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RARE EARTH METALS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) This is a group of 16 elements from atomic number 57 to 71 plus the elements number 39 (Yttrium) and 21 (Scandium). Although some have been used for an appreciable amount of time in industrial settings, no detectable signs of human toxicity have been reported (Stokinger, 1981).

Specific Substances

    A) Cerium
    1) Molecular Formula: Ce
    2) Atomic Number: 58
    Dysprosium
    1) Molecular Formula: Dy
    2) Atomic Number: 66
    Erbium
    1) Molecular Formula: Er
    2) Atomic Number: 68
    Europium
    1) Molecular Formula: Eu
    2) Atomic Number: 63
    Gadolinium
    1) Molecular Formula: Gd
    2) Atomic Number: 64
    Holmium
    1) Molecular Formula: Ho
    2) Atomic Number: 67
    Lanthanum
    1) Molecular Formula: La
    2) Atomic Number: 57
    Lutetium
    1) Molecular Formula: Lu
    2) Atomic Number: 71
    Neodymium
    1) Molecular Formula: Nd
    2) Atomic Number: 60
    Praseodymium
    1) Molecular Formula: Pr
    2) Atomic Number: 59
    Prometheum
    1) Molecular Formula: Pm
    2) Atomic Number: 61
    Samarium
    1) Molecular Formula: Sm
    2) Atomic Number: 62
    Scandium
    1) Molecular Formula: Sc
    2) Atomic Number: 21
    Terbium
    1) Molecular Formula: Tb
    2) Atomic Number: 65
    Thulium
    1) Molecular Formula: Tm
    2) Atomic Number: 69
    Ytterbium
    1) Molecular Formula: Yb
    2) Atomic Number: 70
    Yttrium
    1) Molecular Formula: Y
    2) Atomic Number: 39
    GENERAL TERMS
    1) METALS, RARE EARTH

Available Forms Sources

    A) SOURCES
    1) Ores which contain rare earths include:
    Light lanthanidesMonazite
    Bastnasite
    Heavy lanthanidesGadolinite
    Euxenite
    Xenotime

    2) Light lanthanides or cerium subgroup includes: La, Ce, Pr, Nd, Pm (Parmeggiani, 1983).
    3) Heavy lanthanides or yttrium subgroup includes: Sm, Eu, Gd, Tb, Dy, Y, Yb, Lu, Tm, Er, Ho (Parmeggiani, 1983).
    B) USES
    1) NON-MEDICAL USES: Lanthanides are used in carbon-arc lights, metals alloys, lighter flints, magnesium and ferrous alloys, coloring or decolorization of glass, polishing of optical lenses, surface preparation of mirror glasses and special glasses, ceramics, and television tubes.
    2) MEDICAL USES
    a) Doses of 40 to 100 mg of various lanthanides have been injected for treatment of tuberculosis (Beaser et al, 1942).
    b) Various lanthanides have been injected and tested for their anticoagulant activities in animals and man. The most commonly used are cerium, neodymium, and lanthanum.
    c) Ytterbium 169 DTPA (Pentetate, calcium trisodium by 3M) is available for routine use for cisternography, and Cesium 137 (3M brand) is available for brachytherapy (Blaufox & Freeman, 1976).
    d) Yttrium-90 (collidal suspension of yttrium silicate or yttrium oxide rods) has been used to treat pleural malignancies, malignant ascites, various arthritic conditions, and for pituitary ablation (Reynolds, 1982).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Although these metals have been used for an appreciable amount of time in industrial settings, no detectable signs of human toxicity have been reported. These elements produce a delayed response in acute exposures. Symptoms start within 24 hours and peak between 48 to 72 hours.
    B) The lanthanides have a general depressant activity on all systems. Death is usually due to cardiovascular collapse and respiratory paralysis. Except for when specifically stated, signs and symptoms listed below are from animal studies.
    0.2.4) HEENT
    A) Although all of the lanthanides are irritating to the eyes, only terbium has shown significant and prolonged ocular damage.
    0.2.5) CARDIOVASCULAR
    A) Cardiovascular collapse with decreased blood flow and decreased blood pressure occurred in animals.
    0.2.6) RESPIRATORY
    A) Labored breathing and depressed respirations, leading to respiratory paralysis, were common in animals.
    B) Pneumoconiosis has occurred in man.
    0.2.7) NEUROLOGIC
    A) Ataxia and writhing occurred in animals. Gadolinium encephalopathy has been reported in a patient with renal failure.
    0.2.8) GASTROINTESTINAL
    A) Decreased intestinal tone and ileum contractility diarrhea, and abdominal irritation have been reported.
    0.2.9) HEPATIC
    A) Animal studies have indicated changes in the mitochondria and endoplasmic reticulum of liver cells, acute passive hepatic congestion, and elevations in hepatic enzymes.
    0.2.10) GENITOURINARY
    A) Hemoglobinuria and albuminuria are possible.
    0.2.13) HEMATOLOGIC
    A) Increased prothrombin and coagulation times were reported. The exact mechanism by which lanthanides act as anticoagulants is unknown. The effect may last as long as 5 days.
    0.2.14) DERMATOLOGIC
    A) Skin irritation and dermal nodules have been reported in animals.
    0.2.15) MUSCULOSKELETAL
    A) Muscle pain and abdominal cramps were reported when injected as an anticoagulant in man.
    0.2.17) METABOLISM
    A) Animals with cerium or praseodynium-induced liver toxicity had decreased blood glucose levels.

Laboratory Monitoring

    A) Monitored for anticoagulant effects.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Little is known about human exposures to lanthanides. From animal studies it would appear that the prime areas of concern would be prolonged clotting times, pulmonary congestion, cardiovascular collapse, and respiratory paralysis.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    D) EDTA: The rare earths form stable complexes with EDTA, but this has yet to be tried clinically. It is not known if the complexes themselves are toxic in humans, but they are somewhat toxic in animals.

Range Of Toxicity

    A) The toxicity of cerium and other lanthanides varies considerably by with salt form and by species. Most lanthanides have minimal toxicity under 10 mg/kg. Between 10 and 20 mg/kg anticoagulant activity may occur. Serious cardiovascular and respiratory toxicity has occured in animals in amounts greater than 20 mg/kg of the chloride salts.

Clinical Effects

Summary Of Exposure

    A) Although these metals have been used for an appreciable amount of time in industrial settings, no detectable signs of human toxicity have been reported. These elements produce a delayed response in acute exposures. Symptoms start within 24 hours and peak between 48 to 72 hours.
    B) The lanthanides have a general depressant activity on all systems. Death is usually due to cardiovascular collapse and respiratory paralysis. Except for when specifically stated, signs and symptoms listed below are from animal studies.

Vital Signs

    3.3.3) TEMPERATURE
    A) Chills and fever have been reported when used as an anticoagulant in humans (Beaser et al, 1942). Erbium vapors and dysprosium may cause increased heat sensitivity (Haley et al, 1966).

Heent

    3.4.1) SUMMARY
    A) Although all of the lanthanides are irritating to the eyes, only terbium has shown significant and prolonged ocular damage.
    3.4.3) EYES
    A) Although all of the lanthanides are irritating to the eyes, only terbium was shown significant and prolonged ocular damage (Haley & Upham, 1963).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiovascular collapse with decreased blood flow and decreased blood pressure occurred in animals.
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPOTENSION
    a) In studies done on various animals, cardiovascular toxicity was seen at 20 mg/kg of Tb, Yb, Tm, Pr, Nd, Dy, Ho, Er chlorides (Haley et al, 1964; (Haley et al, 1966). Cardiovascular collapse with decreased blood flow and decreased blood pressure were seen in animals (Graca, 1964; Haley & Upham, 1963).

Respiratory

    3.6.1) SUMMARY
    A) Labored breathing and depressed respirations, leading to respiratory paralysis, were common in animals.
    B) Pneumoconiosis has occurred in man.
    3.6.2) CLINICAL EFFECTS
    A) PNEUMOCONIOSIS
    1) Pneumoconiosis has been reported after long-term exposure to cerium (Sulotto et al, 1986).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PNEUMONITIS
    a) Lanthanon fluorides produced chemical pneumonitis, subacute bronchitis, bronchiolitis, hypertropic emphysema and bronchiolar stricturing in animals, but no focal fibrosis or granulomatosis (Schepers et al, 1955; Schepers et al, 1955).
    2) RESPIRATORY DEPRESSION
    a) Labored breathing and depressed respirations leading to respiratory paralysis were symptoms commonly seen in animals (Haley & Upham, 1963; Graca et al, 1962).

Neurologic

    3.7.1) SUMMARY
    A) Ataxia and writhing occurred in animals. Gadolinium encephalopathy has been reported in a patient with renal failure.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) There have been symptoms of headache and nausea from workers exposed to dust and fumes of La2O used in carbon-lights. The relationship was not conclusively proven (Fairhall, 1957).
    B) TOXIC ENCEPHALOPATHY
    1) A 57-year-old woman with renal failure developed a subacute encephalopathy after alternate day MRI and MR angiograms of the brain with gadolinium contrast boluses over 7 days. The total gadolinium dose over 7 days was approximately 60 to 80 mL. Her mental state declined over the 7 days and MRI revealed multiple subcortical hyperintensities. On day 8, she had a mild left hemiparesis and was drowsy with a fluctuating level of consciousness. Review of earlier MRIs revealed that the CSF had become increasingly hyperintense on successive MRI scans. On day 14, a noncontrast brain MRI showed a marked reduction in the CSF hyperintensity. By 6 weeks, her hemiparesis had resolved. CSF hyperintensity was due to diffusion of gadolinium into the CSF (Maramattom et al, 2005).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ATAXIA
    a) Ataxia and writhing were effects reported in animals poisoned by Pr and Nd chlorides (Haley et al, 1964).

Gastrointestinal

    3.8.1) SUMMARY
    A) Decreased intestinal tone and ileum contractility diarrhea, and abdominal irritation have been reported.
    3.8.2) CLINICAL EFFECTS
    A) DIARRHEA
    1) Decreased intestinal tonus and ileum contractility as well as diarrhea and abdominal irritation have been reported (Stokinger, 1981; Haley & Upham, 1963).

Hepatic

    3.9.1) SUMMARY
    A) Animal studies have indicated changes in the mitochondria and endoplasmic reticulum of liver cells, acute passive hepatic congestion, and elevations in hepatic enzymes.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LIVER FATTY
    a) Intravenous injection of cerium produced fatty infiltrates in rat livers. Cerium was found primarily in the acid soluble fraction of the liver, not the lipid. Females appear to be more susceptible to this effect than males. Changes were seen in both the mitochondria and endoplasmic reticulum of liver cells (Stokinger, 1981).
    2) HEPATITIS
    a) Other animal studies have shown acute passive hepatic congestion (Graca et al, 1962).
    3) HEPATIC ENZYMES INCREASED
    a) Strubelt et al (1980) demonstrated a dose-dependent increase in SGOT, SGPT, and sorbitol dehydrogenase enzymes in rats after IV administration of 3 to 14 mg/kg of praseodymium, cerium, and lanthanum.

Genitourinary

    3.10.1) SUMMARY
    A) Hemoglobinuria and albuminuria are possible.
    3.10.2) CLINICAL EFFECTS
    A) HEMOLYSIS
    1) Hemoglobinuria was extensive enough to rule out the use of lanthanides (especially Ce, Pr, Nd) as anticoagulants when administered to humans by Beaser (1942).
    B) ALBUMINURIA
    1) Albuminuria and cast excretion was also seen.

Hematologic

    3.13.1) SUMMARY
    A) Increased prothrombin and coagulation times were reported. The exact mechanism by which lanthanides act as anticoagulants is unknown. The effect may last as long as 5 days.
    3.13.2) CLINICAL EFFECTS
    A) COAG./BLEEDING TESTS ABNORMAL
    1) Increased prothrombin and coagulation times was reported by Graca (1964). Serum proteins are precipitated at concentrations of 0.25 to 0.7% and dissolved at greater than 1.5%. However, little lanthanide is distributed to the blood (0.02% per ml of the administered dose) so the anticoagulant effect may instead be due to the capacity to act as a phosphate acceptor and, therefore, indirectly decrease prothrombin content of blood.
    2) The exact mechanism by which lanthanides act as anticoagulants is unknown. Doses of 3 to 12.5 mg/kg of cerium (or Nd, La) given by injection to humans decreased coagulability to 0. This effect then gradually decreased over the next 8 hours (Beaser et al, 1942). The minimum effective anticoagulant dose of Nd was approximately 10 mg/kg. The anticoagulant effect peaked in about 1 hour and then decreased. Hemoglobinemia was a significant side effect in Beaser's experiment. This effect lasted as long as 5 days in one patient.

Dermatologic

    3.14.1) SUMMARY
    A) Skin irritation and dermal nodules have been reported in animals.
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) When tested on rabbits, cerium had little dermal effect. Both Er and terbium chloride produced irritation on intact skin (Stokinger, 1981; Haley & Upham, 1963).
    2) SKIN NODULE
    a) As slight a concentration as 1 ppm of these substances has caused dermal nodules when injected interdermally in guinea pigs. This may have implications if the material becomes interdermally injected in an industrial setting (Haley & Upham, 1963).
    3) CALCINOSIS
    a) Garrett & McClure (1981) reported that subcutaneous injection of various lanthanide trichlorides in mice resulted in calcification of the subcutaneous dorsal fascia (calcergy).

Musculoskeletal

    3.15.1) SUMMARY
    A) Muscle pain and abdominal cramps were reported when injected as an anticoagulant in man.
    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) Muscle pain and abdominal cramps were seen when injected as an anticoagulant in man (Beaser et al, 1942).

Carcinogenicity

    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) ANTI-CANCER EFFECTS - Investigators have shown that the stable isotopes of cerium and lanthanide show mild anti-tumor effects.
    2) Certain radioisotopic compounds are mildly carcinogenic (Stokinger, 1981).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitored for anticoagulant effects.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) No toxic levels have been established for the lanthanides.
    2) Patients should be monitored for liver toxicity and anticoagulant effects.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitored for anticoagulant effects.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) These substances are poorly absorbed orally. If a significant amount were to be ingested, gastric decontamination may be of some use.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Support respiratory and cardiovascular function. A chest x-ray may be indicated if there is pulmonary involvement.
    B) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    C) MONITORING OF PATIENT
    1) Some lanthanide studies have shown liver toxicity. Monitor liver function tests.
    2) Lanthanides may definitely increase clotting time when given intravenously. For patients significantly exposed, prothrombin time or international normalized ratio (INR) should be monitored for several days.
    3) Although hematuria and albuminuria have been noted after intentional intravenous use, the significance of these effects after oral ingestion is unknown. If sufficient quantities are taken to produce an increased clotting time, patients may need to be monitored for these effects.
    D) ANALGESIC
    1) May be treated with analgesics.
    E) EXPERIMENTAL THERAPY
    1) METHIONINE: Neither methionine nor choline were protective of the liver toxicity induced by cerium (Stokinger, 1981).
    2) EDTA: The rare earths form stable complexes with EDTA (Wheelwright et al, 1953), but this has yet to be tried clinically. It is not known if the complexes themselves are toxic in humans, but they are somewhat toxic in animals (Graca et al, 1962).

Abstracts

Case Reports

    A) ADULT
    1) PNEUMOCONIOSIS - A case of "rare-earth" pneumoconiosis was reported in a 48-year-old male exposed to cerium for 13 years, with a 17-year period having elapsed since last exposure. The patient was asymptomatic, and exposure was not suspected until a micronodular pattern extending to all lung fields was observed on routine chest x-ray. Pulmonary function tests, however, revealed restrictive spirometric impairment. Bronchoalveolar lavage demonstrated abnormal levels of La, Ce, Nd, Sm, Tb, Yb, and Lu. Abnormal levels of these metals were also found in the patient's nails, suggesting systemic absorption from the lung. The presence of such abnormal findings after so many years suggests a very slow alveolar clearance of these elements, and gives evidence against the reversibility of the damage (Sulotto et al, 1986).

Range Of Toxicity

Summary

    A) The toxicity of cerium and other lanthanides varies considerably by with salt form and by species. Most lanthanides have minimal toxicity under 10 mg/kg. Between 10 and 20 mg/kg anticoagulant activity may occur. Serious cardiovascular and respiratory toxicity has occured in animals in amounts greater than 20 mg/kg of the chloride salts.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The toxicity of cerium and other lanthanides varies considerably by its salt form. Since the non-metallic portions of the compound may change the toxicity greatly, toxicity data on these metals should only be used if the work was done after the 1950's. This is when new purifying techniques were used to obtain the metals for testing (Stokinger, 1981). Literature reports prior to this time may show the lanthanides to be considerably more toxic.
    2) Toxicity varies considerably by species. Which lanthanide is most toxic, and the toxic dose for that species, may be extremely variable. Most lanthanides have minimal toxicity under 10 milligrams/kilogram. Between 10 and 20 milligrams/kilogram one may see some anticoagulant activity. Serious cardiovascular and respiratory toxicity has been seen in animals in amounts greater than 20 milligrams/kilogram of the chloride salts.

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) TERBIUM CHLORIDE
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 550 mg/kg (Haley et al, 1963)
    2) LD50- (ORAL)MOUSE:
    a) 5,100 mg/kg (Haley et al, 1963)
    B) THULIUM CHLORIDE
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 485 mg/kg (Haley et al, 1963)
    2) LD50- (ORAL)MOUSE:
    a) 6,250 mg/kg (Haley et al, 1963)
    C) YTTERBIUM CHLORIDE
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 395 mg/kg (Haley et al, 1963)
    2) LD50- (ORAL)MOUSE:
    a) 6,700 mg/kg (Haley et al, 1963)

Pharmacology Toxicology

Toxicologic Mechanism

    A) Lanthanide salts will form insoluble complexes with nucleic acids (Wheelwright et al, 1953). Toxicity is difficult to determine because of lanthanide protein precipitating capacity (Graca et al, 1962). Human serum proteins precipitated concentrations greater than 0.25% to 0.7% and dissolve at concentrations of 1.5% (Stokinger, 1981). Erbium has an effect as an antiprothrombin and thrombokinase (Haley et al, 1966).

Physicochemical

Physical Characteristics

    A) Cerium group metals are soft; oxides have reduced malleability.

Molecular Weight

    A) Varies

References

General Bibliography

    1) Alaspaa AO, Kuisma MJ, Hoppu K, et al: Out-of-hospital administration of activated charcoal by emergency medical services. Ann Emerg Med 2005; 45:207-12.
    2) Beaser SB, Segel A, & Vandam L: The anticoagulant effects in rabbits and man of the intravenous injection of salts of the rare earths. J Clin Invest 1942; 21:447-454.
    3) Blaufox MD & Freeman LM: Physician's Desk Reference for Radiology and Nuclear Medicine, Medical Economics Company, Montvale, NJ, 1976.
    4) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    5) Dagnone D, Matsui D, & Rieder MJ: Assessment of the palatability of vehicles for activated charcoal in pediatric volunteers. Pediatr Emerg Care 2002; 18:19-21.
    6) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    7) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    8) Fairhall LT: Industrial Toxicology, Williams & Williams, Baltimore, MD, 1957.
    9) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    10) Graca JG, Davidson FC, & Feavel JB: Comparative toxicity of stable rare earth compounds II. Arch Environ Health 1962; 5:437-444.
    11) Graca JG: Comparative toxicity of stable rare earth compounds III. Arch Environ Health 1964; 8:750.
    12) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    13) Guenther Skokan E, Junkins EP, & Corneli HM: Taste test: children rate flavoring agents used with activated charcoal. Arch Pediatr Adolesc Med 2001; 155:683-686.
    14) Haley TJ & Upham AC: Skin reaction to intradermal injection of rare earths. Nature 1963; 200:271.
    15) Haley TJ, Konesu N, & Efios M: Pharmacology and toxicology of praseodymium and neodymium chlorides. Toxicol Appl Pharmacol 1966; 8:37-43.
    16) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    17) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    18) Maramattom BV, Manno EM, Wijdicks EF, et al: Gadolinium encephalopathy in a patient with renal failure. Neurology 2005; 64(7):1276-1278.
    19) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    20) Parmeggiani: Encyclopaedia of Occupational Health and Safety, 3rd revised ed, International Labour Office, Geneva, Switzerland, 1983.
    21) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    22) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    23) Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.
    24) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
    25) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    26) Reynolds JEF: Martindale: The Extra Pharmacopoeia, 28th ed, The Pharmaceutical Press, London, UK, 1982.
    27) Schepers GWH, Delahant AB, & Redlin AJ: An experimental study of the effects of rare earths on animal lungs. AMA Arch Ind Health 1955; 12:297-300.
    28) Spiller HA & Rogers GC: Evaluation of administration of activated charcoal in the home. Pediatrics 2002; 108:E100.
    29) Stokinger HE: The Metals, by Clayton GD & Clayton FE: Patty's Industrial Hygeine and Toxicology, 3rd revised ed, 2A, John Wiley and Sons, New York, NY, 1981, pp 1674-1687.
    30) Sulotto F, Romano C, & Berra A: Rare-earth pneumoconiosis: a new case. Am J Ind Med 1986; 9:567-576.
    31) Thakore S & Murphy N: The potential role of prehospital administration of activated charcoal. Emerg Med J 2002; 19:63-65.