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(Circulation. 2006;114:1347-1349.)
© 2006 American Heart Association, Inc.

Editorial

Low-Level Environmental Exposure to Lead Unmasked as Silent Killer

Tim S. Nawrot, PhD; Jan A. Staessen, MD, PhD

From the Division of Lung Toxicology, Department of Occupational and Environmental Medicine (T.S.N.) and the Studies Coordinating Centre (J.A.S.), Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Diseases, University of Leuven, Leuven, Belgium.

Correspondence to Jan A. Staessen, Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Diseases, Campus Gasthuisberg, Herestraat 49, Box 702, B-3000, Leuven, Belgium. E-mail jan.staessen@med.kuleuven.be or jan.staessen@proximus.be

Key Words: epidemiology • mortality • hypertension • risk factors • lead

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Since the dawn of human civilization, lead has been a ubiquitous environmental pollutant.¹ In 370 BC, Hippocrates described colic in a lead worker.² The industrial application of lead continues to the present day. Lead is a toxic metal that, during a lifetime, accumulates in the human body.¹ Recent evidence^3–6 suggests that lead affects human health at levels of exposure that, until now, were considered safe. The underlying premise is that a dose-related continuum of toxicity exists. Asymptomatic health effects may occur at even a very low dose and may evolve into clinically overt adverse effects if the exposure persists during a person’s lifetime or becomes more intense. The report published by Menke et al⁷ in this issue of Circulation breaks new ground by extending the dose–effect relation to considerably lower blood lead concentrations than reported in previous studies.^3–6

Article p 1388

Menke et al⁷ analyzed the database of the Third National Health and Nutrition Examination Survey (NHANES III) to investigate the relation between total and cause-specific mortality and blood lead in a representative sample of the US population. All 13 946 participants (17 years of age) included in the analysis had a blood lead concentration <0.48 µmol/L (10 µg/dL). (To convert micromoles per liter of lead into micrograms per deciliter, multiply by 20.712.) Follow-up lasted until December 31, 2000. With adjustments applied for confounders, subjects in the highest third of the blood lead distribution (0.17 µmol/L), as compared with those in the lowest third (<0.09 µmol/L), experienced a . . . [Full Text of this Article]