3. Prolonged exposure to lead or lead salts is toxic. To prevent lead poisoning, the current standard for lead paint is 600.0 ppm. Some older paints had a much higher concentration of lead.

Explanation:

Lead exposure has been linked with various types of brain damage. These include

Problems with thinking (cognition);

Difficulties with organizing actions, decisions, and behaviors (executive functions);

Abnormal social behavior (including aggression); and

Difficulties in coordinating fine movements, such as picking up small objects (fine motor control).

Sufficient evidence in children shows that BLLs <5 µg/dL are associated with increased diagnosis of attention-related behavioral problems, greater incidence of problem behaviors, and decreased cognitive performance. This is indicated by

Decreased IQ,

Lower academic achievement, and

Reductions in specific cognitive measures .

Lead causes activation of protein kinase C (PKC) and binds to PKC more avidly than calcium (its physiologic activator). This creates problems with neurotransmitter release. Alteration of PKC function also affects second-messenger systems within the cell which may lead to future changes in gene expression and protein synthesis.

A large body of evidence associates a reduction in IQ performance and other neuropsychological defects with BLLs <10 µg/dL, including reduced hearing.

Neurological adverse effects of lead in children have been documented at exposure levels once thought to cause no harmful effects, including those <10 µg/dL.

Low doses of lead can cause a broad range of functional problems such as loss of self-control, shortened attention span and a host of learning disorders that often cause lead-exposed children to perform poorly in school and ultimately to drop out.

Because otherwise asymptomatic individuals may experience neurological effects from lead exposure, clinicians should have a high index of suspicion for lead exposure, especially in the case of children with developmental delays.

Children suffer neurological effects from lead at much lower blood lead levels than adults.

Subclinical neurological effects may occur at lower BLLs - at or below the regulatory standard of 10 µg/dL, in some cases - and it may not be possible to detect them on clinical examination at the time of the exposure or peak BLLs. Children often show no signs of lead toxicity until they are in school, even as late as middle school, when expectations for academic achievement increase.

Some studies have found, for example, that for every 10 µg/dL increase in BLLs, children's IQ was found to be lowered by 4 to 7 points.

Evidence shows that ADHD and hearing impairment in children increase with increasing BLLs, and that lead exposure may disrupt balance and impair peripheral nerve function [ATSDR 2010].

In children, acute exposures leading to very high blood lead levels (< 70 µg/dL), may produce encephalopathy and other accompanying signs of

Ataxia,

Coma,

Convulsions,

Death,

Hyperirritability, and

Stupor.

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