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CAS 10034-93-2

Hydrazine sulfate

hydrazine saltHAPprobable carcinogen

Hydrazine sulfate is the water-soluble salt form of the highly toxic rocket fuel precursor hydrazine — it gained unexpected notoriety in the 1990s as a controversial alternative cancer treatment before rigorous clinical trials definitively showed it was ineffective and potentially harmful.

Where It Comes From

Hydrazine sulfate (H2NNH2·H2SO4) is manufactured by combining hydrazine with sulfuric acid and has industrial uses as a chemical intermediate in synthesis of pharmaceuticals, antioxidants, and agricultural chemicals, as well as for water treatment and as a reducing agent. [1] Hydrazine itself was first synthesized in 1875 by Curtius and became important in the 20th century as a rocket propellant and chemical intermediate. The sulfate salt is more stable and easier to handle than anhydrous hydrazine. Toxicologically, hydrazine sulfate shares hydrazine's properties: hepatotoxicity, central nervous system toxicity, and carcinogenicity. NTP studies found it caused lung tumors, liver tumors, and vascular tumors in rodents, leading to its classification as a Group B2 probable human carcinogen. [2] A separate and remarkable chapter in its history occurred in the 1970s–1990s when biochemist Joseph Gold proposed that hydrazine sulfate could treat cancer cachexia (wasting) by inhibiting a metabolic enzyme (phosphoenolpyruvate carboxykinase, PEPCK) involved in gluconeogenesis from lactate. Several small, poorly controlled studies reported benefits, and hydrazine sulfate was promoted in alternative cancer medicine circles. However, three large, rigorous NCI-sponsored clinical trials in the early 1990s found no benefit for cancer patients, and some evidence of harm including peripheral neuropathy. [3] The FDA never approved it as a cancer treatment. It remains an industrial chemical tracked under the TRI and HAP programs.

How You Are Exposed

Occupational exposure occurs in chemical manufacturing facilities where hydrazine sulfate is produced or used as a synthetic intermediate. Inhalation of dusts during handling of the white crystalline solid and skin absorption are the primary routes. The general public has very limited direct exposure; historical exposure occurred among individuals taking it as an alternative cancer remedy.

Why It Matters

The carcinogenicity of hydrazine sulfate (shared with the parent hydrazine molecule) is well-established in rodents across multiple tumor types. The mechanism involves reactive metabolites that alkylate DNA. Acute effects include nausea, vomiting, liver damage, hemolytic anemia, and CNS effects including tremors and seizures. Chronic exposure depletes vitamin B6 (pyridoxal phosphate), contributing to neuropathy. [2] The historical episode as a fraudulent cancer treatment serves as a cautionary tale about inadequate clinical evidence in alternative medicine.

Who Is at Risk

Chemical industry workers handling hydrazine sulfate are most at risk. Historically, cancer patients who used it as an alternative treatment were exposed to the carcinogen they were trying to treat themselves with. Current general population risk is low.

How to Lower Your Exposure

1. Industrial handling requires local exhaust ventilation, impermeable gloves, eye protection, and respiratory protection for dust. 2. Treat all hydrazine compound spills as hazardous — neutralize with dilute acid before disposal per waste regulations. 3. Avoid all alternative medicine preparations containing hydrazine sulfate — there is no evidence of benefit and clear evidence of harm. 4. Refer cancer patients asking about this compound to evidence-based oncology care.

References

  1. [1][1] Kirk-Othmer Encyclopedia of Chemical Technology. Hydrazine. John Wiley & Sons.
  2. [2][2] US EPA IRIS. Hydrazine/Hydrazine sulfate (CASRN 302-01-2/10034-93-2). https://cfpub.epa.gov/ncea/iris/iris_documents/documents/subst/0193_summary.pdf
  3. [3][3] Loprinzi CL, et al. (1994). Randomized placebo-controlled evaluation of hydrazine sulfate in patients with advanced colorectal cancer. Journal of Clinical Oncology, 12(6), 1121–1125.

Recovery & Clinical Information

Body Half-Life

Hydrazine sulfate dissociates to hydrazine in aqueous solution. Hydrazine has a plasma half-life of several hours; it is metabolized by acetylation (with polymorphic variation), oxidation, and elimination as acetylhydrazine and other metabolites in urine. Vitamin B6 depletion occurs with repeated exposures. Full metabolic clearance occurs within 1–3 days of a single exposure.

Testing & Biomarkers

Blood or urine hydrazine can be measured by GC or colorimetric methods in research settings. Methemoglobin and liver function tests (ALT, AST) are clinically relevant for acute exposure. Plasma pyridoxal phosphate level can be measured to assess B6 depletion. Routine clinical labs do not typically offer hydrazine testing; request from toxicology or occupational medicine services.

Interventions

For acute exposure: remove from source; if ingested, do not induce vomiting; seek emergency medical care. Pyridoxine (vitamin B6) is the specific antidote for hydrazine-class seizures and neurological effects — IV pyridoxine controls seizures. Supportive care for liver injury. Methylene blue for methemoglobinemia. For chronic low-level exposure, source removal and B6 supplementation under medical supervision.

Recovery Timeline

Acute symptoms resolve within 24–72 hours with appropriate treatment. Liver enzyme elevations may persist for weeks. Neuropathy from B6 depletion gradually improves after B6 repletion and cessation of exposure. Cancer risk from past exposure remains but does not increase after exposure ends.

Recovery References

  1. [1]NIOSH Pocket Guide: Hydrazine. https://www.cdc.gov/niosh/npg/npgd0336.html
  2. [2]Sotaniemi EA, et al. (1971). Liver damage in workers exposed to hydrazine. American Journal of Medicine, 51(1), 32–42.

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