Lithium, Elemental

CAS RN: 7439-93-2

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: Used as drain openers, household cleaners (oven, bathroom), hair relaxers, dishwasher soap, and in automobile air bags. In industry used as cleaners, in cement, and as chemical precursors.
    • B) TOXICOLOGY: Alkaline corrosives cause liquefaction necrosis. They saponify the fats in the cell membrane, destroying the cell and allowing deep penetration into mucosal tissue. In gastrointestinal tissue an initial inflammatory phase may be followed by tissue necrosis (sometimes resulting in perforation), then granulation and finally stricture formation.
    • C) EPIDEMIOLOGY: Exposure is common. Serious effects are rare in the developed world (generally only seen in adults with deliberate ingestion), largely because mostly low concentration corrosives are present in products available in the home. Serious effects are more common in developing countries.
    • D) WITH POISONING/EXPOSURE
      • 1) MILD TO MODERATE ORAL TOXICITY: Patients with mild ingestions may only develop irritation or grade I (superficial hyperemia and edema) burns of the oropharynx, esophagus or stomach; acute or chronic complications are unlikely. Patients with moderate toxicity may develop grade II burns (superficial blisters, erosions and ulcerations) are at risk for subsequent stricture formation, particularly esophageal. Some patients (particularly young children) may develop upper airway edema.
        • a) Alkaline corrosive ingestion may produce burns to the oropharynx, upper airway, esophagus and occasionally stomach. Spontaneous vomiting may occur. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns. The presence of stridor, vomiting, drooling, and abdominal pain are associated with serious esophageal injury in most cases.
        • b) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality.
      • 2) SEVERE ORAL TOXICITY: May develop deep burns and necrosis of the gastrointestinal mucosa. Complications often include perforation (esophageal, gastric, rarely duodenal), fistula formation (tracheoesophageal, aortoesophageal), and gastrointestinal bleeding. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Stricture formation (esophageal, less often oral or gastric) is likely to develop long term. Esophageal carcinoma is another long term complication. Upper airway edema is common and often life threatening. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because alkaline products available in the home are generally of low concentration.
      • 3) INHALATION EXPOSURE: Mild exposure may cause cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, stridor, and rarely acute lung injury.
      • 4) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent visual loss and in severe cases perforation.
      • 5) DERMAL EXPOSURE: Mild exposure causes irritation and partial thickness burns. Metabolic acidosis may develop in patients with severe burns or shock. Prolonged exposure or high concentration products can cause full thickness burns.
0.2.3 VITAL SIGNS
0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: Lithium carbonate is used therapeutically, primarily to treat bipolar disorder; it is less commonly used today due to the wide availability of other psychiatric medications with lesser side effects. It is available in oral formulations, both regular and extended release. Lithium orotate is a dietary supplement. Lithium is an important industrial material used to make batteries, alloys, and flux.
    • B) PHARMACOLOGY: Lithium is a naturally occurring alkali metal and monovalent cation chemically similar to Na+ and K+. The exact mechanism by which it stabilizes mood is not known. It is thought to affect the CNS by altering nerve conduction, cortisol and monoamine metabolism, and increasing serotonin.
    • C) TOXICOLOGY: In the kidney, lithium competes with Na+ and K+ in the renal tubules; conditions that increase renal sodium reabsorption (dehydration) decrease lithium elimination. Chronic toxicity is typically due to decreased clearance caused by dehydration, medication interactions, or renal impairment.
    • D) EPIDEMIOLOGY: Acute poisoning is typically less severe than chronic toxicity. Chronic toxicity develops primarily in elderly patients, those with intercurrent illnesses, and those started on drugs that decrease lithium clearance.
    • E) WITH THERAPEUTIC USE
      • 1) At therapeutic doses, effects such as blurred vision, nystagmus, GI irritation, tremors, slowed mentation, cerebellar dysfunction may occur. Polyneuropathy and Parkinsonian syndrome have been described. ECG changes such as nonspecific ST/T changes, sinus node blocks may be present. Brugada Syndrome has been reported in several chronic lithium users. Nephrogenic Diabetes Insipidus, reduced glomerular filtration, and thyroid abnormalities, particularly hypothyroidism, may also occur. Lithium carbonate crosses the placenta and is also present in breast milk. Congenital malformations have been documented after exposure to lithium during pregnancy.
      • 2) DRUG INTERACTIONS: Lithium clearance is decreased by concomitant use of ACE inhibitors, angiotensin II antagonists, thiazide and loop diuretics, and nonsteroidal anti-inflammatory drugs.
    • F) WITH POISONING/EXPOSURE
      • 1) MILD TO MODERATE POISONING: Toxicity is categorized as acute or chronic. Acute overdose is typically less severe than chronic toxicity and results in gastrointestinal upset, while CNS manifestations are less common due to slow absorption into the brain. Chronic effects are usually less gastrointestinal and more neurological due to prior CNS saturation. Mild to moderate poisoning can cause nausea, vomiting, diarrhea, dehydration, nystagmus, and tremors. Hyperreflexia, cogwheel rigidity, ataxia, agitation, confusion, and lethargy are common. Bradycardia, T-wave abnormalities, hypoventilation may also occur.
      • 2) SEVERE POISONING: Severe effects in acute exposures are rare. Patients with chronic toxicity may manifest severe toxicity despite relatively modestly elevated serum lithium concentrations. Effects include photophobia, dehydration, electrolyte imbalances, thyroid dysfunction, hyperthermia, seizure, coma, rigidity, myoclonus, serotonin syndrome. ECG changes such as nonspecific T-wave abnormalities, QTc prolongation, bundle branch block, bradycardia, junctional rhythm, and hypotension may occur. Hypoventilation, respiratory failure, and ARDS may rarely develop. Bezoars may form in large ingestions.
0.2.3 VITAL SIGNS0.2.20 REPRODUCTIVE HAZARDS
  • A) Lithium is classified as FDA pregnancy category D. Congenital malformations have been reported. The use of lithium should be avoided during pregnancy, especially in the first trimester and one week prior to delivery. Cardiovascular and other teratogenic or toxic effects have been reported in infants born to lithium-treated mothers. In addition, a prospective, observational study showed that significantly more miscarriages and preterm deliveries occurred with lithium exposure during pregnancy (n=18
    • 3) compared with a group of women who were not exposed to any teratogen during pregnancy (n=748). However, other studies have revealed that outcomes of most pregnancies with in utero exposure to lithium have resulted in normal infants, and that use of lithium during pregnancy may possess a lower fetal risk than previously believed. Lithium is present in breast milk at 33% to 50% of the plasma lithium concentration, and may cause hypertonia, hypothermia, cyanosis, and ECG changes in nursing infants and neonates.
0.2.21 CARCINOGENICITY
  • 0.2.21.1 IARC CATEGORY
    • A) IARC Carcinogenicity Ratings for CAS554-13-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
      • 1) Not Listed
  • 0.2.21.2 HUMAN OVERVIEW
    • A) At the time of this review, the manufacturer does not report any carcinogenic potential for lithium in humans.
0.2.22 GENOTOXICITY
  • A) Lithium-treated patients did not demonstrate increased numbers of chromosomal lesions in blood lymphocytes compared with controls (Turecki et al, 1994).
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