Lead Profile Occupational Exposure, Blood
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Lead is a heavy metal commonly found in man's environment that can be an acute and chronic toxin.
Lead was banned from household paints in 1978, but is still found in paint produced for nondomestic use and in artistic pigments. Ceramic products available from noncommercial suppliers (such as local artists) often contain significant amounts of lead that can be leached from the ceramic by weak acids such as vinegar and fruit juices. Lead is found in dirt from areas adjacent to homes painted with lead-based paints and highways where lead accumulates from use of leaded gasoline. Use of leaded gasoline has diminished significantly since the introduction of nonleaded gasolines that have been required in personal automobiles since 1972. Lead is found in soil near abandoned industrial sites where lead may have been used. Water transported through lead or lead-soldered pipe will contain some lead with higher concentrations found in water that is weakly acidic. Some foods (for example: moonshine distilled in lead pipes) and some traditional home medicines contain lead.
Lead expresses its toxicity by several mechanisms. It avidly inhibits aminolevulinic acid dehydratase (ALA-D) and ferrochelatase, 2 of the enzymes that catalyze synthesis of heme; the end result is decreased hemoglobin synthesis resulting in anemia.
Lead also is an electrophile that avidly forms covalent bonds with the sulfhydryl group of cysteine in proteins. Thus, proteins in all tissues exposed to lead will have lead bound to them. The most common sites affected are epithelial cells of the gastrointestinal tract and epithelial cells of the proximal tubule of the kidney.
The typical diet in the United States contributes 1 to 3 mcg of lead per day, of which 1% to 10% is absorbed; children may absorb as much as 50% of the dietary intake, and the fraction of lead absorbed is enhanced by nutritional deficiency. The majority of the daily intake is excreted in the stool after direct passage through the gastrointestinal tract. While a significant fraction of the absorbed lead is rapidly incorporated into bone and erythrocytes, lead ultimately distributes among all tissues, with lipid-dense tissues such as the central nervous system being particularly sensitive to organic forms of lead. All absorbed lead is ultimately excreted in the bile or urine. Soft-tissue turnover of lead occurs within approximately 120 days.
Avoidance of exposure to lead is the treatment of choice. However, chelation therapy is available to treat severe disease. Oral dimercaprol may be used in the outpatient setting except in the most severe cases.
Erythrocyte protoporphyrin is a biologic marker of lead toxicity. Lead inhibits several enzymes in the heme synthesis pathway and causes increased levels of RBC zinc protoporphyrin (ZPP).
Detecting lead toxicity
The Centers for Disease Control and Prevention (CDC) has identified the blood lead test as the preferred test for detecting lead exposure in children. Chronic whole blood lead levels <10 mcg/dL are often seen in children. For pediatric patients, there may be an association with blood lead values of 5 to 9 mcg/dL and adverse health effects. Follow up testing in 3 to 6 months may be warranted. Chelation therapy is indicated when whole blood lead concentration is >45 mcg/dL.
The Occupational Safety and Health Administration (OSHA) has published the following standards for employees working in industry:
-Employees with whole blood lead >60 mcg/dL must be removed from workplace exposure.
-Employees with whole blood lead >50 mcg/dL averaged over 3 blood samplings must be removed from workplace exposure.
-An employee may not return to work in a lead exposure environment until whole blood lead is <40 mcg/dL.
Elevated ZPP levels in adults may indicate long-term (chronic) lead exposure or may be indicative of iron deficiency anemia or anemia of chronic disease.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
High concentrations of gadolinium and iodine are known to interfere with most metals tests. If either gadolinium- or iodine-containing contrast media has been administered, a specimen must not be collected for 96 hours.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
0-6 years: 0.0-4.9 mcg/dL
>or =7 years: 0.0-9.9 mcg/dL
Pediatrics (< or =15 years): > or =20.0 mcg/dL
Adults (> or =16 years): > or =70.0 mcg/dL
Clinical References Provides recommendations for further in-depth reading of a clinical nature
1. Occupational Safety and Health Administration: OSHA Lead Standard-Requirements from the General Industry Standards Lead (1910, 1025), from 29 CFR 1910, 1025, A.M. Best Safety and Security-2000. Retrieved March 2000. Available from URL: http://www.ambest.com/safety/osha/chap10g.html
2. Centers for Disease Control and Prevention. Screening Young Children for Lead Poisoning. Guidance for State and Local Public Health officials. Atlanta, GA: U.S. Department of Health and Human Services. Public Health Service: November 1997 Available from URL: http://www.cdc.gov/nceh/lead/guide/guide97.htm
3. Burbure C, Buchet J-P, Leroyer A, et al: Renal and neurologic effects of cadmium, lead, mercury, and arsenic in children: evidence of early effects and multiple interactions at environmental exposure levels. Environ Health Perspect 2006;114:584-590
4. Kosnett MJ, Wedeen RP, Rothenberg SJ, et al: Recommendations for medical management of adult lead exposure. Environ Health Perspect 2007;115:463-471
5. Jusko T, Henderson C, Lanphear B, et al: Blood lead concentrations <10 mcg/dL and child intelligence at 6 years of age. Environ Health Perspect 2008;116:243-248