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Body lead burden development

Finally, it should be pointed out that, in recent years, techniques have been developed to measure the lead content in bones and teeth in vivo. The method applied is X-ray fluorescence (XRF), and promises to provide a convenient, non-invasive assessment of body lead burden. The possibilities of this technique are described and reviewed by Hu et al. (1989) and Shapiro et al. (1978). [Pg.382]

C. Urinary lead excretion increases and decreases more rapidly than blood lead. Normal urinary lead excretion is less than 50 mcg/day. Several empiric protocols that measure 6- or 24-hour urinary lead excretion after calcium EDTA challenge have been developed to identify persons with elevated body lead burdens. However, since chelatable lead predominantly reflects lead in soft tissues, which in most cases already correlates satisfactorily with blood lead, chelation challenges are seldom indicated in clinical practice. [Pg.240]

Otto, D. A., Benignus, V. A., Muller, K. E. and Barton, C. N. (1981). Effects of age and body lead burdens on CNS function in young children. I. Slow potentials. Electroencephalogr. Clin. Neurophysiol, 52, 229 Overmann, S. R. (1977). Behavioral effects of asymptomatic lead exposure during neonatal development in rats. Toxicol Appl Pharmacol, 41, 459 Overmann, S. R., Zimmer, L. and Woolley, D. E. (1981). Motor development, tissue weights and seizure susceptibility in perinatally exposed rats. Neurotoxicology, 2, 125... [Pg.147]

Drug contamination In India, a 39-year-old man with jaundice developed vomiting and severe abdominal pain after consuming 10-15 ml of kadda (in local language) every morning on an empty stomach for 10 days [24" ]. Lead poisoning was confirmed when the blood lead concentration was measured. A combination of chelation therapy and nutritional supplements reduced the body lead burden. Tlie original syrup had been consumed and could not be tested for lead content. [Pg.992]

The development over the past several decades of x-ray fluorescence (XRF) instrumentation that is capable of measuring bone lead levels noninvasively has contributed to evaluations of body lead burdens and long-term lead... [Pg.17]

In summary, the temporal stability of PbB is a function of age and stage of development. PbB values are most labile in infancy and tend to become more stable with age. In older children this stability is mainly in the form of preservation of rank order, whereas in adults there is also rather good preservation of absolute PbB values. These data suggest that single PbB measurements are least reliable in infancy but become more reliable with increasing age of the subject. The stability of the rank order in children as they get older may represent the relative level of body lead burden in bone. This would parallel what is seen in retired lead workers, where the main determinant of PbB is the bone lead burden (Hryhorczuk et al, 1985). [Pg.137]

Most current epidemiological research has been based on replication from other studies investigating children. The search for effects has become the motivating force, with the result that studies often appear to lack a valid model to explain these effects. Equally there needs to be a model to explain differences in body lead burden in different children from similar environments, and some of the prospective studies have now developed sophisticated models to do this. [Pg.497]

Sauerhoff, M. W. and Michaelson, I. A. (1973). Hyperactivity and brain catecholamines in lead-exposed developing rats. Science, 182, 1022 Scarborough, J. (1969). Roman Medicine. (New York Cornell University Press) Schlaepfer, W. W. (1969). Experimental lead neuropathy a disease of the supporting cells in the peripheral nervous system. J. Neuropathol. Exp. Neurol., 21, 401 Schroeder, H. A. and Mitchener, M. (1971). Toxic effects of trace elements on the reproduction of mice and rats. Arch. Env. Health, 23, 102 Schroeder, H. A. and Tipton, I. H. (1968). The human body burden of lead. Arch. Env. Health, 17, 965... [Pg.149]

We have collected much, often redundant, data, and are now able to examine them systematically to determine which measures are the most useful in predicting a child s mental development. We really do not know how or when low levels of lead contamination disturb brain development. Thus, without imposing any prior restrictions, we should evaluate many measures of lead burden. In the absence of an assay for the bioactive species (ionic ) of lead at the target organ (brain) at the critical time(s), blood lead measurements (which are mostly erythrocyte bound lead, and which represent a very small fraction of the body s total lead level) were used to assess the child s body burden. [Pg.475]

Most of the body burden of lead resides in bone a portion of the maternal bone lead stores is transferred to the fetus during gestation and incorporated into fetal bone during the development of the fetal skeleton. [Pg.357]

Lead. One of the most familiar of the particulates in air pollutants is lead, with young children and fetuses being the most susceptible. Lead can impair renal function, interfere with the development of red blood cells, and impair the nervous system, leading to mental retardation and even blindness. The two most common routes of exposure to lead are inhalation and ingestion. It is estimated that approximately 20% of the total body burden of lead comes from inhalation. [Pg.38]

Taylor JR Disorders of the nervous system, in Principles and Practice of Environmental Medicine. Edited by Tarcher AB. New York, Plenum, 1992, pp 217-240 Thacker SB, Hoffman DA, Smith J, et al Effect of low-level body burdens of lead on the mental development of children limitations of meta-analysis in a review of longitudinal data. Arch Environ Health 47 336-346,1992 Todd AC, Wetmur JG, Moline JM, et al Unraveling the chronic toxicity of lead an essential priority for environmental health. Environ Health Perspect 104 (suppl 1) 141-146, 1996... [Pg.134]

To develop more sensitive techniques to quantify human lead body burden, particularly lead in bone. [Pg.9]

To this end, a variety of analyses have been developed to determine both lead body burden and the effects of lead on critical cellular processes (Table XVIII)... [Pg.113]

The presence of EDCs in the body affects functions such as metabolic and reproductive processes including embryonic development, gonadal formation, sex differentiation, growth, and digestion. They are plausibly linked to diseases including prostate cancer, breast cancer, attention deficit/hyperactivity disorder (ADHD), asthma, and reproductive problems (Myers et al, 2009 Swan et al., 2000). Though not toxins in the conventional sense, EDCs lead to serious adverse health outcomes in both animals and humans. Conditions linked to exposure to EDCs, such as reproductive problems, incidence of certain cancers, asthma, obesity, diabetes, behavioral or learning disorders, and ADHD, are on the increase worldwide. Of this disease burden, 24-33% has been attributed to environmental contributions (Smith et al., 1999). [Pg.186]

Beck, B.D., Mattuck, R.L., Bowers, T.S., Muir, B., 2001. The development of a stochastic physiologically-based pharmacokinetic model for lead. Sci. Total Environ. 274, 15—19. Bergdahl, I.A., Schulz, A., Gerhardsson, L., Jensen, A., Skerfving, S., 1997. Lead concentrations in human plasma, urine and whole blood. Scand. J. Work Environ. Health 23, 359—363. Bert, J.L., van Dusen, L.J., Grace, J.R., 1989. A generalized model for the prediction of lead body burdens. Environ. Res. 48, 117—127. [Pg.341]

Once absorbed, Cd is very poorly excreted, mainly in urine and feces. In humans the amount excreted daily in urine represents only about 0.005-0.015% of the total body burden [39,96]. The mean concentration of urinary Cd in people not exposed to high Cd levels is 0.5-2.0 pg/L [23] and increases with age [97-99] and body burden [2,100,101]. Smokers have higher urinary excretion than non-smokers [97,99]. Increased urinary Cd excretion occurs when tubular proteinuria develops [100,102]. Most of the Cd in urine is transported bound to MT. Tohyama et al. [103] found good correlation between urinary MT and Cd in the general population as well as in smokers [104]. Roels et al. [105] confirmed this correlation in Cd workers. Over a range of doses, an increase in urinary excretion of Cd is associated with an increase of Cd in the renal cortex [106-108]. Chronic studies on several mammalian species have shown that urinary excretion of Cd increases slowly for a considerable time but, as kidney dysfunction develops, a sharp increase in excretion occurs [5,106,107,109]. This leads to a decrease in renal and liver Cd concentrations [5,106]. [Pg.425]

An increased mortality from cerebrovascular disease has been observed in a study on lead battery workers (Dingwall-Fordyce and Lane, 1963). An association between lead absorption and the development of hypertension has been claimed, initially in lead-exposed workers. In a US population-based study on adult males, lead was found to be significantly related to both systolic and diastolic blood pressure after controlling for a number of confounding variables (Schwartz, 1985). However, a British population-based study on men aged 40-59 found only a very weak association between PbB and either systolic or diastolic blood pressure. The investigators commented on the problem of adjusting adequately for all relevant confounders, and concluded that it is premature to consider that an elevated lead body burden has a causal influence on blood pressure (Pocock et al, 1985). [Pg.125]


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