Food & Drink / Compounds / Oxalic acid

Oxalic acid in food: ingestion safety

Moderate risk

Oral ingestion of oxalic acid represents a dose-dependent risk from negligible (normal dietary intake from plant foods) to potentially fatal (concentrated industrial oxalic acid); the unique systemic toxicity via calcium chelation and renal tubular crystal deposition distinguishes oxalic acid from most common organic acids. Normal dietary exposure: plant-food-derived oxalate at 100–300 mg/day is partially absorbed (~10–25% depending on gut microbiome composition and calcium intake) and partially complexed with intestinal calcium — dietary calcium intake reduces oxalate absorption by forming insoluble calcium oxalate in the gut lumen, a fact exploited in kidney stone prevention strategies. Kidney stone formation: even at normal dietary oxalate intake, individuals with hyperoxaluria (primary or secondary), low urine volumes, and low citrate excretion develop calcium oxalate nephrolithiasis — the most prevalent kidney stone type globally; dietary oxalate reduction combined with increased calcium intake and hydration is first-line prevention. Ethylene glycol toxicity connection: ethylene glycol antifreeze is metabolized to oxalic acid via glycolic and glyoxylic acid intermediates — the calcium oxalate crystal deposition in renal tubules and systemically accounts for the delayed acute renal failure in ethylene glycol poisoning; this metabolic pathway demonstrates the toxicological role of oxalic acid as an end-stage toxic metabolite. Industrial oxalic acid ingestion (concentrated): 10% oxalic acid solution ingestion (industrial cleaner concentration) causes immediate GI corrosive injury, severe hypocalcemia with tetany and QT prolongation, and acute renal tubular obstruction — serum calcium and ECG monitoring are essential treatment components. Perioperative oxalate nephropathy: high-dose vitamin C supplementation (ascorbic acid >4 g/day) increases urinary oxalate excretion, contributing to oxalate nephropathy in susceptible patients — a concern emerging from IV vitamin C protocols.

What is oxalic acid?

Also known as: ethanedioic acid, Aktisal, Aquisal, Oxiric acid.

IUPAC name
oxalic acid
CAS number
144-62-7
Molecular formula
C2H2O4
Molecular weight
90.03 g/mol
SMILES
C(=O)(C(=O)O)O
PubChem CID
971

Risk for people

Moderate risk

Oral ingestion of oxalic acid represents a dose-dependent risk from negligible (normal dietary intake from plant foods) to potentially fatal (concentrated industrial oxalic acid); the unique systemic toxicity via calcium chelation and renal tubular crystal deposition distinguishes oxalic acid from most common organic acids. Normal dietary exposure: plant-food-derived oxalate at 100–300 mg/day is partially absorbed (~10–25% depending on gut microbiome composition and calcium intake) and partially complexed with intestinal calcium — dietary calcium intake reduces oxalate absorption by forming insoluble calcium oxalate in the gut lumen, a fact exploited in kidney stone prevention strategies. Kidney stone formation: even at normal dietary oxalate intake, individuals with hyperoxaluria (primary or secondary), low urine volumes, and low citrate excretion develop calcium oxalate nephrolithiasis — the most prevalent kidney stone type globally; dietary oxalate reduction combined with increased calcium intake and hydration is first-line prevention. Ethylene glycol toxicity connection: ethylene glycol antifreeze is metabolized to oxalic acid via glycolic and glyoxylic acid intermediates — the calcium oxalate crystal deposition in renal tubules and systemically accounts for the delayed acute renal failure in ethylene glycol poisoning; this metabolic pathway demonstrates the toxicological role of oxalic acid as an end-stage toxic metabolite. Industrial oxalic acid ingestion (concentrated): 10% oxalic acid solution ingestion (industrial cleaner concentration) causes immediate GI corrosive injury, severe hypocalcemia with tetany and QT prolongation, and acute renal tubular obstruction — serum calcium and ECG monitoring are essential treatment components. Perioperative oxalate nephropathy: high-dose vitamin C supplementation (ascorbic acid >4 g/day) increases urinary oxalate excretion, contributing to oxalate nephropathy in susceptible patients — a concern emerging from IV vitamin C protocols.

Regulatory consensus

5 regulatory and scientific bodies have classified Oxalic acid. The classifications differ — that's the data.

AgencyYearClassificationNotes
EPA CTX / GenetoxGenotoxicity: negative (Ames: negative, 0 positive / 5 negative reports)
EPA CTX / GenetoxGenotoxicity: negative (Ames: negative, 0 positive / 5 negative reports)
FDAGRAS as natural food component; no specific food additive approval
ECHAH302 harmful if swallowed; H312 harmful in contact with skin
OSHAPEL 1 mg/m3 TWA (respirable)

Regulators apply different standards of evidence — animal-data weighting, exposure-pattern assumptions, epidemiological power thresholds — which is why two scientific bodies can review the same data and reach different conclusions. The disagreement is the data.

Where you encounter oxalic acid

  • Industrial FacilitiesManufacturing plants, Chemical storage areas, Waste treatment sites
  • Occupational EnvironmentsFactories, Warehouses, Transportation vehicles
  • Foodprocessed food, beverages, candy, baked goods
  • Natural Foodsspinach, rhubarb, beets, Swiss chard, star fruit
  • Cleaning ProductsBar Keepers Friend, wood bleach/deck brightener, rust removers, metal polish
  • Industrialmarble polishing, textile bleaching, wastewater treatment (precipitant)
  • Automotiveradiator flush, aluminum brightener

Safer alternatives

Lower-risk approaches that achieve a similar outcome to Oxalic acid:

  • Fragrance-free formulations
    Trade-offs: Consumer preference for scented products
    Relative cost: Lower (ingredient elimination)
  • Essential oil-based fragrances (with disclosure)
    Trade-offs: Natural does not mean safe — many essential oils are skin sensitizers
    Relative cost: 2-5× conventional

Frequently asked questions

Is oxalic acid safe for you?

Oral ingestion of oxalic acid represents a dose-dependent risk from negligible (normal dietary intake from plant foods) to potentially fatal (concentrated industrial oxalic acid); the unique systemic toxicity via calcium chelation and renal tubular crystal deposition distinguishes oxalic acid from most common organic acids. Normal dietary exposure: plant-food-derived oxalate at 100–300 mg/day is partially absorbed (~10–25% depending on gut microbiome composition and calcium intake) and partially complexed with intestinal calcium — dietary calcium intake reduces oxalate absorption by forming insoluble calcium oxalate in the gut lumen, a fact exploited in kidney stone prevention strategies. Kidney stone formation: even at normal dietary oxalate intake, individuals with hyperoxaluria (primary or secondary), low urine volumes, and low citrate excretion develop calcium oxalate nephrolithiasis — the most prevalent kidney stone type globally; dietary oxalate reduction combined with increased calcium intake and hydration is first-line prevention. Ethylene glycol toxicity connection: ethylene glycol antifreeze is metabolized to oxalic acid via glycolic and glyoxylic acid intermediates — the calcium oxalate crystal deposition in renal tubules and systemically accounts for the delayed acute renal failure in ethylene glycol poisoning; this metabolic pathway demonstrates the toxicological role of oxalic acid as an end-stage toxic metabolite. Industrial oxalic acid ingestion (concentrated): 10% oxalic acid solution ingestion (industrial cleaner concentration) causes immediate GI corrosive injury, severe hypocalcemia with tetany and QT prolongation, and acute renal tubular obstruction — serum calcium and ECG monitoring are essential treatment components. Perioperative oxalate nephropathy: high-dose vitamin C supplementation (ascorbic acid >4 g/day) increases urinary oxalate excretion, contributing to oxalate nephropathy in susceptible patients — a concern emerging from IV vitamin C protocols.

What products contain oxalic acid?

Oxalic acid appears in: Manufacturing plants (Industrial facilities); Chemical storage areas (Industrial facilities); Factories (Occupational environments); Warehouses (Occupational environments); processed food (Food).

Why do regulators disagree about oxalic acid?

Oxalic acid has been classified by 5 agencies including EPA CTX / Genetox, EPA CTX / Genetox, FDA, ECHA, OSHA, with differing conclusions. Regulators apply different standards of evidence (animal data weighting, exposure-pattern assumptions, epidemiological power thresholds), which is why two scientific bodies can review the same data and reach different conclusions. See the regulatory consensus table on this page for the full picture.

See Oxalic acid in the food app

Look up products containing oxalic acid, compare to alternatives, and explore the full data record.

Open in food View raw API data

Sources (2)

  1. NIOSH: Oxalic Acid — calcium chelation; calcium oxalate nephrolithiasis; hypocalcemia; rhubarb leaf toxicity; industrial cleaner hazard; primary hyperoxaluria; ethylene glycol metabolism (2019) (2019) — regulatory
  2. CDC/ATSDR: Oxalic Acid Toxicological Profile — plant sources; dietary intake; renal tubular deposition; acute poisoning treatment; industrial uses; calcium oxalate crystals; pediatric rhubarb exposure (2020) (2020) — regulatory

Reference data, not professional advice. Aggregates publicly available regulatory and scientific data; not a substitute for veterinary, medical, legal, or regulatory advice. Why we built ALETHEIA →