Changes in bone Pb accumulation: Cause and effect of altered bone turnover

Abstract

This paper assesses the magnitude of Pb uptake in cortical and trabecular bones in healthy animals and animals with altered balance in bone turnover, and the impact of exposure to Pb on serum markers of bone formation and resorption. The results reported herein provide physiological evidence that Pb distributes differently in central compartments in Pb metabolism, such as cortical and trabecular bone, in healthy animals and animals with altered balance in bone turnover, and that exposure to Pb does have an impact on bone resorption resulting in OC-dependent osteopenia. These findings show that Pb may play a role in the etiology of osteoporosis and that its concentration in bones varies as a result of altered bone turnover characteristic of this disease, a long standing question in the field. In addition, data collected in this study are consistent with previous observations of increased half-life of Pb in bone at higher exposures. This evidence is relevant for the necessary revision of current physiologically based kinetic models for Pb in humans. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Abstract This paper assesses the magnitude of Pb uptake in cortical and trabecular bones in healthy animals and animals with altered balance in bone turnover, and the impact of exposure to Pb on serum markers of bone formation and resorption. The results reported herein provide physiological evidence that Pb distributes differently in central compartments in Pb metabolism, such as cortical and trabecular bone, in healthy animals and animals with altered balance in bone turnover, and that exposure to Pb does have an impact on bone resorption resulting in OC-dependent osteopenia. These findings show that Pb may play a role in the etiology of osteoporosis and that its concentration in bones varies as a result of altered bone turnover characteristic of this disease, a long standing question in the field. In addition, data collected in this study are consistent with previous observations of increased half-life of Pb in bone at higher exposures. This evidence is relevant for the necessary revision of current physiologically based kinetic models for Pb in humans. Keywords Pb exposureBone turnover Osteoporosis Kinetic models 1

Differences in cadmium transfer from tobacco to cigarette smoke, compared to arsenic or lead

“…The body burden of cadmium was assessed as being approximately two-fold higher in smokers than in non-smokers [18] , [7] , [19] . The impact of smoking on the lead body burden is observed through a sequestration in bones [20] , [21] , [22] , but not in blood [23] , [24] , while no effect from smoking could be observed in the case of arsenic [25] , or mercury [26] , [27] . Surveys also showed that smoking is not an important source for nickel [28] .…”

Relationships between Bone Turnover and Energy Metabolism

“…Most biochemical markers of bone resorption are related to collagen breakdown products or to various collagen crosslinks and telopeptides [11–13]. At present, serum C-terminal peptide-bound crosslinks of type I collagen (CTX-1) have been chosen as the reference standard for bone resorption rate, whereas osteocalcin is considered a good marker of bone formation [14–16]. Also, osteocalcin is a bone-specific protein that acts as a hormone regulating glucose metabolism.…”

Lead Exposure and Environmental Health

“…Bone accumulates lead throughout most of the human life span but, at the same time, lead is mobilised from bone by remodelling. In adults, approximately 90 % of the total body burden of lead found in bones (Brito et al, 2014). However, in children, only 70 % of the body burden is found…”