Mercuric Nitrate

CAS RN: 10045-94-0

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • A) USES: Common mercury salts include mercury II (mercuric) chloride (corrosive sublimate), mercury I (mercurous) chloride (calomel), mercury II oxide, mercury II iodide, and mercury II sulfide (cinnabar). Mercuric chloride is used as a disinfectant and pesticide. In the past, inorganic mercury compounds were used as diuretics, antibacterials, antiseptics, ointments, laxatives, and antisyphilitic agents. Most of these products have now been discontinued. Mercury poisoning due to ingestion of stool fixative containing 4.5% of mercuric chloride (675 mg) and 5% of polyvinyl alcohol has been reported. Skin lightening creams from Asia and Latin America and some Chinese herbal medicines have been found to contain inorganic mercury.
  • B) PHARMACOLOGY: Inorganic mercurials have antiseptic properties though they are no longer formulated for therapeutic use.
  • C) TOXICOLOGY: Inorganic mercury causes caustic injury to the gastrointestinal tract and kidney tubules due to direct oxidative effects of mercury salts. Mercury ions bind to sulfhydryl groups and also have an affinity for phosphoryl, carboxyl, amide, and amine groups. The structure and function of key proteins and enzymes are disturbed, receptor affinities altered, and cellular metabolism impaired, among other effects. Mercury II chloride is considered more toxic that mercury I chloride.
  • D) EPIDEMIOLOGY: Inorganic mercury exposure is uncommon and acute toxicity is rare.
  • E) WITH POISONING/EXPOSURE
    • 1) MILD TO MODERATE TOXICITY: Nausea, vomiting, and diarrhea are likely to be the first symptoms of acute inorganic mercury salt ingestion. Oropharyngeal burns may occur. Renal insufficiency may occur within 24 hours of exposure.
    • 2) SEVERE TOXICITY: GASTROINTESTINAL: Hemorrhagic gastroenteritis may occur due to the caustic effects of inorganic mercury salts on the gastrointestinal mucosa. Grayish discoloration of the mucosa and metallic taste may accompany caustic effects in the oropharynx. Massive fluid losses due to vomiting and diarrhea toxicity may lead to hypotension and shock over the first several days of poisoning. RENAL: In addition to caustic gastrointestinal effects, renal injury is the primary toxicity of inorganic mercury exposure. Acute tubular necrosis due to the oxidative effects of mercury salts may lead to renal failure. RESPIRATORY: Aspiration or inhalation of inorganic mercury can lead to pneumonitis and acute lung injury.
    • 3) CHRONIC TOXICITY: Gastrointestinal, renal, and neurologic symptoms predominate chronic inorganic mercury toxicity. Gastrointestinal symptoms consist of abdominal pain, nausea, metallic taste, gingivostomatitis, loose teeth, and hypersalivation. Renal insufficiency due to acute tubular necrosis may occur. While inorganic mercury does not easily cross the blood brain barrier, long-term exposure may lead to conversion to organic mercury compounds which deposit into the CNS. Neurologic symptoms include tremor, neurasthenia, and withdrawn behavior (erethism). However, inorganic mercury exposure is unlikely to cause significant neurotoxicity. Chronic exposure to mercurial powders has led to acrodynia (Pink Disease), characterized by a morbilliform rash and erythematous edematous hyperkeratotic induration of the palms and soles associated with excessive sweating, tachycardia, photophobia, paraesthesias, and decreased reflexes.
0.2.3 VITAL SIGNS
  • A) Hypotension may occur.
0.2.5 CARDIOVASCULAR
  • A) Tachycardia, hypotension, hypovolemic shock and cardiovascular collapse can occur following ingestion of inorganic salts of mercury.
0.2.6 RESPIRATORY
  • A) Dyspnea, rales, and severe tracheal, laryngeal and pulmonary edema have occurred following ingestion and aspiration of inorganic mercury salts. Clinical findings similar to the adult respiratory distress syndrome (ARDS) have also been reported.
0.2.7 NEUROLOGIC
  • A) Tremor, confusion, loss of coordination, hyperreflexia, and lethargy may follow acute mercuric chloride ingestion.
  • B) Chronic exposure can cause fatigue, headache, weakness, decreased concentration, anxiety, emotional lability, irritability, delirium and neurocognitive impairment.
0.2.8 GASTROINTESTINAL
  • A) Inorganic mercury salts are corrosive. Gastritis, ulceration and necrosis of the gastrointestinal system can occur. Signs and symptoms include nausea, vomiting, diarrhea, dysphagia, abdominal pain, hematemesis and hematochezia. Death due to fluid and blood loss may result.
0.2.10 GENITOURINARY
  • A) Proteinuria, anuria, hematuria and glycosuria may result from ingestion of lower concentrations of inorganic mercury salts, or as a result of dermal application of products which contain inorganic mercury salts.
  • B) Acute renal failure and acute tubular necrosis may develop after ingestion of higher concentrations of inorganic mercury salts, and also as a result of injection or peritoneal exposure to these compounds.
0.2.12 FLUID-ELECTROLYTE
  • A) Severe fluid and electrolyte imbalances may occur secondary to GI losses after ingestion.
0.2.13 HEMATOLOGIC
  • A) There are limited reports of anemia and disseminated intravascular coagulation primarily secondary to the corrosive effects of these compounds.
0.2.14 DERMATOLOGIC
  • A) Mercury pigmentation, dermatitis and symptoms of acrodynia have resulted from use of creams containing inorganic mercury salts. Burns or irritation can result from some inorganic mercury compounds. Systemic toxicity resulted from chronic dermal absorption.
0.2.15 MUSCULOSKELETAL
  • A) Evidence of rhabdomyolysis was seen in a case of acute mercuric chloride ingestion. Muscular weakness occurs with chronic poisoning from inorganic mercurials.
0.2.20 REPRODUCTIVE
  • A) Mercuric chloride has been associated with spontaneous abortions in humans. It has been embryotoxic, fetotoxic, and teratogenic, and has affected the testes and sperm in rodents.
0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: Nitrites are commonly found in the manufacturing industry; they are used in the manufacture of diazo dyes, potassium salts, nitroso compounds, and nitrogen oxide, dyeing and printing textile fabrics, in photography, as reagents in analytical chemistry, as a key chemical in metal treatment and finishing operations, and bleaching flax, silk, and linen. Nitrites are also used in meat curing and preserving, and high inorganic nitrite (KNO2, NaNO
      • 2) levels may be found in well water contaminated by septic tanks, municipal sewage, fertilizers, and feed lots where bacteria reduce nitrates to nitrites. Medically, sodium nitrite is used as an adjunct to disinfectant fluids to prevent rusting of the instruments. Sodium nitrite is also used as an antidote to cyanide poisoning in combination with sodium thiosulfate. Please refer to "SODIUM NITRITE" management for more information.
    • B) PHARMACOLOGY: Sodium nitrite acts as a vasodilator and relaxes maximally contracted smooth muscles, especially at the level of the small blood vessels. In the setting of cyanide toxicity, sodium nitrite has its therapeutic effect by creating methemoglobin which scavenges cyanide and possibly by increasing hepatic blood flow. Nitrites oxidize normal (ferrous) hemoglobin to ferric hemoglobin (methemoglobin).
    • C) TOXICOLOGY: Toxic effects of sodium nitrite are caused by an extension of therapeutic mechanisms. Significant vasodilation may cause hypotension and end-organ hypoperfusion. Excess methemoglobinemia may lead to functional hypoxia. The toxic effects of other nitrites are similar to sodium nitrite's effects.
    • D) EPIDEMIOLOGY: Overdose is rare.
    • E) WITH POISONING/EXPOSURE
      • 1) MILD TO MODERATE TOXICITY: Hypotension with syncope and tachycardia are common findings in toxicity. Cyanosis may also be noted due to methemoglobinemia. Other common symptoms include headache, nausea, vomiting, and abdominal pain.
      • 2) SEVERE TOXICITY: In cases of severe toxicity, patients may develop severe hypotension, distributive shock, coronary ischemia, cerebrovascular disease, and seizures. Profound methemoglobinemia may lead to respiratory depression, and coma. Death due to nitrite poisoning is caused by uncontrolled vasodilation and hypoperfusion, or by profound methemoglobinemia and functional hypoxia.
0.2.20 REPRODUCTIVE HAZARDS
  • A) Behavioral deficits were observed in the adult offspring of rats who received sodium nitrite prenatally.
0.2.21 CARCINOGENICITY
  • 0.2.21.2 HUMAN OVERVIEW
    • A) Sodium nitrite has shown a potential for carcinogenicity in animals.
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