옥살산 디암모늄

Fire Extinguishing Agents: Water, foam (USCG, 1999)

Use water spray, powder, foam, carbon dioxide.

Fresh air, rest. Seek medical attention if you feel unwell.

Remove contaminated clothes. Rinse and then wash skin with water and soap.

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

Rinse mouth. Refer for medical attention .

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Sweep spilled substance into sealable containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

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.

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.

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.

Cough. Sore throat.

Redness. Burning sensation. Pain.

Redness. Pain. Burns.

Abdominal pain. Vomiting. Convulsions. Drowsiness. Dullness. Shock or collapse.

Oxalic acid poisoning symptoms include weakness, burning in the mouth, death from cardiovascular collapse, on the respiratory system, throat – burning in the throat, abdominal pain, nausea, vomiting, diarrhea, convulsions, and coma.

SYMPTOMATOLOGY: 1. BURNING PAIN IN THROAT, ESOPHAGUS, & STOMACH. EXPOSED AREAS OF MUCOUS MEMBRANE TURN ALMOST IMMEDIATELY AN OPAQUE WHITE...NO CORROSIVE ACTIONS ON LIPS & FACE. 2. VOMITING (OFTEN BLOODY OR WITH A COFFEE GROUND APPEARANCE), INTENSE BURNING PAIN, SEVERE PURGING. 3. PULSE BECOMES WEAK, IRREGULAR, & SOMETIMES IMPERCEPTIBLE. HYPOTENSION & USUAL SIGNS OF CARDIOVASCULAR COLLAPSE APPEAR. 4. IF DEATH IS DELAYED FOR A FEW HR, NERVOUS OR NEUROMUSCULAR SYMPTOMS DEVELOP: HEADACHE, MUSCLE CRAMPS...TETANY, SOMETIMES CONVULSIONS, STUPOR, COMA, & DEATH. 5. RENAL DAMAGE, AS EVIDENCED BY OLIGURIA. ALBUMINURIA, & HEMATURIA MAY PERSIST FOR WK. /OXALATE/

INGESTION OR EXCESSIVE INHALATION OF DUST CAUSES SYSTEMIC POISONING; POSSIBLE SYMPTOMS INCLUDE PAIN IN THROAT, ESOPHAGUS, & STOMACH; MUCOUS MEMBRANES TURN WHITE; VOMITING, SEVERE PURGING, WEAK PULSE, CARDIOVASCULAR COLLAPSE, NEUROMUSCULAR SYMPTOMS. /MONOHYDRATE/

IF...A LARGE ENOUGH QUANTITY OF OXALATE IS INGESTED SOME OF IT WILL BE ABSORBED UNCHANGED & THUS LEAD TO OXALATE POISONING. /OXALIC ACID/

...ABSORBED INTO BLOOD... IT MAY PRODUCE ACUTE HYPOCALCEMIA LEADING TO RAPID DEATH. THE MOST COMMON EFFECT...KIDNEY DAMAGE OWING TO BLOCKING OF TUBULES BY CRYSTALS OF CALCIUM OXALATE. ...OXALATES MAY CRYSTALLIZE OUT IN BRAIN TISSUE & CAUSE...PARALYSIS & OTHER DISORDERS OF CNS. MAY LEAD TO THE BREAKDOWN OF RED BLOOD CELLS. /OXALIC ACID/

...SYMPTOMS INCLUDE DULLNESS & LOSS OF APPETITE. HEAD IS LOWERED & ANIMAL IS UNWILLING TO KEEP WITH FLOCK. WITH ACUTE POISONING...SALIVATION & NASAL DISCHARGE WITH PROGRESSIVE WEAKNESS, RAPID SHALLOW BREATHING & COLLAPSE... LUNGS MAY BE DARK RED & FILLED WITH BLOOD AND THERE MAY BE PETECHIAL OR LARGER HEMORRHAGES. /OXALIC ACID/

AMMONIUM OXALATE CAUSED CHANGES IN BREATHING RHYTHM & DECR OF 8-16% IN OXYGEN INTAKE OF GAMMARUS FOSSARUM & INCR OF 18.23% IN CO2 EXCRETION.

AMMONIUM OXALATE WAS AMONG TOXIC CMPD WHICH DECR OXYGEN CONSUMPTION BY BARYTELPHUSA CUNICULARIS.