Volume 9, Issue 5 pp. 286-303
Original Paper

Experimental Lead Paint Poisoning in Nonhuman Primates

II. Clinical Pathologic Findings and Behavioral Effects1

B.C. Zook

Corresponding Author

B.C. Zook

Department of Pathology, School of Medicine and Health Sciences, and Department of Psychology, The George Washington University, Washington, D.C.

Infectious Disease Branch, Collaborative and Field Research, National Institute of Neurological Diseases and Stroke, NIH, Bethesda, Md.

Pathology Division, National Zoological Park, Smithsonian Institution, Washington, D.C.

Bernard C. Zook, DVM, The George Washington University, Ross Hall, B-12, 2300 I Street, N.W., Washington, DC 20037 (USA)Search for more papers by this author
W.T. London

W.T. London

Department of Pathology, School of Medicine and Health Sciences, and Department of Psychology, The George Washington University, Washington, D.C.

Infectious Disease Branch, Collaborative and Field Research, National Institute of Neurological Diseases and Stroke, NIH, Bethesda, Md.

Pathology Division, National Zoological Park, Smithsonian Institution, Washington, D.C.

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J.F. DiMaggio

J.F. DiMaggio

Department of Pathology, School of Medicine and Health Sciences, and Department of Psychology, The George Washington University, Washington, D.C.

Infectious Disease Branch, Collaborative and Field Research, National Institute of Neurological Diseases and Stroke, NIH, Bethesda, Md.

Pathology Division, National Zoological Park, Smithsonian Institution, Washington, D.C.

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L.A. Rothblat

L.A. Rothblat

Department of Pathology, School of Medicine and Health Sciences, and Department of Psychology, The George Washington University, Washington, D.C.

Infectious Disease Branch, Collaborative and Field Research, National Institute of Neurological Diseases and Stroke, NIH, Bethesda, Md.

Pathology Division, National Zoological Park, Smithsonian Institution, Washington, D.C.

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RM. Sauer

RM. Sauer

Department of Pathology, School of Medicine and Health Sciences, and Department of Psychology, The George Washington University, Washington, D.C.

Infectious Disease Branch, Collaborative and Field Research, National Institute of Neurological Diseases and Stroke, NIH, Bethesda, Md.

Pathology Division, National Zoological Park, Smithsonian Institution, Washington, D.C.

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J.L. Sever

J.L. Sever

Department of Pathology, School of Medicine and Health Sciences, and Department of Psychology, The George Washington University, Washington, D.C.

Infectious Disease Branch, Collaborative and Field Research, National Institute of Neurological Diseases and Stroke, NIH, Bethesda, Md.

Pathology Division, National Zoological Park, Smithsonian Institution, Washington, D.C.

The authors thank Margaret R. Ashworth, Robert L. Brown, and Sherry L. Thomas for their technical assistance. Dr. Sauer is presently with the Gillette Medical Evaluation Laboratories in Rockville, Md. A portion of this work by J.F. DiMaggio has been accepted by The George Washington University in partial fulfillment for a Master of Arts degree.Search for more papers by this author
First published: 01 October 1980
1
This work was supported in part by grant Nr. NIH 5 SO1 RR 5359 14 of the National Institutes of Health, Department of Health, Education and Welfare.

Abstract

Oral administration of lead-containing paint to rhesus monkeys induced anemia, more profound in older primates. Erythrocytes were microcytic and hypochromic, but tended to become macrocytic terminally. Stippled erythrocytes were increased in all poisoned monkeys, especially in those with high blood lead levels and anemia. Proteinuria, glycosuria, casts and sloughed tubular cells containing acid-fast inclusion bodies were found on urinalysis. Terminal elevations of blood urea nitrogen were associated with profound anemia and renal tubular damage. Repeated blood lead values over 200 μg/dl were associated with a moribund termination while monkeys which had levels under 100 μg/dl remained apparently healthy. Behavioral studies in a small number of subclinically poisoned juveniles and neonates failed to reveal deficiencies of visual acuity or cognitive ability, nor was there evidence of alterations in levels of activity.

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