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Manganese intoxication generally is caused by chronic exposure. Sources of inorganic manganese exposure include mining, metal working, smelting, foundries, and welding. Recent studies also suggest a possible link between an organic manganese fungicide (Maneb) and chronic neurologic toxicity. An organic manganese gasoline additive, methylcyclopentadienyl manganese tricarbonyl (MMT), has not yet been introduced in the United States because of public health concerns but is used elsewhere. Finally, parenteral exposure to inorganic manganese has occurred through injection drug abuse of potassium permanganate–adulterated substances and through manganese-containing total parenteral nutrition.

  1. Mechanism of toxicity. The precise mechanism is not known. The CNS is the target organ, specifically regions within the basal ganglia.

  2. Toxic dose. The primary route of exposure is inhalation, but there is evidence that absorption to the CNS through the olfactory system may play a role in toxicity. IV injection also leads to effective delivery of this toxin. Metallic inorganic manganese is poorly absorbed from the GI tract; potassium permanganate ingestion, however, can cause systemic toxicity. MMT can be absorbed across the skin. The OSHA workplace limit (permissible exposure limit—ceiling [PEL-C]) for inorganic manganese is 5 mg/m3; the ACGIH-recommended workplace exposure limit (threshold limit value–8-hour time-weighted average [TLV-TWA]) is considerably lower at 0.2 mg/m3. The ACGIH TLV-TWA for MMT is 0.1 mg/m3 (skin). The air level of manganese considered immediately dangerous to life or health (IDLH) is 500 mg/m3.

  3. Clinical presentation. Acute high-level manganese inhalation can produce an irritant-type pneumonitis, but this is rare (See Gases, Irritant). More typically, toxicity occurs after chronic exposure to low levels over months or years. The time course following injection of manganese is considerably foreshortened. The patient may present with a psychiatric disorder that can be misdiagnosed as schizophrenia or atypical psychosis. Organic signs of neurologic toxicity, such as parkinsonism and other extrapyramidal movement disorders, usually appear later, up to years after any primarily psychiatric presentation. Ingestion of potassium permanganate can cause severe acute hepatic and renal toxicity and methemoglobinemia.

  4. Diagnosis depends on a thorough occupational, drug abuse, and psychiatric history.

    1. Specific levels. Testing of whole blood, serum, or urine may be performed, but the results should be interpreted with caution, as they may not correlate with clinical effects. Whole-blood levels are 20 times higher than levels in serum or plasma, and red blood cell contamination can falsely elevate serum or plasma levels.

      1. Normal serum manganese concentrations are usually less than 1.2 mcg/L.

      2. Elevated urine manganese concentrations (>2 mcg/L) may confirm recent acute exposure. Exposures at the OSHA PEL usually do not raise urinary levels above 8 mcg/L. Chelation challenge does not have a role in diagnosis.

      3. Hair and nail levels are not useful.

    2. Other useful laboratory studies include arterial blood gases or oximetry and chest radiography (after acute, heavy, symptomatic inhalation exposure if acute lung injury is suspected). Magnetic resonance imaging (MRI) of the brain may show findings suggestive of manganese deposition.

  5. Treatment

    1. Emergency and supportive measures

      1. Acute inhalation. Administer supplemental ...

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