Experimental Lead Paint Poisoning in Nonhuman Primates
III. Pathologic Findings
Corresponding Author
B.C. Zook
Department of Pathology, The George Washington University School of Medicine and Health Sciences, Washington, D.C.
Infectious Disease Branch, Collaborative and Field Research, NIH, Bethesda, Md.
Department of Otolaryngology, Thomas Jefferson University Medical School, Philadelphia, Pa.
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 authorW.T. London
Department of Pathology, The George Washington University School of Medicine and Health Sciences, Washington, D.C.
Infectious Disease Branch, Collaborative and Field Research, NIH, Bethesda, Md.
Department of Otolaryngology, Thomas Jefferson University Medical School, Philadelphia, Pa.
Search for more papers by this authorC.R. Wilpizeski
Department of Pathology, The George Washington University School of Medicine and Health Sciences, Washington, D.C.
Infectious Disease Branch, Collaborative and Field Research, NIH, Bethesda, Md.
Department of Otolaryngology, Thomas Jefferson University Medical School, Philadelphia, Pa.
Search for more papers by this authorJ.L. Sever
Department of Pathology, The George Washington University School of Medicine and Health Sciences, Washington, D.C.
Infectious Disease Branch, Collaborative and Field Research, NIH, Bethesda, Md.
Department of Otolaryngology, Thomas Jefferson University Medical School, Philadelphia, Pa.
The authors thank Margaret R. Ashworth, Robert L. Brown, and Sherry L. Thomas for their technical assistance.Search for more papers by this authorCorresponding Author
B.C. Zook
Department of Pathology, The George Washington University School of Medicine and Health Sciences, Washington, D.C.
Infectious Disease Branch, Collaborative and Field Research, NIH, Bethesda, Md.
Department of Otolaryngology, Thomas Jefferson University Medical School, Philadelphia, Pa.
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 authorW.T. London
Department of Pathology, The George Washington University School of Medicine and Health Sciences, Washington, D.C.
Infectious Disease Branch, Collaborative and Field Research, NIH, Bethesda, Md.
Department of Otolaryngology, Thomas Jefferson University Medical School, Philadelphia, Pa.
Search for more papers by this authorC.R. Wilpizeski
Department of Pathology, The George Washington University School of Medicine and Health Sciences, Washington, D.C.
Infectious Disease Branch, Collaborative and Field Research, NIH, Bethesda, Md.
Department of Otolaryngology, Thomas Jefferson University Medical School, Philadelphia, Pa.
Search for more papers by this authorJ.L. Sever
Department of Pathology, The George Washington University School of Medicine and Health Sciences, Washington, D.C.
Infectious Disease Branch, Collaborative and Field Research, NIH, Bethesda, Md.
Department of Otolaryngology, Thomas Jefferson University Medical School, Philadelphia, Pa.
The authors thank Margaret R. Ashworth, Robert L. Brown, and Sherry L. Thomas for their technical assistance.Search for more papers by this authorAbstract
Necropsies were performed on 25 rhesus monkeys, three cebus monkeys and three baboons which had been fed leaded paint or lead acetate at various doses up to 666 days. The 31 test primates and six controls ranged in age from five days to about eight years. In addition, the brains of 13 subadult squirrel monkeys fed lead oxide and two controls were studied grossly and microscopically. Lead content of liver, kidney and brain correlated with clinical outcome and typical histologic changes. Neuropathologic lesions, most severe in the young, occurred in 28 of 43 test primates despite a paucity of neurological signs. Brain lesions were similar to those occurring in human lead encephalopathy and included degenerative and proliferative changes of small vessels, ring hemorrhages, edema, perivascular hyalin droplets, rosette-like deposits of proteinaceous exudates, focal loss of myelin, astrogliosis and necrosis of hippocampal neurons.
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