Oxalic Acid

Other Classes -> Organic Acids

Corrosives

-0.81

-0.81

1.9 at 59 °F (USCG, 1999) - Denser than water; will sink

1.90 @ 17 DEG/4 °C, ALPHA

1.9 g/cm³

1.90

1.9 @ 17°C

1.90

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].

50 to 100 mg/mL at 75 °F (NTP, 1992)

100 G AQ SOLN SATURATED @ 15 °C CONTAINS 6.71 G; 100 G AQ SOLN SATURATED @ 20 °C CONTAINS 8.34 G; 100 G AQ SOLN SATURATED @ 25 °C CONTAINS 9.81 G

VERY SOL IN ETHANOL; SLIGHTLY SOL IN ETHER; INSOL IN BENZENE, CHLOROFORM, PETROLEUM ETHER

Water solubility of 220,000 mg/l at 25 °C

220 mg/mL at 25 °C

Sublimes (NIOSH, 2024)

sublimes

Sublimes

372 °F (Decomposes) (NTP, 1992)

189.5 °C (DECOMPOSES)

189.5 °C

189.5 °C

372 °F

4.3 (NTP, 1992) - Heavier than air; will sink (Relative to Air)

4.3

Warning

H302: Harmful if swallowed [Warning Acute toxicity, oral]

P264, P270, P280, P301+P317, P302+P352, P317, P321, P330, P362+P364, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for 0.2% (2 of 1282) of reports.

Danger

H302 (99.8%): Harmful if swallowed [Warning Acute toxicity, oral]

Chemical: Ethanedioic acid

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

Status: Active Update: 25-07-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/14786

Oxalic acid: Does not have an individual approval but may be used under an appropriate group standard

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Special Hazards of Combustion Products: Generates poisonous gases (USCG, 1999)

Combustible. Gives off irritating or toxic fumes (or gases) in a fire.

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)

Liquid causes second or third degree burns after short contact. [CHRIS] TLV Basis is irritation (eye, skin and upper respiratory tract); [ACGIH] Solutions range from irritating to corrosive. Inhalation of high concentrations may induce chemical pneumonitis. Ingestion of oxalic acid or soluble oxalate compounds causes acute hypocalcemia and deposition of calcium oxalate crystals in the brain, heart, kidney, and other organs. In plant poisoning cases, ingestion of insoluble oxalate compounds causes irritation and swelling of the mouth, throat, and esophagus. [Olson, p. 360-1] A corrosive substance that can cause pulmonary edema after inhalation of aerosol; [ICSC] May cause kidney damage, hypocalcemia, and hepatic necrosis in severe poisoning cases following ingestion; [HSDB]

Residues of oxalic acid are exempted from the requirement of a tolerance when used as a calcium chelating hard water inhibitor in accordance with good agricultural practices as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops or to raw agricultural commodities after harvest. Limits: No more oxalic acid should be used than is necessary to chelate calcium and, in no case, should more than 2 lb oxalic acid per acre be used.

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.

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].

Fires involving this compound may be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)

Use water spray, powder, foam, carbon dioxide. In case of fire: keep drums, etc., cool by spraying with water.

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.

Rinse mouth. Do NOT induce vomiting. Refer immediately for medical attention.

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.

(General first aid procedures)

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/

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.

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.

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.

Acute Exposure: If oxalic acid is swallowed, immediately give the person water or milk, unless instructed otherwise by a health care provider. DO NOT give water or milk if the person is having symptoms (such as vomiting, convulsions, or a decreased level of alertness) that make it hard to swallow. If acute exposure occurs to the eyes, irrigate opened eyes for several minutes under running water. Chronic exposure: in some patients with primary hyperoxaluria type 1, pyridoxine treatment (vitamin B6) may decrease oxalate excretion and prevent kidney stone formation.

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.

Because it binds vital nutrients such as calcium, long-term consumption of foods high in oxalic acid can be problematic. Healthy individuals can safely consume such foods in moderation, but those with kidney disorders, gout, rheumatoid arthritis, or certain forms of chronic vulvar pain (vulvodynia) are typically advised to avoid foods high in oxalic acid or oxalates. The calcium oxalate precipitate (better known as kidney stones) obstruct the kidney tubules. Conversely, calcium supplements taken along with foods high in oxalic acid can cause calcium oxalate to precipitate out in the gut and drastically reduce the levels of oxalate absorbed by the body (by 97% in some cases.) Chronically high levels of oxalic acid are associated with at least 2 inborn errors of metabolism including: Type I primary hyperoxaluria and Primary hyperoxaluria. Oxalate stones in primary hyperoxaluria tend to be severe, resulting in relatively early kidney damage (before age 20), which impairs the excretion of oxalate leading to a further acceleration in accumulation of oxalate in the body. After the development of renal failure patients may develop oxalate deposits in the bones, joints and bone marrow. Severe cases may develop haematological problems such as anaemia and thrombocytopaenia. The deposition of oxalate in the body is sometimes called "oxalosis" to be distinguished from "oxaluria" which refers to oxalate in the urine.

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).

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).

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

The affinity of divalent metal ions is sometimes reflected in their tendency to form insoluble precipitates. Thus in the body, oxalic acid also combines with metals ions such as Ca2+, Fe2+, and Mg2+ to deposit crystals of the corresponding oxalates, which irritate the gut and kidneys. (2) Therefore the toxicity of oxalic acid is due to kidney failure caused by precipitation of solid calcium oxalate, the main component of kidney stones. Oxalic acid can also cause joint pain due to the formation of similar precipitates in the joints. Ingestion of ethylene glycol results in oxalic acid as a metabolite that can also cause acute kidney failure.

OXALATE CONTENT OF PLANTS IS HIGHEST AT LEAFY STAGE OF GROWTH & PLANTS WHICH ARE NORMALLY NOT DANGEROUS TO STOCK MAY BECOME SO @ CERTAIN TIMES OF YR. HALOGETON MAY CONTAIN ... 34.5% OF OXALATE, MANGELS UP TO 12% & SOURSOB 5.9% (DRY WT). /OXALATE/

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). 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). Oxylate concns ranged from 0.1 to 5.0% in several plant species that are potential sources of the oxylates in sediments of Searsville Lake, CA, Lake Tahoe, CA, Big Soda Lake, NV, and a south San Francisco Bay mud flat and salt marsh(3).

Residues of oxalic acid are exempted from the requirement of a tolerance when used as a calcium chelating hard water inhibitor in accordance with good agricultural practices as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops or to raw agricultural commodities after harvest. Limits: No more oxalic acid should be used than is necessary to chelate calcium and, in no case, should more than 2 lb oxalic acid per acre be used.

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.

Oxalic acid is not metabolized but excreted in the urine.

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.

Used in metal cleaning, chemical synthesis, dye and rubber manufacturing, and textile stripping/finishing; Also used as a disinfectant (swimming pool and drainage system) and bathroom sanitizer; [ACGIH] Several species of plants contain soluble and insoluble oxalate salts. [Olson, p. 360] Used in photography (toner and platinum printing); Also used as a mordant in textile dyeing; [www.ci.tucson.az.us/arthazards/medium.html]

Using Disinfectants or Biocides [Category: Clean]

Textile arts [Category: Hobbies]

SCOURING AGENT IN TEXTILE FINISHING, STRIPPING, CLEANING; FOR BLEACH & STAIN REMOVER; RUST, GREASE, AND WAX REMOVING AGENT IN METAL CLEANING; CHEM INT

AS ANALYTICAL REAGENT; IN CALICO PRINTING & DYEING; BLEACHING STRAW (HATS) & LEATHER; MFR OXALATES; BLUE INK; REMOVING PAINT OR VARNISH, RUST OR INK STAINS; CLEANING WOOD; MFR CELLULOID; INT & DYES; IN METAL POLISHES; IN INDIGO DYEING; IN PURIFYING METHANOL; FOR DECOLORIZING CRUDE GLYCEROL; FOR STABILIZING HYDROCYANIC ACID; AS GENERAL REDUCING AGENT; IN CERAMICS & PIGMENTS; IN METALLURGY AS CLEANSER; IN PAPER INDUSTRY; IN PHOTOGRAPHY; IN PROCESS ENGRAVING; IN RUBBER MFR INDUSTRY; IN MAKING GLUCOSE FROM STARCH; AS CONDENSING AGENT IN ORG CHEMISTRY; VET: IN 5% SOLN WITH 5% MALONIC ACID AS HEMOSTATIC AGENT

OXALIC ACID & OXALATE SALTS ARE SOMETIMES USED AS ANTICOAGULANTS IN BLOOD SPECIMENS DRAWN FOR CHEMICAL ANALYSIS.

(1972) NEGLIGIBLE

1.68X10+8 g

(1972) 8.6X10+8 G

(1975) 1.73X10+9 G

(1984) 9.31X10+9 g

2023: 2,500,000 - <4,000,000 lb

(1972) 1.0X10+10 G

(1974) 8.17X10+9 G

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)

MADE BY PASSING CARBON MONOXIDE INTO CONCENTRATED SODIUM HYDROXIDE OR BY HEATING SODIUM FORMATE IN PRESENCE OF SODIUM HYDROXIDE OR SODIUM CARBONATE.

OXALIC ACID IS PRODUCED COMMERCIALLY BY NITRIC ACID OXIDATION OF STARCH, SUGAR, OR ETHYLENE GLYCOL

OXALIC ACID IS A CO-PRODUCT OF THE FERMENTATION OF MOLASSES TO CITRIC ACID. OXALIC ACID CAN BE MADE BY FUSING SAWDUST (OR OTHER FORMS OF CELLULOSE) WITH A MIXTURE OF SODIUM HYDROXIDE AND POTASSIUM HYDROXIDE. TEXACO WAS GRANTED A PATENT IN 1973 FOR THE ELECTROLYTIC SYNTHESIS OF OXALIC ACID FROM CARBON DIOXIDE AND HYDROGEN.

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

Fragrance Ingredients

Cosmetics -> Chelating

Not Known or Reasonably Ascertainable

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