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Hematologic consequences ascribed to lead toxicity may be basophilic stippling, mild anemia, and reticulocytosis. Other characteristics of toxicity may include increased urine δ-aminolevulinic acid, increased erythrocyte protoporphyrins, and decreased aminolevulinic acid dehydrase. Lead lines on gums or at the metaphyses of long bones in children may also be present.² Early symptoms of lead poisoning include anorexia, apathy or irritability, fatigue, and anemia.³ Toxic effects include GI distress, joint pain, colic, headache, stupor, convulsions, and coma. Another test that may be used to evaluate lead intoxication is free erythrocyte protoporphyrin (FEP); however, a blood lead assay is the definitive test.⁴

Lead and organic lead compounds have numerous commercial and industrial applications, including paints, plastics, storage batteries, bearing alloys, insecticides, and ceramics. Exposure may also occur through the inhalation of dust containing lead emitted by automobile exhaust. A common source of lead exposure among children is through the mouthing of inanimate objects, specifically objects with paint and paint chips that contain lead. Acute lead exposure is rare; however, toxicity may occur through acute ingestion of a lead salt or acetate. Blood is the preferred specimen by which the extent of an acute or recent exposure to lead may be measured.

BEI® are reference values intended as guidelines for evaluation of occupational exposure. BEI® represent biological levels of chemicals that correspond to workers with inhalation exposure equivalent to the threshold limit value (TLV®) of the chemicals. TLVs refer to the airborne concentrations of substances and represent conditions under which it is believed that nearly all workers may be repeatedly exposed, day after day, without adverse health effects.¹