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Howard Hu, MD, MPH, ScD; Hirokastsu Watanabe, MD; Marinelle Payton, MD, PhD, MPH; Susan Korrick, MD, MPH; Andrea Rotnitzky, PhD

JAMA. 1994;272(19):1512-1517.

Abstract
Objective.
—To determine whether the concentration of lead in bone constitutes a biological marker that is more sensitive for chronic toxicity than blood lead levels.

Design.
—Survey.

Setting.
—A construction trade union with members who engage in carpentry, demolition, and other construction activities.

Participants.
—Members of the construction trade union.

Main Outcome Measures.
—We measured blood pressure, serum creatinine, hematocrit, and hemoglobin. We measured blood lead by anodic stripping voltametry and used a cadmium 109 K x-ray fluorescence instrument to make in vivo measurements of lead in the tibia (a heavily cortical bone) and the patella (a heavily trabecular bone). Information was also collected on medical history, smoking, and alcohol ingestion.

Results.
—Bone lead levels in the patella were found to be significantly correlated with a decrease in hemoglobin and hematocrit, even after adjusting for age, blood lead, body mass index, cigarette smoking, and alcohol ingestion and removing outliers. Blood lead levels were low (mean=0.40 µmol/L [8.3 µg/dL]) and were not correlated with either hemoglobin or hematocrit. In the final multivariate regression model that corrected for measurement error, an increase in patella bone lead level from the lowest to highest quintile in this study population (37 µg/g) was associated with a decrease in hemoglobin and hematocrit of 11 g/L (95% confidence interval [CI], 2.7 to 19.3 g/L) and 0.03 (95% CI, 0.01 to 0.05), respectively.

Conclusion.
—We conclude that patella bone lead levels are associated with decreased hematocrit and hemoglobin levels despite the presence of low blood lead levels. This conclusion may reflect a subclinical effect of bone lead stores on hematopoiesis and is the first epidemiological evidence that bone lead may be an important biological marker of ongoing chronic toxicity.

(JAMA. 1994;272:1512-1517)

Author Affiliations
From the Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School (Drs Hu, Watanabe, Payton, and Korrick), the Occupational Health Program, Department of Environmental Health (Drs Hu and Korrick), and the Department of Biostatistics (Dr Rotnitzky), Harvard School of Public Health, Boston, Mass; and Osaka (Japan) Medical College (Dr Watanabe).

Footnotes
Reprint requests to Channing Laboratory, 180 Longwood Ave, Boston, MA 02115 (Dr Hu).

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