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Lead

Lead poisoning is an environmental public health problem.  Lead based paint was banned in 1978 and lead-based gasoline was phased out in 1986. Today, the most common source of lead poisoning is dust and paint chips created by deteriorating lead paint found in millions of homes built before 1978.  Home renovation and demolition can also create airborne lead dust.  Other sources of lead include soil contaminated by lead paint, some insecticides, and highway pollution.  The water supply can become contaminated from lead pipes, fixtures, or solder.  Food stored in poorly glazed pottery or grown in contaminated soil can be a major source of lead. Industrial sources of lead include the manufacture of lead acid batteries, secondary lead smelters, nonferrous foundries, and the refurbishing of lead painted structures.  Lead is a potential hazard for ceramic artists. Employees of firing ranges are at risk due to the leaching of lead from bullets into the soil. Moonshine liquor may be contaminated with lead. Many Asian and Chinese herbal remedies are contaminated with heavy metals such as lead, arsenic, and mercury.  Indian Aryurvedic medicines sold in the U.S. are also heavily contaminated with lead.

Lead enters the body primarily through ingestion and inhalation.  Lead inhaled into the lungs is completely absorbed into the bloodstream.  Young children are susceptible to lead ingestion because of frequent hand to mouth activities.  Adults absorb 10 to 15% of ingested lead from the GI tract, while pregnant women and children absorb 50%.  Iron or calcium deficiency and fasting greatly increase lead absorption. Lead is stored in the blood, soft tissues, and bone.  Most lead is stored in bone as a labile component that readily exchanges with blood lead. Most of the blood lead is excreted in the urine.  About 25% of blood lead is transferred to the soft tissues, where the average half life is 40 to 120 days.  Bone lead has an average half-life of 15 to 20 years. Because of this long half-life, bone contains more than 95% of the body’s total lead burden. Following chronic lead exposure, blood lead levels may remain elevated for months or years after all sources of lead are removed from the environment because of the slow release of lead from the skeleton.

At low levels, lead poisoning in children may cause intelligence quotient deficiencies, reading and learning disabilities, impaired hearing, reduced attention span, hyperactivity, and behavior problems. Low level lead exposure from maternal blood may cause low birth weight and premature birth. 

Acute lead toxicity may begin at blood lead levels of 40 to 60 ug/dL. Early symptoms include irritability, anorexia, malaise, and headache.  As intoxication advances, abdominal pain and renal damage may develop.  Peripheral neuropathy is characterized by extensor muscle weakness with minimal sensory loss.  Intense exposure may cause cerebral edema, coma and death. 

Children insured through Medicaid are required to have blood lead level tests at ages 1 and 2, but some children are not screened. Some states require testing, but requirements vary. The American Academy of Pediatrics recommends blood lead level testing only for children who are determined to be at risk for lead exposure or who live in high prevalence areas. Likewise, CDC’s 2012 recommendation discourages universal screening in favor of primary prevention.

In 1991, CDC recommended that state or local health departments should perform follow-up testing of children with blood lead levels (BLLs) ≥10 µg/dL. In 1995, the Council of State and Territorial Epidemiologists (CSTE), in collaboration with CDC, added elevated BLLs to the list of reportable conditions. CDC asks state and local health departments to report all blood lead test data for children to the Healthy Homes and Lead Poisoning Prevention Program (HHLPPP), regardless of the BLL.

In May 2012, the Advisory Committee on Childhood Lead Poisoning Prevention (ACCLPP) recommended using reference ranges to identify elevated BLLs. ACCLPP recommended that the upper value of the reference range should be based on the 97.5th percentile of the lead levels contained in the National Health and Nutritional Examination Survey (NHANES). Currently, a cutoff value of 5 µg/dL is used by clinical and public health care providers to identify children with elevated BLLs. At this low level, the total allowable error is +/-4 ug/dL. 

In 2015, the National Institute for Occupational Safety and Health (NIOSH) changed the upper limit of the reference range for blood lead levels in adults to 5 µg/dL from 10 ug/dL.  An elevated BLL is defined as a BLL ≥5 µg/dL. NIOSH Lead Standards require workers to be removed from lead exposure when BLLs are equal or greater than 50 µg/dL in the construction industry or 60 µg/dL in general industry.

Workers to return to work when the BLL falls below 40 µg/dL.Lead has a half life of 25 days in blood and complete removal from the source may lead to a 3 to 5 ug/dL reduction of blood lead level per week. Chelating therapy is rarely performed for blood lead concentrations below 60 ug/dL and is usually performed for levels of 80 ug/dL or higher.

Specimen requirement is one royal blue top (EDTA) trace element blood collection tube or one metal free lavender top (EDTA) Microtainer.  Fingerstick samples may give falsely elevated lead values if the skin is not thoroughly cleansed.

Raymond J and Brown MJ, Childhood Blood Levels in Children Aged <5 years – United States, 2009-2014. MMWR Surveillance Summaries, Jan 20, 2017;66 (3):1-10. 

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