Modeling normal aging bone loss, with consideration of bone loss in osteoporosis.
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A physiologically based model of normal bone loss in human aging is presented. The model is a modification of an existing physiologically based model of body and bone growth from birth to maturity. To account for loss of bone after peak bone mass is reached between ages 25 and 30 years, a slow first-order loss of bone is incorporated into the existing model. The rate constants for this first-order loss are the same for men and women but differ with the type of bone, being 3%/decade for cortical bone and 7-11%/decade for trabecular bone. In women, a 10-year period of more rapid loss of both cortical and trabecular bone is superimposed on the slow loss, beginning at the time of menopause. The superimposed loss occurs at the same relative rate in cortical and trabecular bone. Alterations in parameter values allow simulation of bone mass in osteoporotic men and women. The model is calibrated to quantitative estimates of cortical and trabecular bone mass as functions of age; in particular, to data sets of fractional vertebral bone volume as functions of age, and it is compared to the International Commission on Radiological Protection trend curves for skeletal mass in men and women to age 60. It is also applied to the question of whether loss of bone in women after menopause could create a hazard related to the return to blood of lead previously stored in bone. In agreement with observations made during 1976-1980, the model simulates an increase due to bone resorption of approximately 1 microg/dl in blood lead concentration in a postmenopausal (60-year-old) woman compared with a premenopausal (50-year-old) woman with typical lifetime ambient lead exposure. (+info)
Age of Neoproterozoic bilatarian body and trace fossils, White Sea, Russia: implications for metazoan evolution.
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A uranium-lead zircon age for a volcanic ash interstratified with fossil-bearing, shallow marine siliciclastic rocks in the Zimnie Gory section of the White Sea region indicates that a diverse assemblage of body and trace fossils occurred before 555.3 +/- 0.3 million years ago. This age is a minimum for the oldest well-documented triploblastic bilaterian Kimberella. It also makes co-occurring trace fossils the oldest that are reliably dated. This determination of age implies that there is no simple relation between Ediacaran diversity and the carbon isotopic composition of Neoproterozoic seawater. (+info)
Cd(II), Pb(II) and Zn(II) ions regulate expression of the metal-transporting P-type ATPase ZntA in Escherichia coli.
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ZntA is a cation-translocating ATPase which exports from Escherichia coli Cd(II) and Pb(II), as well as Zn(II). The metal-dependent ATP hydrolysis activity of purified ZntA was recently characterised and showed a specificity for Cd(II), Pb(II) and Zn(II). zntA expression has been reported to be up-regulated primarily by Zn(II), mediated by the regulatory protein ZntR, belonging to the MerR transcriptional regulator family. In contrast to previous claims, we now show, using a Phi(zntA-lacZ) monolysogen, that Cd(II) is the most effective inducer of zntA, which is also induced significantly by Pb(II). The Cd(II)- and Pb(II)-dependent transcriptional up-regulation of zntA is also mediated by ZntR. (+info)
Neonatal lead exposure impairs development of rodent barrel field cortex.
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Childhood exposure to low-level lead can permanently reduce intelligence, but the neurobiologic mechanism for this effect is unknown. We examined the impact of lead exposure on the development of cortical columns, using the rodent barrel field as a model. In all areas of mammalian neocortex, cortical columns constitute a fundamental structural unit subserving information processing. Barrel field cortex contains columnar processing units with distinct clusters of layer IV neurons that receive sensory input from individual whiskers. In this study, rat pups were exposed to 0, 0.2, 1, 1.5, or 2 g/liter lead acetate in their dam's drinking water from birth through postnatal day 10. This treatment, which coincides with the development of segregated columns in the barrel field, produced blood lead concentrations from 1 to 31 microg/dl. On postnatal day 10, the area of the barrel field and of individual barrels was measured. A dose-related reduction in barrel field area was observed (Pearson correlation = -0.740; P < 0.001); mean barrel field area in the highest exposure group was decreased 12% versus controls. Individual barrels in the physiologically more active caudoventral group were affected preferentially. Total cortical area measured in the same sections was not altered significantly by lead exposure. These data support the hypothesis that lead exposure may impair the development of columnar processing units in immature neocortex. We demonstrate that low levels of blood lead, in the range seen in many impoverished inner-city children, cause structural alterations in a neocortical somatosensory map. (+info)
Effect of exposure to lead on postural control in workers.
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OBJECTIVES: To examine the effect of lead on postural control of workers who have been exposed to lead. METHODS: 63 Male, lead battery workers mean (SD) age 41.0 (7.4) were compared with 48 age matched male controls after excluding those with acute or chronic diseases. Exposed workers had mean (SD) past blood lead concentrations of 37.5 (9.2) micrograms/dl and 11.2 (5.7) years of employment. Postural control was measured with a computerised postural sway measurement system which measured both sway and total movements. RESULTS: Workers standing straight with eyes open on the bare plates had sway and total movements which were not notably different from controls. On the other hand increased movements were needed in the exposed workers to maintain stability (the general stability quotient 18.2 (5.4) v 15.4 (4.4) in controls, p < 0.01) when standing directly on the foot-plates with closed eyes,, and with the head tilted (15.0 (3.8) v 11.5 (3.0) in controls, p < 0.001). Exposed workers also had a trend for less ability to synchronize anterior posterior and lateral sway in the stress positions (0.0625) than had non-exposed workers. Significant but low correlations were found between the estimate of the chronic internal dose of lead and three of 10 of the postural control measurements, and present lead blood concentrations and only one of the 10 measurements and (r values ranged from 0.21 to 0.31, p < or = 0.03). CONCLUSIONS: These findings suggest that lead affects postural control in asymptomatic workers. Further studies are warranted to find whether workers with decreased postural control are at increased risk of accidents and the relation, if any, of these measurements with subsequent morbidity. (+info)
The technique of (109)Cd-based X-ray fluorescence (XRF) measurements of lead in bone is well established. A paper by some XRF researchers [Gordon CL, et al. The Reproducibility of (109)Cd-based X-ray Fluorescence Measurements of Bone Lead. Environ Health Perspect 102:690-694 (1994)] presented the currently practiced method for calculating the variance of an in vivo measurement once a calibration line has been established. This paper corrects typographical errors in the method published by those authors; presents a crude estimate of the measurement error that can be acquired without computational peak fitting programs; and draws attention to the measurement error attributable to covariance, an important feature in the construct of the currently accepted method that is flawed under certain circumstances. (+info)
A pilot study examining changes in dust lead loading on walls and ceilings after lead hazard control interventions.
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The U.S. Department of Housing and Urban Development (HUD) guidelines on lead hazard control instruct contractors to clean floors, windows, walls, ceilings, and other horizontal surfaces to remove lead-contaminated dust and debris after lead interventions are conducted. This dust removal activity adds costs to each project. The need to clean floors and windows is well documented in the HUD guidelines. However, there is substantially less documentation to support the recommendation to clean walls and ceilings. We examined whether it is necessary to clean walls and ceilings after lead hazard control (LHC) interventions by comparing dust lead loadings measured on these surfaces before an LHC intervention to dust lead loadings after the intervention. Twenty-two dwelling units undergoing substantial LHC measures consistent with the HUD guidelines were enrolled in the study. There was a significant increase in dust lead loading on walls and ceilings between the pre- and postintervention. The change in wall dust lead loading was substantial and created potentially harmful lead exposures. Although statistically significant, the change in ceiling dust lead loading was minimal and the postintervention dust lead loadings were far below the existing federal floor dust lead clearance standard. These results strongly support the recommendations in the HUD guidelines to clean walls after LHC interventions and do not provide sufficient justification to alter the current recommendation to clean ceilings after lead work. (+info)
Biomarkers of lead exposure.
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Biomarkers of exposure, effect, and susceptibility are reviewed in relation to lead exposure. Of the biomarkers of lead exposure, blood lead (Pb-B), mainly red cell lead, is a representative of soft tissue lead, and most widely used as measures of body burden and absorbed (internal) doses of lead. Urine lead (Pb-U) as well as plasma lead (Pb-P) increases exponentially with increasing Pb-B under a steady-state situation and is a reflection of recent exposure. The amount of lead in plasma and urine (MPb-P and MPb-U) after administration of a chelating agent (e.g. CaEDTA) can be useful for biomarkers of internal exposure of lead, reflecting the mobilizable pool of lead which consists of mainly blood and soft tissue lead with only a small fraction derived from bones. The critical effects in bone marrow arise mainly from the interaction of lead with some enzymatic process responsible for heme synthesis. The effects can be used for the biomarkers of effects. They are the inhibition of delta-aminolevulinic acid dehydratase (ALAD) and the variation in some metabolite concentrations (e.g. delta-aminolevulinic acid in urine (ALA-U), blood (ALA-B) or plasma (ALA-P), coproporphyrin in urine (CP), zinc protoporphyrin (ZP) in blood). The activities of pyrimidine nucleotidase (P5'N) and nicotinamide adenine dinucleotide synthetase (NADS) in blood are also decreased in lead exposure, and nucleotide contents in blood is altered in lead exposure. These effects of lead on human can be also useful biomarkers of effect. The differences in levels of heme precursors between two types of ALAD genotypes might be attributable to those in the affinity of different ALAD isozymes to lead. ALAD1 homozygotes have higher levels of ZP and ALA in comparison with ALAD2 carriers at the high lead exposure, suggesting that ALAD1 homozygotes might be more susceptible for disturbance in heme biosynthesis by lead than ALAD2 carriers. (+info)