Lead toxicity, a review of the literature. Part 1: Exposure, evaluation, and treatment.
The phasing out of leaded gasoline for transportation vehicles between 1973 and 1995 and the removal of lead from paint by federal mandate by 1978 have resulted in substantial lowering of mean blood lead levels in all segments of the U.S. population. However, because lead is a persistent metal, it is still present in the environment - in water, brass plumbing fixtures, soil, dust, and imported products manufactured with lead. Diagnosis of lead toxicity has traditionally been based on significantly elevated blood lead levels. However, data now implicates low-level exposures and blood lead levels previously considered normal as causative factors in cognitive dysfunction, neurobehavioral disorders, neurological damage, hypertension, and renal impairment. Chelation is the conventional recommendation in the case of blood levels associated with acute toxicity and encephalopathic damage. Issues surrounding the assessment of body lead burden and the consequences of low-level environmental exposure are critical in the treatment of chronic disease related to lead toxicity.
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D002318:Cardiovascular Diseases / Q000139:chemically induced; D015913:Chelation Therapy / Q000379:methods; D004781:Environmental Exposure / Q000009:adverse effects; D006801:Humans; D007674:Kidney Diseases / Q000139:chemically induced; D007854:Lead / Q000378:metabolism; D007855:Lead Poisoning / Q000175:diagnosis / Q000209:etiology / Q000628:therapy; D008099:Liver / Q000378:metabolism; D014018:Tissue Distribution
D007854:Lead