Lead Poisoning: the Evolving Definition

Correspondence to Richard P. Wedeen, MD, Department of Veterans Affairs New Jersey Health Care System 385, Tremont Ave, East Orange, NJ 07018, USA Tel: +1-973-395-7877 E-mail: Rrichard.Wedeen@va.gov Lead poisoning has been recognized for thousands of years but remains an occupational and environmental hazard worldwide. While some have attributed its first recognition to Hippocrates around 500 BC, the first description that approximates modern understanding of the disease is found in a poem by Nikander of Colophon in 200 BC. The major symptoms of lead poisoning can be identified in Nikander’s poem including lead colic (abdominal pain), peripheral neuropathy (wrist drop), encephalitis (mental confusion), and anemia (pallor). But early physicians had difficulty in separating lead colic from the far more common infectious gastroenteritis. Modern recognition of the symptom complex of acute lead poisoning dates to a series of essays by Sir George Baker in 1767 who unraveled the cause of the Devonshire Colic. Baker recognized that lead introduced into the local apple cider by soldered repairs to the cider presses was the cause. He was aided in this seminal insight by Benjamin Franklin who reported to Baker that New Englanders suffered from the “dry gripes,” (abdominal pain without diarrhea) from West Indian rum contaminated by lead from the “lead worms” (condensation coils) used in the stills. Saturnine gout was added to this description by Alfred Barring Garrod in 1859 who devised a method for measuring uric acid in blood and recognized that many of his hyperuricemic gout patients in 19 century Britain were lead workers. Current investigations indicate that uric acid itself contributes to the development of hypertension and renal failure. 4 Baker’s classical description remained the clinical standard for recognition of acute lead poisoning until the 20 century when blood lead measurement became available. The exponential increase in the use of lead during the industrial revolution exploded further with the introduction of tetraethyl lead as an anti-knock agent in gasoline in 1923. Under the influence of Robert Kehoe, research on the health effects was largely limited to studies in children. Kehoe, an industrial hygienist, who was simultaneously the Medical Director of the Ethyl Gasoline Corporation and the Kettering Laboratory of Applied Physiology at the University of Cincinnati declared blood lead levels of 80 μg/dL as acceptable for lead workers. At this level of exposure, symptomatic lead poisoning was usually present. Seizures, sometimes fatal, occurred in children who consumed leadpaint chips in deteriorating lead-painted housing, a practice called “pica.” These children had blood lead levels of 80 μg/dL or higher. While studies of childhood lead poisoning in the 20 century established the long-term impairment of cognitive development induced at even low levels of lead absorption, few studies of the effect of lead on adults were performed until the 1970s. On the basis of epidemiologic data, the acceptable blood lead level for children promulgated by the Center for Disease Control and Prevention (CDC) was progressively reduced from 60 μg/dL Editorial