Hormone replacement therapy may reduce the return of endogenous lead from bone to the circulation.

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 35 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 microgram/g bone mineral. For women on HRT, tibia bone lead was 19.37 +/- 8.62 micrograms/g bone mineral on low-dose HRT and 16.87 +/- 11.68 micrograms/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.ImagesFigure 1.

Lead Exposure and Spine Bone Mineral Density

“…HRT is effective in diminishing postmenopausal bone loss and has been considered a cornerstone in preventing osteoporosis. 46 In several prospective trials, HRT increased BMD in older women. [47][48][49][50] Regression analysis revealed that weight was a more important predictor of spine BMD in 1994 and 2000 than exercise habit (data not shown).…”

Prospective Study of Blood and Tibia Lead in Women Undergoing Surgical Menopause

“…A small cross-sectional study of blood lead concentrations among postmenopausal women either on ERT or calcium supplementation found that ERT may reduce the release of lead from bone (Webber et al 1995). However, this was evident only for cortical (tibia) and not trabecular (calcaneus) bone, even though trabecular bone is thought to be more sensitive to estrogen declines than is cortical bone.…”

Lead-induced hypertension: Role of oxidative stress

“…Although the presence of lead in the bone is not necessarily toxic, it can serve as a proxy for lead-induced renal and cardiovascular disease, owing to the steady exposure of target organs to low levels of lead released from bone storage compartment. It is important to recognize that lead may be mobilized from the skeleton during periods of increased bone demineralization, such as pregnancy and lactation [26], very old age [27], and menopause [28], and that during these periods, the risk for HTN may be increased.…”