Archive Issue

2017, Volume 27, Number 1

Measurement of Lead Levels in Blood

William G. Finn, MD, Medical Director, Warde Medical Laboratory

A renewed public interest in lead toxicity was spurred by the water crisis in Flint, Michigan in 2014. (1) In an effort to save money, a state-appointed emergency manager established plans to change the Flint water supply from water purchased from the Detroit Water and Sewerage Department to a new pipeline under construction in Lake Huron.

Pending completion of that pipeline, the Flint water supply was temporarily switched to the Flint River as its principal source. The new source yielded water that was more corrosive than the existing source, resulting in the leaching of lead from the antiquated system of pipes that constituted the Flint water distribution system. As a result, the number of children in Flint with elevated blood levels essentially doubled, from 2.4% prior to the switch to 4.9% after the switch. (1)

Historical Perspective


Recognition of lead poisoning dates back thousands of years. (2) Anemia, encephalopathy, “lead palsy,” and “lead colic” are some of the oldest known manifestations of lead poisoning. However, the recognition of lower level lead exposure as an ongoing environmental and public health threat is a relatively recent phenomenon.

For centuries, lead control efforts were aimed at preventing ingestion or exposure to clinically toxic lead levels, with little awareness of the risk of lower level or chronic environmental lead exposure. Today it is broadly recognized that lead serves no beneficial function to human life, and that there is no such thing as a safe level of lead exposure. (2,3)

Attempts to monitor and control lead poisoning in industrial workers in the early 20th century paved the way for modern occupational health initiatives, developed through such works as Legge and Goadby’s Lead Absorption in 1912, (2,4) and by the pioneering work of Alice Hamilton—cited by some as the inventor of “industrial medicine.” (2,5) Still, however, the focus was mainly on the detection and management of frank toxicity, rather than prevention.

Unfortunately, awareness of the deleterious effects of even low-level lead exposure didn’t develop until the latter part of the 20th century. The development of this awareness was hampered by the activism of commercial interests (particularly in the petroleum industry), and by the nearly ubiquitous contamination of laboratory equipment and operators by environmental lead (likely due to the use of tetraethyl lead as a gasoline additive dating to the 1920s). (2)
This widespread contamination resulted in the interpretation of baseline lead levels observed in individuals and in the environment as natural rather than man-made.

Dr. Clair Patterson, a geologist whose interest in lead began with his research on the calculation of the age of the Earth, published compelling evidence that lead levels deemed “natural” by others in the field (including Robert Kehoe, a leading skeptic of Patterson’s work who did not believe in the concept of subclinical lead poisoning) were actually the result of man-made environmental pollution, and orders of magnitude higher than truly natural environmental levels. (6)

Surprisingly, the two greatest contributors to lead toxicity in modern society—the use of lead-based paint and the use of tetraethyl lead as a gasoline additive—were only banned in the United States in 1978 and 1996, respectively (although a gradual phase-out of tetraethyl lead had begun some two decades earlier). Today, exposure to lead paint in houses built before 1978 remains a principal source of childhood lead poisoning.

CDC Guidelines

Prior to 2012, the Centers for Disease Control and Prevention (CDC) had established a whole blood lead concentration of 10 ug/dL as a “level of concern” for the screening of children for lead toxicity. However, in 2012 the CDC’s Advisory Committee on Childhood Lead Poisoning Prevention (ACCLPP) recommended that the term “level of concern” be eliminated from all guidance documents, since cognitive deficits are well documented in children whose peak blood levels never exceeded 10 ug/dL, and since there is a growing consensus that no level of lead exposure is considered safe. (3)

The ACCLPP recommended instead the establishment of a childhood blood lead reference value of 5 ug/dL to “identify children and environments associated with lead exposure hazards” based on the 97.5th percentile of childhood lead levels according to the CDC’s National Health and Nutrition Examination Survey (NHANES). The Committee further recommended that this reference level be reviewed periodically based on population data.

Screening for Elevated Lead Levels


Measurement of whole blood lead is the recommended method for screening for lead exposure and toxicity. (3) While the measurement of zinc protoporphyrin (ZPP) level may be useful in assessing the chronicity of lead toxicity in the setting of known occupational or industrial exposure, ZPP lacks both sensitivity and specificity in assessing for environmental exposure or more acute lead toxicity (7) and is not recommended for populational screening.

The World Health Organization (WHO) and the Clinical and Laboratory Standards Institute (CLSI) recognize three main methods for the determination of blood lead levels: atomic absorption spectrometry (AAS), anodal stripping voltammetry (ASV), and inductively coupled plasma mass spectrometry (ICP-MS). (8,9)

While ASV has gained popularity due to its relative ease of use and adaptability to portable or point-of-care platforms, it is relatively insensitive, with detection limits (particularly in point-of-care applications) that may not satisfy the current CDC recommendations for whole blood lead level detection.

Warde Medical Laboratory currently uses a graphite furnace AAS method that is highly sensitive and provides rapid results for the accurate determination of blood lead levels.


References

  1. Hanna-Attisha M, LaChance J, Sadler RC, Schnepp AC: Elevated blood lead levels in children associated with the Flint drinking water crisis: a spatial analysis of risk and public health response. Am J Public Health 2016; 106(2):283-290.
  2. Hernberg S: Lead poisoning in a historical perspective. Am J Industrial Med 2000; 38:244-254.
  3. Centers for Disease Control and Prevention: Low level lead exposure harms children. A renewed call for primary prevention. Report of the Advisory Committee on Childhood Lead Poisoning Prevention 2012; https://www.cdc.gov/nceh/lead/acclpp/final_document_030712.pdf. Accessed February 28, 2017.
  4. Legge TM, Goadby KW: Lead poisoning and lead absorption. Longman (New York), 1912.
  5. Hamilton A: Exploring the dangerous trades. Little, Brown (Boston), 1943.
  6. Patterson CC: Contaminated and natural lead environments of man. Arch Environ Health 1965; 11:344-360.
  7. Martin CJ, Werntz III CL, Ducatman AM: The interpretation of zinc protoporphyrin changes in lead intoxication: a case report and review of the literature. Occupational Med 2004; 54:587-591.
  8. Inter-Organization Programme for the Sound Management of Chemicals (IOMC):
    Brief guide to analytical methods for measuring lead in blood. World Health Organization, 2011;
    http://www.who.int/ipcs/assessment/public_health/lead_blood.pdf
  9. CLSI. Measurement Procedures for the Determination of Lead Concentrations in Blood and Urine; Approved Guideline—Second Edition. CLSI document C40-A2. Wayne, PA: Clinical and Laboratory Standards Institute; 2013.