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Hormone Replacement Therapy May Reduce the Return of Endogenous Lead from Bone to the Circulation
Colin E. Webber,1 David R. Chettle,2 Robert J. Bowins,3 Lesley F. Beaumont,1 Christopher L. Gordon,1 Xinni Song,1 Jennifer M, Blake,4 and Robert H. McNutt3
1 Department of Nuclear Medicine, Chedoke-McMaster Hospitals, Hamilton, Ontario, L8N 3Z5 Canada
2Department of Physics and Astronomy and 3Department of Geology, McMaster University, Hamilton, Ontario, L8S 4M1 Canada
4Department of Obstetrics and Gynecology, McMaster University Medical Centre, Hamilton, Ontario, L8N 3Z5 Canada
Abstract
Hormone replacement therapy (HRT) in postmenopausal women suppresses the increase in bone resorption expected as circulating levels of endogenous estrogen decline. We tested the hypothesis that bone lead content might remain elevated in women on HRT. Fifty-six women who at recruitment were on average 3.5 years postmenopausal were placed on calcium supplementation. Six months later, 33 of these women were prescribed either low dose or moderate dose hormone replacement in addition to the calcium supplementation. After approximately 4 years of hormone replacement, lead content was measured at the tibia and calcaneus by in vivo fluorescence excitation, and lead concentrations were measured in serum, whole blood and urine.
Women not taking hormones had significantly lower lead concentrations in cortical bone compared to all women on HRT (p = 0.007). Tibia lead content (mean ± SD) for women on calcium only was 11.13 ± 6.22 µg/g bone mineral. For women on HRT, tibia bone lead was 19.37 ± 8.62 µg/g bone mineral on low-dose HRT and 16.87 ± 11.68 µg/g bone mineral) on moderate-dose HRT. There were no differences between groups for lead concentrations measured in trabecular bone, whole blood, serum or urine. Hormone replacement maintains cortical bone lead content. In women not on HRT, there will be a perimenopausal release of lead from bone. Key words: bone resorption, endogenous lead, estrogen, hormone replacement, menopause. Environ Health Perspect 103:1150-1153 (1995)
Address correspondence to C. E. Webber, Department of Nuclear Medicine, Chedoke-McMaster Hospitals, 1200 Main Street West, Hamilton, Ontario L8N 3Z5 Canada.
This work was supported by a grant (LH-432/416) from the International Lead and Zinc Research Organization.
Received 22 June 1995; accepted 23 August 1995.
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