The toxic effects of lead vary greatly, manifesting as the potential fatal encephalopathy of acute lead poisoning or as subtle changes in neurocognitive function in low level exposure. As exposure progresses, symptoms may manifest differently [30].
Brain damage is common in high exposure (blood levels above 100-120 μg/dL for adults and 80 -100μg/dL in children, causing encephalopathy and can also be fetal or permanently disabling resulting in dementia [31,32] Chronic exposure to high lead concentration results in cognitive deficits in the domains of viso-spatial perception, attention, recognition memory and new learning as well as neurological impairment such as gait ataxia, dysdiachokinesia, increased tendon reflexes and can also lead to toxic encephalopathy [33,34].
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Results of more recent cross-sectional and prospective studies indicate that postnatal lead exposure resulting in blood levels as low as 25μg/dL, and probably lower, are also associated with deficits in intellectual attainment and affect behavior [35]. Baker reported various neurobehavioural in workers with blood lead concentrations between 40 and 60 micrograms/100 ml which showed impaired performance on tests of verbal concept formation, visual/motor performance, memory, and mood. Furthermore this impairment occurred in the absence of peripheral nervous system derangement and increased in severity with increasing lead dose [40]. Similar results obtained other studies that associated lead exposure with subclinical decrements of neurocognitive function