25 and 4.28(1), respectively; oxalic acid is expected to exist as an ion under environmental conditions (pH 5-9). The aquatic oxidation rate for the reaction of hydroxyl radicals in water with the oxalate ion has been experimentally determined to be 7.7X10+6 L/mole-s at pH 6(1). Based on this rate and a hydroxyl radical concn of 1X10-17 mole/L in water under continuous sunlight(3), the half-life for the aquatic oxidation of oxalic acid can be estimated to be 285 yrs(SRC). Oxalic acid may react slowly with OH in water, but it is removed rapidly by direct photolysis; the daytime persistence of oxalic acid is not expected to exceed a few hours(5).

Based on an average experimental water solubility of 220,000 mg/L at 25 °C(1) and a regression derived equation(2), the BCF for oxalic acid can be estimated to be approximately 0.6(SRC) and therefore should not be expected to bioconcentrate in aquatic organisms(SRC).

Based on an average experimental water solubility of 220,000 mg/L at 25 °C(1) and a regression derived equation(2), the Koc for undissociated oxalic acid can be estimated to be approximately 5. This Koc value indicates that oxalic acid will have very high mobility in soil(3); therefore, adsorption to soil and sediment may not be an important fate process. Based on pKa1 and pKa2 values of 1.25 and 4.28(4) respectively, oxalic acid will exist primarily as the oxalate ion under environmental conditions (pH 5-9). No experimental data are available to determine whether the oxalate ion will adsorb to sediment or soil more strongly than its estimated Koc value indicates(SRC).

Based on an experimental Henry's Law constant of 1.4X10-10 atm-cu m/mole at 25 °C(1), oxalic acid is essentially nonvolatile from water(2).

GROUNDWATER: Oxalic acid was detected at a site in Germany at a concn of about 1 mg/kg in groundwater 610 to 640 cm below the surface; however, it was not detected in groundwater 640 to 670 cm below the surface(1).|RAIN/SNOW: Oxalic acid was detected in two samples of mist collected in Los Angeles, CA on June 9, 1983 and June 11, 1983 at concns of 23.3 and 4 uM, respectively(1). In the same study, oxalic acid was detected in 4 fog samples in June of 1983 at concns ranging from 17.3 to 18.7 uM at an average concn of 18 uM(1). Also, oxalic acid was detected in 8 rain samples collected in Los Angeles, CA in August and September of 1983 at concns ranging from 2.8 to 20.7 uM at an average concn of 15.9 uM(1).

Oxalic acid is present in many plants and vegetables, notably in those of the Oxalis and Rumex families, where it occurs in the sap of the plant as the potassium or calcium salt(2). Oxalic acid was qualitatively detected in raw cassava (Manihot esculenta, Crantz) which is one of the major staple foods of the tropics(1). Gari and Farine (Farinha demandioca), both products of cassava, were determine to be 0.04% and 0.2% oxalic acid, respectively(1).

Exposure of the general population to oxalic acid is expected to occur through consumption of foods in which it is naturally contained, inhalation of contaminated air and consumption of contaminated groundwater(1-7,SRC). In occupational settings, exposure to oxalic acid may occur through inhalation of vapors and through eye and skin contact(SRC).|NIOSH (NOHS Survey 1972-1974) has statistically estimated that 705,215 workers are potentially exposed to oxalic acid in the USA(1). NIOSH (NOES Survey 1981-1983) has statistically estimated that 130,128 workers are potentially exposed to oxalic acid in the USA(2).

Oxalic acid calcium salt is a major constituent of kidney stones(1).

Ascorbic acid ingestion in high doses is associated with oxalate deposition in tissue in dialysis patients. /Oxalates/

Materials that add an electron to an element or compound, that is, decrease the positiveness of its valence. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed) (See all compounds classified as Reducing Agents.)

TARTARIC & OXALIC ACIDS ARE EXCRETED IN URINE UNCHANGED.|The absorption of (14)C-labelled oxalic acid was studied in Wistar rats, CD-1 mice and NMRI mice. Oxalic acid in solution was given to the animals by gavage either with water alone or with 0.625 g/kg body wt of xylitol. Both xylitol adapted animals and animals not previously exposed to xylitol were used. Adaptation to xylitol diets enhanced the absorption and urinary excretion of the label (oxalic acid) in both strains of mice but not in rats. Earlier studies have indicated a high incidence of bladder calculi in mice but not in rats fed high amounts of xylitol. The results of the present study offer one likely explanation for the increased formation of bladder calculi as a result of over saturation of urine with oxalate.

IN RABBIT, MAJOR END-PRODUCT OF METAB OF (14)C-ETHYLENE GLYCOL IS RESP CARBON DIOXIDE (60% OF DOSE IN 3 DAYS), & METABOLITES EXCRETED IN URINE ARE UNCHANGED ETHYLENE GLYCOL (10%) & OXALIC ACID (0.1%). ... GLYCOLALDEHYDE, GLYCOLLIC ACID & GLYOXYLIC ACID ARE INTERMEDIATES IN CONVERSION TO CARBON DIOXIDE.|IN OXIDATIVE METAB OF ETHYLENE GLYCOL IN MAMMALS, SPECIES VARIATIONS OCCUR WHICH EXPLAIN ... DIFFERENCES IN TOXICITY. GLYCOL IS OXIDIZED BY MAJOR PATHWAY INTO CARBON DIOXIDE, & BY MINOR PATHWAY TO ... OXALIC ACID. EXTENT OF FORMATION OF OXALIC ACID IS DEPENDENT ON DOSE LEVEL, BUT HAS ... BEEN SHOWN TO VARY WITH SPECIES ...|INITIAL STEPS IN OXIDATION OF ETHYLENE GLYCOL TO DIALDEHYDE (GLYOXAL) & TO GLYOXYLIC ACID SEEM TO BE MEDIATED BY ALC DEHYDROGENASE; DECARBOXYLATION OF GLYOXYLIC ACID YIELDS CARBON DIOXIDE & FORMIC ACID. GLYOXYLIC ACID IS ALSO OXIDIZED TO OXALIC ACID.|Piridoxilate is an association of glyoxylic acid and pyridoxine in which pyridoxine is supposed to facilitate in vivo transformation of glyoxylic acid to glycine rather than to oxalic acid. However, it has recently been shown that long term treatment with piridoxilate may result in over production of oxalic acid and in calcium oxalate nephrolithiasis. A patient in whom piridoxilate induced both oxalate nephrolithiasis and chronic oxalate nephropathy with renal insufficiency, an association that has not been previously described, was reported. Therefore, piridoxilate should be added to the list of chemicals responsible for chronic oxalate nephropathy.|Cyclosporin A interferes with oxalate metabolism and, therefore, should be given with utmost caution in patients with primary hyperoxaluria.

Metabolically its toxicity is believed due to the capacity of oxalic acid to immobilize calcium and thus upset the calcium-potassium ratio in critical tissues.

As dust or as a solution, can cause severe burns of eyes, skin, or mucous membranes. Ingestion of 5 grams has caused death with symptoms of nausea, shock, collapse, and convulsions coming on rapidly. Repeated or prolonged skin exposure can cause dermatitis and slow-healing ulcers. (USCG, 1999)|Corrosives

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)|(See procedures)

Fresh air, rest. Half-upright position. Refer immediately for medical attention.

Remove contaminated clothes. Rinse skin with plenty of water or shower for at least 15 minutes. Refer for medical attention .

Rinse with plenty of water (remove contact lenses if easily possible). Refer immediately for medical attention.

Treatment should be rapidly instituted by giving a dilute solution of calcium lactate, lime water, finely pulverized chalk, plaster, and/or milk to supply large amounts of calcium to inactivate oxalate by forming an insoluble calcium salt in the stomach. Gastric lavage is controversial, since this may compound an already severe corrosive lesion in the esophagus or stomach. However, if used, gastric lavage should be done with limewater (calcium hydroxide). Intravenous gluconate or calcium chloride solutions should be given to prevent hypocalcemic tetany; in severe cases parathyroid extract also has been given. ... Additionally, acute renal failure should be anticipated, and careful fluid management is necessary. /Oxalates/|Metabolically its toxicity is believed /to be/ due to the capacity of oxalic acid to immobilize calcium and thus upset the calcium-potassium ratio in critical tissues. Effective therapy against burns from oxalic acid involves replacement of calcium.

SYMPTOMATOLOGY: 1. BURNING PAIN IN THROAT, ESOPHAGUS, & STOMACH. EXPOSED AREAS OF MUCOUS MEMBRANE TURN ... OPAQUE WHITE ... 2. VOMITING (OFTEN BLOODY OR WITH COFFEE-GROUND APPEARANCE), INTENSE BURNING PAIN, SEVERE PURGING. 3. PULSE BECOMES WEAK, IRREGULAR, SOMETIMES IMPERCEPTIBLE. HYPOTENSION AND USUAL SIGNS OF CARDIOVASCULAR COLLAPSE APPEAR. 4. IF DEATH IS DELAYED FOR FEW HR, NERVOUS OR NEUROMUSCULAR SYMPTOMS DEVELOP: HEADACHE ... TETANY, SOMETIMES CONVULSIONS, STUPOR, COMA, AND DEATH. 5. RENAL DAMAGE, AS EVIDENCED BY OLIGURIA, ALBUMINURIA, AND HEMATURIA, MAY PERSIST FOR WEEKS. /ORAL; OXALATE/|CHRONIC SKIN EXPOSURE TO SOLN OF OXALIC ACID ... /HAS/ BEEN REPORTED TO HAVE CAUSED LOCALIZED PAIN & CYANOSIS IN FINGERS OR EVEN GANGRENOUS CHANGES ... APPARENTLY DUE TO LOCALIZED ABSORPTION ... & RESULTANT ARTERITIS.|THE NEUROMUSCULAR EFFECTS CAN BE EXPLAINED LARGELY BY CALCIUM-COMPLEXING ACTION OF OXALATE, WHICH DEPRESSES THE LEVEL OF IONIZED CALCIUM IN BODY FLUIDS. THIS HYPOCALCEMIA PRODUCES SEVERE DISTURBANCES IN ACTIONS OF HEART & NERVOUS SYSTEM; DEATH MAY RESULT ... /OXALATE/|... HAS CAUSED BURNS OF HUMAN EYE ... WHEN SOLN ACCIDENTALLY CAME IN CONTACT WITH EYE.|For more Human Toxicity Excerpts (Complete) data for OXALIC ACID (15 total), please visit the HSDB record page.

Acid, Oxalic

The substance can be absorbed into the body by inhalation of its aerosol and by ingestion. Serious local effects by all routes of exposure.|inhalation, ingestion, skin and/or eye contact

irritation eyes, skin, mucous membrane; eye burns; localized pain, cyanosis; shock, collapse, convulsions; kidney damage

Cough. Sore throat. Burning sensation. Shortness of breath. Laboured breathing. Headache.

Redness. Pain. Skin burns.

Redness. Pain. Blurred vision. Burns.

Eyes, skin, respiratory system, kidneys

27% FOR TEXTILE FINISHING, STRIPPING AND CLEANING; 27% FOR METAL AND EQUIPMENT CLEANING; 25% AS A CHEMICAL INTERMEDIATE; 2% FOR LEATHER TANNING; 19% FOR MISC APPLICATIONS (1971)|33% FOR TEXTILE /APPLICATIONS/; 20% FOR METAL; 7% FOR LEATHER; 20% FOR OXALATES; AND 20% FOR OTHER USE (1983)

Technical (crystals and powder); chemically pure: a grade designation signifying a minimum of impurities, but not 100% purity.|THE COMMERCIAL PRODUCT IS COMPRISED OF WHITE TO COLORLESS MONOCLINIC PRISMS OR GRANULES CONTAINING 71.42 wt% ANHYDROUS OXALIC ACID AND 28.58 wt% WATER

All other basic inorganic chemical manufacturing|Ethanedioic acid: ACTIVE|IT IS A PRODUCT OF THE METABOLISM OF MANY MOLDS, SEVERAL SPECIES OF PENICILLIUM & ASPERGILLUS CONVERT SUGAR INTO CALCIUM OXALATE WITH 90% YIELD UNDER OPTIMUM CONDITIONS.|BY 1983, /MOST USA PRODUCERS/ HAD ENDED PRODUCTION AND USA DEMAND HAS BEEN FILLED BY IMPORTS, PRINCIPALLY FROM CHINA AND BRAZIL

VEGETABLE PRODUCTS: TITRATION OR ATOMIC ABSORPTION SPECTROPHOTOMETRY.|AIR SAMPLE. PROCEDURE: TITRATION.

APPLICATION: SERUM OR URINE. METHOD: FLUORESCENCE ANALYSIS.

Health Hazards -> Corrosives|Cosmetics -> Chelating