The Turkish Journal Of Occupational / Environmental Medicine and Safety

Abstract

Metal neurotoxicity has address the molecular, pathological, and
functional responses of central and peripheral nervous systems. Lead, mercury,
arsenic, manganese and aluminum are the most common neurotoxic metals.

Lead: Lead occurs naturally in trace amounts in soil, rocks and water.
Acute lead encephalopathy is most commonly seen in occupationally exposed
adults or in children following ingestion of lead-containing items. Children
tend to present with lethargy, confusion, ataxia and impaired motor functions,
and irritability. Hallucinations, seizures, and coma can occur in patients.
Brain edema occurs with higher levels of exposure and can mimic a mass lesion
with papilledema, positive Babinski sign, and even focal or lateralizing
deficits. Neurological sequelae are more persistent in children, with the most
profound effect on intelligence quotient levels.

Mercury: Mercury has three forms, elemental, organic, and inorganic
forms. Neurological manifestations of methylmercury toxicity range from mild
paresthesias and tremor to severe ataxia, spasticity, seizure, memory loss,
insomnia, hallucination and visual and hearing loss. Encephalopathy may be a
prominent feature and in severe cases may progress to coma and death. The rate
of encephalopathy depends on the rate of peripheral metabolism and their
ability to cross the blood brain barrier.

Arsenic: Arsenic is used in different industries.  Neurotoxicity can result in a profound
leukoencephalopathy following either acute or chronic exposures. Acute toxicity
primarily manifests as confusion, with headache initially. In the hours to days
following, delirium, hallucinations, and seizures may occur. Diffuse
encephalopathy at may be profound as well. Chronic encephalopathy is more
commonly caused by exposure to organic than inorganic arsenic. Chronic arsenic
encephalopathy generally manifests with confusion and irritability. Paranoid
delusions and auditory or visual hallucinations can occur. Brain imaging and
EEG is often normal.

Manganese: Manganese (Mn) is essential and act as cofactor for several
enzymatic reactions in human body.

The classic and most prominent manifestation of Mn toxicity is
parkinsonism, but encephalopathy also occurs with both acute and chronic exposures.
Acute toxicity can cause frank psychosis, with visual and auditory
hallucinations, euphoria, and compulsive behaviors. Headache, irritability, and
memory disturbance can be seen with acute or chronic Mn encephalopathy. With
continued exposure, behavioral changes progress. Emotional lability, compulsive
laughter, and hallucinations may all present before the appearance of the
typical motor features. Tremor, dysarthria, increased tone, and gait
disturbance occur relatively late in the process. Brain magnetic imaging
studies reveals increased signal on T1-weighted images within basal ganglia.

Aluminum: Encephalopathy is a primary feature of acute or chronic
aluminum toxicity. Motor incoordination, poor memory, impaired cognition, and
depression are the hallmark symptoms.

Dialysis-induced encephalopathy is due to the toxic effects of aluminum
in dialysis fluid and in the phosphate binders used in dialysis patients. This
syndrome occurs in patients after 2 to 7 years of dialysis. Often presenting
initially with isolated speech abnormalities, neurological symptoms progress at
varying rates and include episodic confusion, behavioral changes, myoclonus,
seizures, and frank dementia. Blood levels can be used to evaluate patients
with potential aluminum toxicity.