Lead toxicity has been a hot topic in the lay press since the news broke of contaminated water in Flint, MI. Over 4% of children less than 6 years old had blood lead levels (BLL) greater than 5 mcg/dL, the CDC recommended upper reference interval threshold. While Flint has caught much attention, lead toxicity is not an isolated problem. In the US, there are at least 12 states with elevated BLL prevalence higher than that of the Michigan town. For example, in 2014, Pennsylvania reported 8.5 percent of children tested had high BLL. Ohio reported a prevalence 3 times that of Flint.
Globally, lead toxicity accounts for 0.6% of the burden of disease. Some researchers suggest that 26 million people are at risk for lead toxicity, worldwide.
Lead toxicity occurs from environmental exposure. The leading causes of lead exposure include:
- Lead added to gasoline
- Lead from active industry, such as mining (especially in soils)
- Lead based paints and pigments
- Lead solder in food cans
- Ceramic glazes
- Drinking water systems with lead solder and lead pipes
- Lead in products, such as herbal and traditional medicines, folk remedies, cosmetics and toys
- Lead released by incineration of lead-containing waste
- Lead in electronic waste (e-waste)
- Lead in the food chain, via contaminated soil
- Lead contamination as a legacy of historical contamination from former industrial sites
In the United States, lead exposure is primarily from lead paint, followed by lead in the soil and lead in pipes. Leaded paint and pipes are found mostly in older homes and buildings in urban areas. In fact, zip codes associated with high numbers of pre-1950s housing were significantly associated with high BLLs in children <6 years old (1). Unfortunately, these are more likely to be inhabited by low income families.
Lead exposure can cause irreversible cognitive and behavioral impairment. Lead toxicity is due to several mechanisms. Lead can disrupt cellular pathways by binding to metal-binding enzymes, and sulfhydryl and amide groups on enzymes. Lead is particularly detrimental to the heme synthesis pathway, because it can downregulate 3 of the 7 enzymes in the pathway.
Lead can be measured in whole blood by AAP or ICP. Venous whole blood should be collected in metal-free phlebotomy tubes. Screening for elevated BLL can be done at the point of care with the LeadCare II, the only FDA-approved, CLIA-waived POCT device that measures lead currently on the market. The LeadCare measures lead by anodic stripping, and is designed to use capillary blood samples. While elevated capillary blood samples should be confirmed with mass spectrometry on venous blood, the POCT does have the advantage of a quick result while at the patient’s side, increasing the likelihood of obtaining that confirmatory sample.
Despite the availability of fast and affordable testing for lead exposure, the US is not doing a great job maintaining screening programs. 2012, CDC released new guidelines moving the threshold from 10 mcg/dL to 5 mcg/dL. At the same time, federal funding for lead screening programs was cut – from $29 million to $2 million! According to the CDC, we are currently testing ~10% of our at-risk, less than 6 year old population. Only 11 states have federally supported lead screening programs. While Medicaid requires all enrolled children to be screened for lead exposure at 1 and 2 years of age, this requirement is not enforced. Based on Medicaid payment claims, in Ohio only 41% of children enrolled in the program and living in high-risk zip codes were screened for lead exposure. Other states, like Missouri, have state-run programs. Still others have no recommended guidelines for lead screening. Many states do not report lead screening results to the CDC, meaning that lead exposure in the US might be severely under-reported.
On October 20, 2016, the EPA released a Management Alert recommending clarification of EPA authority to issue emergency orders to protect the public. Some argue this is too little too late. Should all the blame go to the EPA? Should we as laboratory professionals join the effort to eradicate lead exposure? We can help by championing and advocating for lead screening programs in our states and consistently and thoroughly reporting lead testing results.
| Blood Lead Concentration (mcg/dL) | Effect(s) |
| 10-20 | Impaired cognition and behavior, fine-motor coordination, hearing, growth |
| 20-40 | Reduced nerve conduction velocity, impaired vitamin D metabolism, decreased hemoglobin synthesis, increased blood pressure, peripheral neuropathy |
| 40-90 | Colic, frank anemia, nephropathy, encephalopathy |
| 90-150 | Encephalopathy, death |
Table: Some clinical manifestations of lead poisoning in children.
Reference:
- McClure LF, Niles JK, Kaufman HW. Blood lead levels in young children: US, 2009-2015. J Pediatr 2016; 175: 173-81.
-Sarah Brown, PhD, DABCC, is an Assistant Professor of Pediatrics and Pathology and Immunology at Washington University in St. Louis School of Medicine. She is passionate about bringing the lab out of the basement and into the forefront of global health.
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