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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 358
CCOHS Chemical Name: Oxalic acid

Synonyms:
Ethanedioic acid
Ethanedionic acid
Dicarboxylic acid
Oxiric acid
Oxalic acid, anhydrous
Oxalic acid dihydrate
Anhydrous oxalic acid

Chemical Name French: Acide oxalique
Chemical Name Spanish: Acido oxálico
CAS Registry Number: 6153-56-6
Other CAS Registry Number(s): 144-62-7
RTECS Number(s): RO2450000
EU EINECS/ELINCS Number: 205-634-3
Chemical Family: Saturated aliphatic carboxylic acid / saturated aliphatic dicarboxylic acid / alkanedioic acid / oxalic acid
Molecular Formula: C2-H2-O4
Structural Formula: HO-C(=O)-C(=O)-OH

SECTION 2. DESCRIPTION

Appearance and Odour:
Transparent, colourless, odourless crystals, powder or granular solid.(2,37) The anhydrous form of oxalic acid is hygroscopic (absorbs moisture from the air to form the dihydrate).(37,38)

Odour Threshold:
Not applicable (odourless).

Warning Properties:
NONE - Oxalic acid is odourless.

Composition/Purity:
Oxalic acid can exist as the anhydrous compound (CAS 144-62-7) and as the dihydrate ((COOH)2.2H2O) (CAS 6153-56-6). The dihydrate is industrially produced and is the typical commercial form. The anhydrous form does not exist in nature and is produced from the dihydrate.(37,38) Oxalic acid is available in grades of purity of 98% to greater than 99%. It is also available as a 5-10% solution in water or a 0.1N standard volumetric solution.

Uses and Occurrences:
Oxalic acid is used in metal treatment (e.g. in coatings for the protection of stainless steel, nickel alloys, chromium steel alloys, and titanium and in the anodizing of aluminum); for rust removal; as a constituent of metal cleaners with rust protection; for the cleaning of materials for electronic devices; for the separation and recovery of rare-earth elements; in textile cleaning; as a mordant for the printing and dyeing of wool and cotton; as a catalyst in the manufacture of wrinkle-free and permanent-press fabrics; for flameproofing of cellulosic fabrics; in bleaching of pulp, cork, wood, straw, cane, and waxes; in the tanning and bleaching of leather; for marble polishing; as a raw material of various agrochemicals and pharmaceuticals; for the manufacture of oxalates; as a reagent in organic synthesis; and as an analytical reagent. It is also used for the production of cobalt; for the manufacture of electronic materials; for the extraction of tungsten from ore; for the manufacture of zirconium and beryllium oxide; for the production of metal catalysts and regeneration of deactivated catalysts; in the preparation of small particles or powders used for magnetic recording tape; as a polymerization initiator; in photography; in the production of inks, pigments and paints; for removing calcium in waste water treatment; and for the stabilization of sodium hydrosulfite and hydrocyanic acid.(37,38,40)
Oxalic acid is formed in plants and in the body. It is found in spinach and rhubarb. Oxalic acid is a product of metabolism of fungi and bacteria, and also occurs in human and animal urine.(37,38)


SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:
Transparent, colourless, odourless crystals, powder or granular solid. Anhydrous oxalic acid is hygroscopic. Can burn if strongly heated. Can decompose at high temperatures forming formic acid and carbon monoxide. Forms explosive oxalate salts with silver and mercury. TOXIC. May be harmful if swallowed. Can cause kidney damage. Inhalation of dusts or mists can cause irritation of the nose, throat and upper respiratory tract. CORROSIVE to the eyes and skin. May cause blindness and permanent scarring.



POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Oxalic acid is a solid, which essentially does not form a vapour at room temperature. Inhalation can occur following exposure to the dust or to mists or vapours formed from heated or misted solutions. Oxalic acid is a relatively strong acid and it is expected to cause irritation of the nose, throat and upper respiratory tract, if inhaled. Coughing and throat irritation were reported in 7/15 workers exposed to "high" levels of oxalic acid steam for 2-3 hours/day.(34)

Skin Contact:
Brief contact with the solid or solutions may cause mild to moderate irritation, based on limited human and animal information. However, with longer contact (several hours or repeatedly over a few days), oxalic acid can bind to calcium in human tissues causing very severe skin effects, including ulcerations. Therefore, oxalic acid should be considered corrosive.
Oxalic acid is a skin absorption hazard.
Historical case reports describe symptoms such as twitching of the muscles of the face, hands and feet (cyanosis); pain, numbness and tingling in the hands and feet; a bluish discoloration and brittleness of the nails; and ulcerations in the nail bed.(5,26) In a recent case report, a man who used a chainsaw to trim an ornamental plant, the Century Plant or Agave americanus, developed itching and stinging in his lower legs within minutes followed by a rash within a few hours, and then fever, sore muscles and general discomfort. The sap of this plant contains calcium oxalate crystals. The authors suggest that the oxalic acid crystals propelled into the skin by the chain saw caused oxalic acid toxicity, in addition to irritant contact dermatitis.(27) Patch tests with a 7% oxalic acid solution in water showed no irritation in 10 volunteers, whereas 8/10 people showed a positive response to a 9.1% concentration (saturated solution). Reactions with the 9.1% solution were reported as 1+ for one person, 2+ for 5 people and 3+ for two people.(5) The amount of oxalic acid and the duration of exposure are not reported and the definitions for 1+, 2+ and 3+ are not provided.

Eye Contact:
Oxalic acid is corrosive to the eyes, based on pH and limited human and animal evidence. Corrosive materials can cause severe eye injury, including blindness. Oxalic acid has been reported to cause corneal burns in humans, which healed within 2 days when treated.(28)

Ingestion:
Oxalic acid is toxic to humans if ingested, based on human case reports. There are numerous historical case reports of non-occupational poisoning with oxalic acid.(4,30) More recently, the incidence of poisoning is much lower. If ingested, oxalic acid causes local corrosive effects on the mouth, throat, esophagus, stomach and intestines with symptoms such as burning pain in the throat, esophagus and stomach, vomiting (often bloody), low blood pressure, weak and irregular pulse and cardiac arrest. If the victim survives, absorbed oxalic acid causes calcium ion deficiency and symptoms such as headache, muscle cramps, and tetany (sharp flexion of the wrist and ankle joints, muscle twitching, cramps and convulsions) develop. The absorbed oxalic acid forms calcium oxalate, which is deposited in the kidneys, liver and other body tissues, and fatal kidney damage can develop.(4,29,30,31) The single oral lethal dose for humans is estimated to be 50-500 mg/kg.(4) The most commonly reported lethal oral dose for humans is 7-30 grams.(4,30) Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

Prolonged or repeated skin contact with concentrated oxalic acid solutions can cause severe skin effects (early stages of gangrene), with numbness and tingling. In one study, long-term exposure to high airborne concentrations of oxalic acid was associated with an increased incidence of kidney stones.

Skin:
In a case report, a painter was diagnosed with early stages of gangrene after using a solution of 1 pound oxalic acid in 1-1.5 gallons of hot water (approximately 6.7% to 10% solution - 9.1% is a saturated solution at room temperature) to wash floors, without hand protection, over a prolonged period (12-15 hours/week for 2 months and infrequently for 2 years). Symptoms included blue discolouration of the skin (cyanosis), yellow nails, pain, and numbness and tingling sensations, and the hands felt cold.(33) Similar effects have also been observed following shorter exposures (several hours or a few days) to oxalic acid solutions.

Skin Sensitization:
Oxalic acid is not an occupational skin sensitizer.
The only report located, which is not available in English, describes positive results from skin testing with oxalic acid in 53.8% of 26 patients with eczema on their feet from leather.(53, unconfirmed) There are no further details available for evaluation.

Kidneys/Urinary System:
A human study suggests that exposure to high airborne concentrations of oxalic acid may cause a higher incidence of kidney stones in exposed workers. The study examined 409 workers exposed to saturated oxalic acid solutions, oxalic acid in steam, and airborne oxalic dust for several years in a Norwegian railroad shop. Workers exposed to oxalic acid for a median duration of 7.5 years (range: 1-28 years) had significantly higher levels of urinary stone incidents (urolithiasis) than unexposed workers. The workers with the highest exposures washed railway cars with a saturated solution of oxalic acid, which was then washed off with boiling water, exposing them to steam containing oxalic acid for 2-3 hours/day. The incidence of urinary stones in these workers was 53.3%. Other workers exposed to oxalic acid dust for about 1 hour/day had a urinary stone incidence of 32.0% and unexposed workers an incidence of 11.9%. This difference is highly significant and dose-dependent.(34)

OTHER:
It is not possible to draw general conclusions from a single historical case report involving extreme inhalation exposure, and possible skin and ingestion exposure. A man using a boiling solution of oxalic acid in water to clean radiators in a poorly ventilated room for several months became completely disabled. Nervous system symptoms were severe, including almost continuous headaches, extreme nervousness, loss of motion in his legs, severe lower back pain and pain throughout his body. Many of these symptoms were still present at the time of the report, one and a half years after exposure had stopped. Respiratory symptoms were inflamed nasal membranes, frequent nosebleeds, and coughing up of membranous tissue. Weakened heart action and repeated vomiting, which persisted for several months, were also observed.(32)

Carcinogenicity:

There is no human or animal information available.

The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.

The American Conference of Governmental Industrial Hygienists (ACGIH) has not assigned a carcinogenicity designation to this chemical.

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

Teratogenicity and Embryotoxicity:
There is no human information available. It is not possible to conclude that oxalic acid causes developmental toxicity, based on the available animal information.

Reproductive Toxicity:
There is no human information available. Reproductive toxicity was observed in mice in one study, but the effects were observed in the presence of a significant reduction in water consumption in the parents of the first generation and increased kidney weight in the second generation. Therefore, it is not possible to conclude that oxalic acid is a reproductive toxin.

Mutagenicity:
There is no human or animal information. Negative results have been obtained for oxalic acid in tests using cultured mammalian cells and in bacteria, both with and without metabolic activation.

Toxicologically Synergistic Materials:
It is not possible to draw conclusions based on one limited study. Fifteen women and 3 men worked packing cleaning powders, containing 96% silicon dioxide and 4% oxalic acid, under extremely dusty conditions, with no personal protection. The airborne concentrations of oxalic acid were not measured. Twelve workers were diagnosed with silicosis or silicotuberculosis after exposure periods of 9 months to 8 years. The author suggested that the oxalic acid exposure contributed to the relatively rapid development of the silicosis.(35) However, there is insufficient information available to verify this claim.

Potential for Accumulation:
Oxalic acid is excreted in the urine at a rate of 8-40 mg/day in healthy normal men and women. About half is excreted as oxalic acid and half as magnesium, calcium or other salts.(29) Ingested oxalic acid is also excreted in the feces. In rats, approximately half of ingested oxalic acid is destroyed by bacterial action and about 25% is excreted unchanged in the feces.(36) In humans, calcium oxalate is deposited in the kidneys as crystals and may be deposited in non-crystalline form, bound to lipid, in the liver and other body tissues.(31)

Health Comments:
Oxalic acid occurs naturally in the body, formed primarily from ascorbic acid and/or glycine. It is also found in many plants and the daily dietary intake is reported to vary from 70-920 mg for a typical Western diet.(29)


SECTION 4. FIRST AID MEASURES

Inhalation:
If symptoms are experienced, remove source of contamination or move victim to fresh air. Obtain medical advice.

Skin Contact:
Avoid direct contact. Wear chemical protective clothing, if necessary. As quickly as possible, remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). Immediately flush with lukewarm, gently flowing water for at least 30 minutes. DO NOT INTERRUPT FLUSHING. If necessary, and it can be done safely, continue flushing during transport to emergency care facility. Quickly transport victim to an emergency care facility. Completely decontaminate clothing, shoes and leather goods before re-use or discard.

Eye Contact:
Avoid direct contact. Wear chemical protective gloves, if necessary. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for at least 30 minutes, while holding the eyelid(s) open. If a contact lens is present, DO NOT delay irrigation or attempt to remove the lens. Neutral saline solution may be used as soon as it is available. DO NOT INTERRUPT FLUSHING. If necessary, continue flushing during transport to emergency care facility. Take care not to rinse contaminated water into the unaffected eye or onto the face. Quickly transport victim to an emergency care facility.

Ingestion:
NEVER give anything by mouth if victim is rapidly losing consciousness, is unconscious or convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. Have victim drink 60 to 240 mL (2 to 8 oz) of water. If vomiting occurs naturally, have victim rinse mouth with water again. Quickly transport victim to an emergency care facility.

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest).
Consult a doctor and/or the nearest Poison Control Centre for all exposures except minor instances of inhalation or skin contact.
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
No flash point is available. Oxalic acid can burn if strongly heated.

Lower Flammable (Explosive) Limit (LFL/LEL):
Not available

Upper Flammable (Explosive) Limit (UFL/UEL):
Not available

Autoignition (Ignition) Temperature:
Not available

Sensitivity to Mechanical Impact:
Probably not sensitive. Stable material.

Electrical Conductivity:
Not available

Minimum Ignition Energy:
No information available.

Potential for Dust Explosions:
No specific information is available, but like other dicarboxylic acids (e.g. adipic acid) anhydrous oxalic acid may be capable of causing a dust explosion.(12) However, this is unlikely to occur as the material is hygroscopic and readily water from the air. There are no reports of oxalic acid being involved in dust explosions.(37)

Combustion and Thermal Decomposition Products:
Carbon monoxide, carbon dioxide, formic acid and other irritating and toxic fumes.(10)

Fire Hazard Summary:
Oxalic acid is not flammable, but can burn if strongly heated. The decomposition products, formic acid and carbon monoxide, are flammable and toxic. During a fire, irritating/toxic smoke and fumes may be generated. Closed containers may rupture violently and suddenly release large amounts of product when exposed to fire or excessive heat for a sufficient period of time.

Extinguishing Media:
Carbon dioxide, dry chemical, alcohol resistant foam or water spray. Water may cause frothing of molten oxalic acid.(10) Foam manufacturers should be consulted for recommendations regarding types of foams and application rates.

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance or protected location. Approach fire from upwind to avoid toxic decomposition products. such as formic acid.
Closed containers may rupture violently when exposed to the heat of fire and suddenly release large amounts of products. If possible, isolate materials not yet involved in the fire and move containers from fire area if this can be done without risk. Protect personnel. Otherwise, use water in flooding quantities to keep fire-exposed containers, drums, or tanks cool and absorb heat to help prevent rupture.
Water or foam may cause frothing of molten oxalic acid. The frothing may be violent and could endanger personnel close to the fire. However, a water spray or fog that is carefully applied to the surface of the liquid, preferably with a fine spray or fog nozzle, will cause frothing that will blanket and extinguish the fire. In addition, water can be used in the form of spray or fog to absorb heat, prevent dust formation, flush spills away from ignition sources and dilute spills to non-combustible mixtures. Dike fire control water for appropriate disposal. Solid streams of water may be ineffective and spread material.

Protection of Fire Fighters:
Oxalic acid is toxic and corrosive. Do not enter without wearing specialized equipment suitable for the situation. Firefighter's normal protective clothing (Bunker Gear) will not provide adequate protection. Chemical protective clothing (e.g. chemical splash suit) and positive pressure self-contained breathing apparatus (NIOSH approved or equivalent) may be necessary.



NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA - Health: 3 - Short exposure could cause serious temporary or residual injury. (dihydrate)
NFPA - Flammability: 1 - Must be preheated before ignition can occur. (dihydrate)
NFPA - Instability: 0 - Normally stable, even under fire conditions, and not reactive with water. (dihydrate)

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 90.04 (anhydrous); 126.07 (dihydrate)

Conversion Factor:
Not applicable

Physical State: Solid
Melting Point: 101.5 deg C (215 deg F) (dihydrate) (loses water to form anhydrous acid).(39) Anhydrous acid decomposes at 187 deg C (369 deg F).(37,38)**
Boiling Point: Not applicable. Decomposes at the melting point.(37,38)
Relative Density (Specific Gravity): Dihydrate: 1.653 at 20 deg C.(37,38) Anhydrous: 1.90 at 17 deg C.(39,40) (water = 1)
Solubility in Water: Dihydrate: Soluble (8.7 g/100 g at 20 deg C; 10.6 g/100 g at 25 deg C) (calculated).(38) Anhydrous: Soluble (9.5 g/100 g at 20 deg C).(37)
Solubility in Other Liquids: Anhydrous and dihydrate: Very soluble in polar solvents, such as ethanol, methanol, acetone, dioxane and tetrahydrofuran; practically insoluble in benzene, chloroform and petroleum ether.(37,38) The anhydrous form is soluble in diethyl ether, while the dihydrate is slightly soluble.(38)
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = -1.74 (estimated) (42)
pH Value: 1.3 (0.1 M solution in water) (38,40)
Acidity: Strong acid (37,38)
Dissociation Constant: pKa1 = 1.27 (K1 = 5.4 x 10(-2)), pKa2 = 4.27 (K2 = 5.5 x 10(-5)).(50) Also reported as pKa1 = 1.19 (K1 = 6.5 x 10(-2)), pKa2 = 4.22 (K2 = 6.0 x 10(-5)).(37,38)
Viscosity-Dynamic: Not applicable
Surface Tension: Not applicable
Vapour Density: Not applicable
Vapour Pressure: Very low at 25 deg C.(41)
Saturation Vapour Concentration: Not applicable
Evaporation Rate: Not available; very low
Henry's Law Constant: 1.45 x 10(-5) Pa.m3/mol (cited as 1.43 x 10(-10) (atm.m3/mol) at 25 deg C (41); log H = -8.23 (dimensionless constant; calculated)

Other Physical Properties:
**Sublimation begins at about 100 deg C (212 deg F), proceeds rapidly at 125 deg C (257 deg F) and can be carried out up to 157 deg C (314.6 deg F), when it begins to decompose.(37,38)


SECTION 10. STABILITY AND REACTIVITY

Stability:
Normally stable.

Hazardous Polymerization:
Does not occur.

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.


STRONG OXIDIZING AGENTS (e.g. potassium permanganate) - may react violently. Risk of fire and explosion.(2,10,43)
SODIUM CHLORITE and WATER - forms highly explosive chlorine dioxide.(9,44)
SILVER or MERCURY- form explosive silver oxalate or explosive mercury oxalate, respectively.(9,44)
ALKALI METALS (e.g. sodium or potassium) - may react violently and produce flammable hydrogen gas.(12)
STRONG ALKALIS (e.g. sodium hydroxide or potassium hydroxide) - may react vigorously or violently.(2,10,12)
ACID CHLORIDES - may react vigorously, producing toxic fumes.(12)
IRON AND IRON COMPOUNDS (e.g. ferric oxide) or COPPER- may react rapidly to form explosive oxalates.

Hazardous Decomposition Products:
None reported.

Conditions to Avoid:
High temperatures, generation of dust.

Corrosivity to Metals:
Oxalic acid solutions (5% to saturated) are corrosive to carbon steel (types 1010, 1020, 1075 and 1095), stainless steel (types 304 and 347), cast iron (unspecified), type 5052 aluminum and lead at 21 deg C.(45,46,47). Oxalic acid is corrosive to type 3003 aluminum at 93 deg C.(45,46) Oxalic acid solutions (5% to saturated) are not corrosive to types 3003 and Cast B-356 aluminum, types 316 and 400 series stainless steels, 20 Carpenter Cb 3, copper, bronze (unspecified), aluminum bronze, naval bronze, silicon bronze, admiralty brass, naval brass, nickel base alloys, Hastelloy, Monel, Inconel, Incoloy, tantalum and zirconium at 21 deg C.(45,46) Dry oxalic acid is not corrosive to metals.(12)

Corrosivity to Non-Metals:
Oxalic acid attacks plastics, such as acetal, nylon and polyethylene terephthalate (PET); elastomers, such as nitrile Buna-N, chlorinated polyethylene, soft rubber and polysulfides; and general purpose and chemical resistant epoxy coatings at 21 deg C.(46,48,49) It does not attack plastics, such as Teflon and other fluorocarbons, acetonitrile-butadiene-styrene (ABS), polyesters, polyvinylidene chloride (Saran), chlorinated polyvinyl chloride (CPVC), polyethylene, polypropylene, polystyrene and polyvinyl chloride (PVC); elastomers, such as ethylene propylene diene, Viton and other fluorocarbons, butyl rubber, isoprene, natural rubber, neoprene and silicone rubbers; and coatings, such as coal tar epoxy, polyester and vinyls at 21 deg C.(46,48,49)

Stability and Reactivity Comments:
Oxalic acid is a mild reducing agent and is easily oxidized.(38)


SECTION 11. TOXICOLOGICAL INFORMATION

LD50 (oral, female rat): 7.5 mL/kg (administered as a 5% water solution); this value can be converted to 375 mg/kg or 7500 mg/kg; depending how the original data is interpreted (13)
LD50 (oral, male rat): 9.5 mL/kg (administered as a 5% water solution); this value can be converted to 475 mg/kg or 9500 mg/kg; depending how the original data is interpreted (13)

LD50 (dermal): greater than 20000 mg/kg (administered as a 5% water solution) (13)

Eye Irritation:

Oxalic acid is corrosive to the eyes.

Application of 100 mg of oxalic acid powder to rabbits caused extreme irritation when not rinsed (score 91.67 to 107.67 after 24 hours), extreme irritation when rinsed after 30 seconds (score 70.17 to 76.17 after 24 hours), and severe irritation when rinsed after 4 seconds (score 35.67 after 24 hours).(1) Application of an unspecified amount of a 5% solution of oxalic acid to rabbits for 30 seconds caused coagulation of the corneal epithelium, but recovery occurred within 6 days.(8, unconfirmed)

Skin Irritation:

Results from studies using accepted test methods were not located. Limited information suggests that brief exposure to oxalic acid is mildly irritating.

Immersion of the ear of a rabbit in 9.1% oxalic acid (saturated solution in water) for one minute did not cause irritation. Immersion of the ear of another rabbit for 5 minutes caused redness, which was still present with scaliness after 24 hours. A disc wet with saturated oxalic acid solution placed on a shaved area on the back of a rabbit for 24 hours caused no irritation.(5) Application of 500 mg (form unspecified) of oxalic acid for 24 hours to rabbits cause mild irritation.(3, unconfirmed)

Effects of Short-Term (Acute) Exposure:

Skin Contact:
Application of 0.1 mL of oxalic acid at concentrations of 1% (pH 1.5), 5% (pH 1.2) and 10% (pH 1.1), once a day for 10 days, to the skin of guinea pigs, caused a dose-related increase in skin-fold thickness (a measure of swelling). Redness was observed at day 3 for the 5% and 10% concentrations, and at day 9 for the 1% concentration.(15)

Ingestion:
Ingestion of 0.25%, 0.5%, and 1.0% oxalic acid in drinking water for 2 weeks caused a dose-related decrease in body-weight gain for male mice, but not for females. Reported doses were 340, 590, and 1060 mg/kg/day for males and 450, 690, and 1180 mg/kg/day for females. Concentrations of 2.5% and 5% caused a dose-related decrease in body weight in both males and females. Reported daily doses were 1710 and 3410 mg/kg/day for males, and 1570 and 3680 mg/kg/day for females. By day 14, 7/8 males and 7/8 females in the 2.5% dose group had died and 7/8 males and 6/8 females in the 5% dose group had died.(21)

Effects of Long-Term (Chronic) Exposure:

Mice orally dosed with approximately 275 mg/kg/day for two generations, had reduced water consumption and increased kidney weights in the second generation. Approximately 2000 mg/kg/day for 70 days caused decreased body weight and growth rates in rats, while approximately 5000 mg/kg/day for 70 days caused increased mortality, kidney stones and kidney damage. In a limited study, slight liver damage was observed in rats orally exposed to doses as low as 40 mg/kg/day for 2 years.

Ingestion:
Rats fed 2.5% or 5% oxalic acid in the diet for 70 days experienced decreased body weight and growth rates, which were more severe at 5%. Also at 5%, organ weights were lower than the controls and kidney stones and kidney damage were observed. Mortality was 25% at the higher dose and less than 10% at the lower dose. Reported doses were 1980 or 5300 mg/kg/day for females and 1780 or 5200 mg/kg/day for males.(6) Another study also used rats fed 2.5% or 5% oxalic acid in the diet for 70 days. Reported doses were 2100 or 5300 mg/kg/day for females and 1900 or 5300 mg/kg for males. Reduced growth was observed at both doses, with more severe effects at 5%. At both doses, males and females showed a significant decrease in thyroid weight and in radioactive iodine uptake. Thyroid stimulating hormone was increased at both doses, but the increase was only significant at the 5%. These results indicate that prolonged ingestion of very high doses of oxalic acid could cause reduced thyroid function.(7) In a 2-generation study with mice dosed continuously with 0.2% oxalic acid in their drinking water (approximate dose 275 mg/kg/day), kidney weights were significantly increased over controls for second-generation mice.(21) In a limited study, rats fed 0.1%, 0.5%, 0.8%, or 1.2% oxalic acid in the diet for two years, had no differences in mortality or weight gain compared to controls. Approximate doses were 40, 250, 400 or 600 mg/kg/day for females and 60, 300, 480 or 720 mg/kg/day for males. Detailed autopsy indicated slight liver damage in 11/83 treated animals; 5/21 of these were in the 0.1% dose group, otherwise doses were not specified. No other differences were reported.(17) In another study, rats were fed oxalic acid, in the form of potassium oxalate, with dietary oxalate concentrations ranging from 0.032-1.32%. Approximate doses were 12-680 mg/kg/day for males and females. Treated rats maintained for 10 weeks on a diet with optimal amounts of calcium, phosphorous and vitamin D showed no significant differences in growth rate or food consumption for any of the treatments. The only effect noted was a decrease in the ash content of the bones, at 1.32%. According to the authors, this effect may indicate somewhat less efficient calcium (or phosphorus) utilization.(16) In a limited study, two dogs given oxalic acid in the form of sodium oxalate or potassium oxalate, twice a week, with total doses of 940 mg/kg (equivalent to 16 mg/kg/day) oxalate over 58 days and 2100 mg/kg (equivalent to 20 mg/kg/day) oxalate over 105 days, accumulated large quantities of oxalic acid in the kidney. Examination of cells from the organs of the dog dosed with 2100 mg/kg, indicated kidney damage and deposits of large quantities of oxalate crystals.(18)

Skin Sensitization:
Oxalic acid, usually considered an irritant rather than a sensitizer, was found to give a positive result in the murine local lymph node assay, a predictive assay for allergens.(19) This assay is known to give false positive results for some irritants, including oxalic acid.

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
It is not possible to conclude that oxalic acid causes developmental toxicity, based on the available information.
A continuous breeding study with mice exposed to oxalic acid in drinking water did not show significant developmental effects.(21,22) See "REPRODUCTIVE TOXICITY" for a review of this study. In a limited study, female rats (10/group) were orally given 0.5 mL of 0, 0.035 or 0.045 gm/day of an oxalic acid solution (approximate doses were 0, 175 or 225 mg/kg/day) starting from day 7 after mating for an unreported duration. Mean birth weights of newborns were the same for treated animals and controls. No abortions or malformed fetuses were observed. However, litter sizes were smaller in the treated groups compared to controls. No statistical analysis of the data was conducted. In the mothers, oxalate crystals were found in the kidneys of 7/10 animals at the higher dose and 5/10 of the lower dose, but in none of the controls. In the offspring, no oxalate crystals or kidney damage was observed.(20)

Reproductive Toxicity:
It is not possible to conclude that oxalic acid is a reproductive toxin based on the available information. Reproductive toxicity was observed in mice in one study, but the effects were observed in the presence of a significant reduction in water consumption in the parents of the first generation and increased kidney weight in the second generation.
In a continuous breeding study, mice were treated with 0.0, 0.05, 0.1 or 0.2% oxalic acid in drinking water for 18 weeks, including a one-week pre-mating period, a 14-week period of male/female cohabitation, and a 6-week holding period. During this time of continuous exposure, litters are produced approximately 3-4 weeks apart. Reported doses were approximately 0, 89, 162, or 275 mg/kg/day. There were no signs of toxicity in the adults, except a significant reduction in water consumption (approximately 25%) at 0.1 and 0.2% and slightly smaller prostate glands in males. At 0.05% and 0.1%, oxalic acid had no significant effect on litter size, proportion of live births, sex ratio or weight of newborns. Treatment at 0.2% caused small, but significant, decreases in the number of litters produced/pair (5%) and in the weight of newborns, which reversed during the postnatal period. The relative frequency of estrous (fertility cycle) was increased in females exposed to 0.2% (11% in controls vs. 21% in the treatment group).(21,22) A second-generation study was carried out on the last litter (10/sex) from the 0.2% dose group. These animals continued to receive oxalic acid, first through lactation and then in drinking water at a 0.2% concentration. They were mated at 74 days of age and produced 1 litter. There was a significant decrease (20%) in the number of live pups/litter for the treated animals, but no differences in the proportion of live births, sex ratio or weight of newborns. Treated males had smaller prostate weights and a significant increase in the percentage of abnormal sperm compared to the controls. However, the percentage of abnormal sperm was still less than controls in the first generation study. The relative frequency of estrous was again increased in females exposed to 0.2% (31% in controls vs. 37% in the treatment group). Increased kidney weight was observed in the males (absolute) and females (relative). The authors concluded that prolonged ingestion of oxalic acid may interfere with the female fertility cycle and with spermatogenesis in males.(21,22) In another study, ingestion of 2.5% or 5% oxalic acid in the diet (reported doses were 1980 or 5300 mg/kg/day) for 70 days caused disruption of the female fertility cycle in rats.(6) These doses caused severe toxicity in the rats.

Mutagenicity:
The available information does not indicate that oxalic acid is mutagenic.
Negative results (chromosome aberrations) were obtained in a test using cultured mammalian cells.(25) Negative results (gene mutation) were also obtained in tests using bacteria, both with and without metabolic activation.(23,24,25)


SECTION 16. OTHER INFORMATION

Selected Bibliography:
(1) Guillot, J.P., et al. Evaluation of the ocular-irritation potential of 56 compounds. Food and Chemistry Toxicology. Vol. 20, no. 5 (1982). p. 573-582
(2) Oxalic acid. In: NIOSH pocket guide to chemical hazards. National Institute for Occupational Safety and Health, June 1997. p. 238-239 Cathy
(3) National Institute for Occupational Safety and Health (NIOSH). Oxalic acid. Last updated: 2000-12. In: Registry of Toxic Effects of Chemical Substances (RTECS(R)). [CD-ROM]. Canadian Centre for Occupational Health and Safety (CCOHS). Issue: 2001-4. Also available from World Wide Web: <http://ccinfoweb.ccohs.ca/rtecs/search.html>
(4) Gosselin, R.E., et al. Clinical toxicology of commercial products. 5th ed. Williams & Wilkins, 1984. p. II-198, III-326-III-328
(5) Klauder, J.V., et al. Industrial uses of compounds of fluorine and oxalic acid. Cutaneous reaction and calcium therapy. A.M.A. Archives of Industrial Health. Vol. 12 (1955). p. 412-419
(6) Goldman, M., et al. Effect of dietary ingestion of oxalic acid on growth and reproduction in male and female Long-Evans rats. Research Communications in Chemical Pathology and Pharmacology. Vol. 18, no. 2 (1977). p. 369-372
(7) Goldman, M., et al. The effect of dietary ingestion of oxalic acid on thyroid function in male and female rats. Toxicology and Applied Pharmacology. Vol. 48 (1979). p. 409-414
(8) Grant, W.M., et al. Toxicology of the eye. 4th ed. Charles C. Thomas, 1993. p. 1081-1084
(9) Urben, P.G., ed. Bretherick's reactive chemical hazards database. [CD-ROM]. 6th ed. Version 3.0. Butterworth-Heinemann Ltd., 1999
(10) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 49; NFPA 491
(11) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002
(12) Oxalic acid; oxalic acid dihydrate. The Sigma-Aldrich library of chemical safety data. Ed II. Vol. 2. Edited by R.E. Lenga. Sigma-Aldrich Corporation, 1988. p. 2661A,D
(13) Vernot, E.H., et al. Acute toxicity and skin corrosion data for some organic and inorganic compounds and aqueous solutions. Toxicology and Applied Pharmacology. Vol. 42, no. 2 (1977). p. 417-423
(14) European Economic Community. Commission Directive 93/72/EEC. Sept. 1, 1993
(15) Wahlberg, J.E. Measurement of skin-fold thickness in the guinea pig. Assessment of edema-inducing capacity of cutting fluids, acids, alkalis, formalin and dimethyl sulfoxide. Contact Dermatitis. Vol. 28, no. 3 (1993). p. 141-145
(16) Mackenzie, C.G., et al. Some effects of dietary oxalate on the rat. The American Journal of Hygiene. Vol. 25, no. 1 (Jan. 1937). p. 1-10
(17) Fitzhugh, O.G., et al. The comparative chronic toxicities of fumaric, tartaric, oxalic and maleic acids. Journal of the American Pharmaceutical Association, Scientific Edition. Vol. 36. no. 7 (1947). p. 217-219
(18) Heubner, W. Toxicity studies on dogs (oxalate). Archiv fuer Experimentelle Pathologie und Pharmakologie. Vol. 178 (1935). p. 749-754
(19) Montelius, J., et al. Murine local lymph node assay for predictive testing of allergenicity: two irritants caused significant proliferation. Acta Derm Venereol. Vol. 78, no. 6 (Nov. 1998). p. 433-437
(20) Sheik-Omar, A.R., et al. Effects of feeding oxalic acid to pregnant rats. Pertanika. Vol. 3, no. 1 (1980). p. 25-31
(21) Gulatti, D.K., et al. Oxalic acid: reproduction and fertility assessment in CD-1 mice when administered in drinking water. RACB84064. US National Toxicology Program, 1985
(22) Chapin, R.E., et al. Reproductive assessment by continuous breeding: evolving study design and summaries of ninety studies. Oxalic acid. Environmental Health Perspectives. Vol. 105, suppl. 1 (Feb. 1997). p. 199-205; 229-230
(23) Sayato, Y., et al. Mutagenicity of products formed by ozonation of naphthoresorcinol in aqueous solutions. Mutation Research. Vol. 189, no. 3 (1987). p. 217-222
(24) Haworth, S., et al. Salmonella mutagenicity test results for 250 chemicals. Environmental Mutagenesis. Vol. 5, suppl. 1 (1983). p. 3-142
(25) Ishidate, M., et al. Primary mutagenicity screening of food additives currently used in Japan. Vol. 22, no. 8 (1984). p. 623-636
(26) Schwartz, L. Dermatoses caused by inorganic and organic acids. In: A textbook of occupational diseases of the skin. 3rd ed. Lea and Febiger, 1948. p. 234-244
(27) Cherpelis, B.S., et al. Purpuric irritant contact dermatitis induce by Agave Americana. Cutis. Vol. 66, no. 4 (Oct. 2000). p. 287-288
(28) McLaughlin, R.S. Chemical burns of the cornea. American Journal of Ophthalmology. Vol. 29, no. 11 (1946). p. 1355-1362
(29) Hodgkinson, A., et al. Oxalic acid metabolism in man: a review. Calcified Tissue Research. Vol. 2 (1968). p. 115-132
(30) Brown, S.A., et al. A study of oxalic acid poisoning. Proceedings of the Society of Experimental Biology and Medicine. Vol. 19 (1922). p. 204-208
(31) Zarembeski, P.M., et al. Plasma oxalic acid and calcium levels in oxalate poisoning. Journal of Clinical Pathology. Vol. 20 (1967). p. 283-285
(32) Howard, C.D. Chronic poisoning by oxalic acid: with report of a case and results of a study concerning the volatilization of oxalic acid from aqueous solution. The Journal of Industrial Hygiene. Vol. 14, no. 8 (Oct. 1932). p. 283-290
(33) Grolnick, M., et al. Case of early gangrene due to oxalic acid immersion. New York State Journal of Medicine. Vol. 29, no. 23 (1929). p. 1461
(34) Laerum, S. et al. Urolithiasis in railroad shopmen in relation to oxalic acid exposure at work. Scandinavian Journal of Work, Environment and Health. Vol. 11, no. 2 (1985). p. 97-100.
(35) Strutek, J. Silicosis in workers packing cleansing powder - accelerating effect of oxalic acid, Casopis Lekaru Ceskych. Vol. 87 (1948). p. 343-346
(36) Menon, M., et al. Oxalate metabolism and renal calculi. Journal of Urology. Vol. 127, no. 1 (Jan. 1982). p. 148-151
(37) Riemenschneider, W. Oxalic acid. In: Ullmann's encyclopedia of industrial chemistry. 5th completely revised ed. Vol. A 18. VCH Publishers, 1991. p. 247-259
(38) Sawada, H., et al. Oxalic acid. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 17. John Wiley and Sons, 1996. p. 882-902
(39) Dean, J.A. Lange's handbook of chemistry. 15th ed. McGraw-Hill, Inc., 1999. p. 1.289, 8.63
(40) Oxalic acid. The Merck index: an encyclopedia of chemicals, drugs and biologicals. Edited by M.J. O'Neil, et al. 13th ed. Merck and Company, 2001. p. 1237
(41) Syracuse Research Corporation. The Physical Properties Database (PHYSPROP). Interactive PhysProp Database Demo. Date unknown. Available from World Wide Web: <http://www.syrres.com/esc/physdemo.htm>
(42) Syracuse Research Corporation. Interactive LogKow (KowWin) Database Demo. Date unknown. Available from World Wide Web: <http://syrres.com/esc/kowdemo.htm>
(43) Oxalic acid. In: Chemical safety sheets: working safely with hazardous chemicals. Kluwer Academic Publishers, 1991. p. 666
(44) Armour, M-A. Oxalic acid. In: Hazardous laboratory chemicals disposal guide. 2nd ed. Lewis Publishers, 1996. p. 348-349
(45) Pruett, K.M. Chemical resistance guide to metals and alloys: a guide to chemical resistance of metals and alloys. Compass Publications, 1995. p. 242-253
(46) Schweitzer, P.A. Corrosion resistance tables: metals, nonmetals, coatings, mortars, plastics, elastomers and linings, and fabrics. 4th ed. Part b, E-O. Marcel Dekker, Inc., 1995. p. 2085-2100
(47) Corrosion data survey: metals section. 6th ed. National Association of Corrosion Engineers, 1985. p. 92-6 to 93-4
(48) Pruett, K.M. Chemical resistance guide for plastics: a guide to chemical resistance of engineering thermoplastics, fluoroplastics, fibers and thermoset resins. Compass Publications, 2000. p. 362 to 373
(49) Pruett, K.M. Chemical resistance guide for elastomers II: a guide to chemical resistance of rubber and elastomeric compounds. Compass Publications, 1994. p. C-266 to C-271
(50) Streitweiser, Jr., A., et al. Introduction to organic chemistry. 3rd ed. Macmillan Publishing Company, 1985. p. 864
(51) Occupational Safety and Health Administration (OSHA). Oxalic Acid. In: OSHA Analytical Methods Manual. Revision Date: Apr. 2003. Available from World Wide Web: <http://www.osha.gov/dts/sltc/methods/partial/pv2115/pv2115.html>
(52) National Institute for Occupational Safety and Health (NIOSH). Particulates, Not Otherwise Regulated, total. In: NIOSH Manual of Analytical Methods (NMAM(R)). 4th ed. Edited by M.E. Cassinelli, et al. DHHS (NIOSH) Publication 94-113. Aug. 1994. Available from World Wide Web: <http://www.cdc.gov/niosh/nmam/nmammenu.html>
(53) Health Council of the Netherlands: Committee on Updating of Occupational Exposure Limits. Oxalic acid: health-based reassessment of administrative occupational exposure limits. 2000/15OSH/106. The Hague: Health Council of the Netherlands, 2004.

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.


Review/Preparation Date: 2005-08-25



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