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Shirng-Wern Tsaih,¹ Joel Schwartz,^2,3 Mei-Ling Ting Lee,^3,4,5 Chitra Amarasiriwardena,³ Antonio Aro,^3,6 David Sparrow,⁷ and Howard Hu^3,6

¹Department of Epidemiology; ²Environmental Epidemiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115 USA
³Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115 USA
⁴Department of Biostatistics, Harvard School of Public Health, Boston, MA 02115 USA
⁵Biostatistics Center, Massachusetts General Hospital, Boston, MA 02114 USA
⁶Occupational Health Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115 USA
⁷The Normative Aging Study, Department of Veterans Affairs Outpatient Clinic, Boston, MA 02114 USA

Abstract

Plasma is the component of blood from which lead is free to cross cell membranes and cause organ toxicity. Plasma lead levels, however, are extremely low and difficult to measure. Urinary lead originates from plasma lead that has been filtered at the glomerular level ; thus, urinary lead adjusted for glomerular filtration rate serves as a proxy for plasma lead levels. In this investigation we examined the interrelationships of lead levels in whole blood corrected by hematocrit [i.e., erythrocyte lead (EPb) ], trabecular bone (TBoPb) , cortical bone (CBoPb) , and urine excreted over 24 hr (UPb) ; all samples were obtained from 71 middle-aged and elderly men with no known occupational lead exposures. Lead was measured by graphite furnace atomic absorption spectroscopy (blood) , K-X-ray fluorescence (bone) , and inductively coupled plasma mass spectroscopy (urine) . Lead levels were generally low, with mean EPb, TBoPb, and CBoPb values of 13.8, 31.1, and 21.7 µg/g, respectively, and a median UPb value of 6.15 µg/day. In generalized additive models adjusted for body weight and creatinine clearance rate, both EPb and bone lead variables remained independently and significantly associated with UPb. This finding suggests that bone influences plasma lead in a manner that is independent of the influence of erythrocytic lead on plasma lead. Thus, the superiority of bone lead over blood lead in predicting some chronic forms of toxicity may be mediated through bone's influence on plasma lead. In addition, this study suggests that measurement of urinary lead might be useful as a proxy for plasma lead levels in studies of lead toxicity. Key words: blood, bone, environmental exposure, K-X-ray fluorescence, lead, urine. Environ Health Perspect 107:391-396 (1999) . [Online 6 April 1999]

http://ehpnet1.niehs.nih.gov/docs/1999/107p391-396tsaih/ abstract.html

Address correspondence to S-W. Tsaih, Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115 USA.

The authors gratefully acknowledge the research management of Soma Datta, Gail Fleischaker, Randi Heldman, Sybil Harcourt, and Nicola Lupoli.

Support for this research was provided by NIEHS R01 ES05257, NIEHS P42-ES05947, NIH NCRR GCRC M01 RR02635, NIEHS Center grant 2 P30 ES00002, and the Cooperative Studies Program/Epidemiology Research Information Centers of the Department of Veterans Affairs. Support was also provided by NIEHS 5 P42 ES-05947, with funding provided by the EPA. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIEHS, NIH, or EPA. The KXRF instrument used in this work was developed by ABIOMED, Inc., of Danvers, MA, with support from NIH SBIR 2R44 ES03918-02.

Received 7 October 1998 ; accepted 25 January 1999.