that chelation treatment for lead encephalopathy be initiated with an intramuscular injection of dimercaprol, followed in 4 hours by concurrent administration of dimercaprol and EDTA. Parenteral chelation is limited to 5 or fewer days, at which time oral treatment with another chelator, succimer (DMSA), may be instituted. In symptomatic lead intoxication without encephalopathy, treatment may sometimes be initiated with succimer. The end point for chelation is usually resolution of symptoms or return of the blood lead concentration to the premorbid range. In patients with chronic exposure, cessation of chelation may be followed by an upward rebound in blood lead concentration as the lead re-equilibrates from bone lead stores.
Although most clinicians support chelation for symptomatic patients with elevated blood lead concentrations, the decision to chelate asymptomatic subjects is more controversial. Since 1991, the Centers for Disease Control and Prevention (CDC) has recommended chelation for all children with blood lead concentrations of 45 mcg/dL or greater. However, a randomized, double-blind, placebo-controlled clinical trial of succimer in children with blood lead concentrations between 25 and 44 mcg/dL found no benefit on neurocognitive function or long-term blood lead reduction. Prophylactic use of chelating agents in the workplace should never be a substitute for reduction or prevention of excessive exposure.
Management of elevated blood lead levels in children and adults should include a conscientious effort to identify and reduce all potential sources of future lead exposure. Many local, state, or national governmental agencies maintain lead poisoning prevention programs that can assist in case management. Blood lead screening of family members or coworkers of a lead poisoning patient is often indicated to assess the scope of the exposure. In 2012, the CDC adopted a new policy that defined as elevated any childhood blood lead concentrations at or exceeding a reference value corresponding to the 97.5th percentile of quadrennial reports of the National Health and Nutrition Examination Survey (NHANES). The blood lead reference value established in 2012 was 5 mcg/dL, and it is projected to decline in the future. Because there is no blood lead concentration known to be devoid of deleterious effects, the finding of a blood lead concentration exceeding the reference value (ie, elevated in relation to the general population) should prompt clinical and environmental investigation (https://www.cdc.gov/nceh/lead/acclpp/final_document_030712.pdf ). Although the US Occupational Safety and Health Administration (OSHA) lead regulations introduced in the late 1970s mandate that workers be removed from lead exposure for blood lead levels higher than 50–60 mcg/dL, an expert panel in 2007 recommended that removal be initiated for a single blood lead level >30 mcg/dL or when two successive blood lead levels measured over a 4-week interval are 20 mcg/dL or greater (https://www.ncbi.nlm.nih.gov/pmc/ articles/PMC1849937/pdf/ehp0115-000463.pdf ). The longer-term goal should be for workers to maintain blood lead levels <10 mcg/dL, and for pregnant women to avoid occupational or avocational exposure that would result in blood lead levels higher than 5 mcg/dL. Environmental Protection Agency (EPA) regulations effective since 2010 require that contractors who perform renovation, repair, and painting projects that disturb lead-based paint in pre-1978 residences and child-occupied facilities must be certified and must follow specific work practices to prevent lead contamination (see Box: Prevention of Lead Poisoning: An Ongoing Effort).
B. Organic Lead Poisoning
Initial treatment consists of decontaminating the skin and preventing further exposure. Treatment of seizures requires appropriate use of anticonvulsants. Empiric chelation may be attempted if high blood lead concentrations are present.