Hematologic consequences ascribed to lead toxicity
may be basophilic stippling, mild anemia, and reticulocytosis. Other
characteristics of toxicity may include increased urine d-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.
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
