Body lead burden

Landrigan PJ, Froines JR, Mahaffey KR. 1985. Body lead burden Summary of epidemiological data and its relation to environmental sources and toxic effects Chapter 14. In Magaffev KR, ed. Dietary and environmental lead Human health effects. Amsterdam, The Netherlands Elsevier Sci Publisher BV, 421451. 

Otto DA, Benignus VA, Muller KE, et al. 1981. Effects of age and body lead burden on CNS function in young children I. Slow cortical potentials. Electroencephalogr Clin Neurophysiol 52 229-239. 

In the cladoceran Daphnia magna, about 90% of the total body lead burden is adsorbed to the exoskeleton (Berglind et al. 1985). In animals with a vertebral column, total amounts of lead tend to increase with age. By far the most lead is bound to the skeleton, especially in areas of active bone formation (Barth et al. 1973 Tsuchiya 1979 USEPA 1980 Hejtmancik et al. 1982 Mykkanen etal. 1982 Peter and Strunc 1983 De Michele 1984 Eisler 1984 Berglind etal. 1985 Marcus 1985). The retention of lead stored in bone pools poses a number of difficulties for the usual multicompartmental loss-rate models. Some lead in bones of high medullary content, such as the... 

Marsden PA Increased body lead burden - cause or consequence of chronic renal insufficiency N Eng J Med 2003 348 345-... 

Lin J-A, Ho H-H, Yu C-C. Chelation therapy for patients with elevated body lead burden and progressive renal insufficiency. A randomized controlled trial. Ann Intern Med 1999 130 7-13. 

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). 

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. 

D. Noninvasive in vivo x-ray fluorescence measurement of lead In bone, a test predominantly available in research settings, may provide the best index of long-term cumulative lead exposure and total body lead burden. 

An additional course of treatment may be considered based on posttreatment blood lead levels and on the persistence or recurrence of symptoms. Although blood lead levels may decline by more than 50% during treatment, patients with high body lead burdens may experience rebound to... 

Nationwide, there has been a significant decline in lead concentrations of whole freshwater fish from 1976-77 to 1984, continuing a decrease that became evident in 1978-79. Nationwide monitoring of freshwater fishes conducted periodically by the U.S. Fish and Wildlife Service showed that whole body lead burdens were highest for Atlantic coast streams, the Great Lakes drainage, the Mississippi River system, the Columbia Etiver... 

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... 

King BG (1971) Maximum daily intake of lead without excessive body lead-burden in children. Am. J. Dis. Child. 122 337... 

In addition to a large database on lead exposures assembled empirically, a number of biokinetic models to ascertain exposure biomarkers and body lead burdens exist in the more recent lead literature, mainly in the form of such biomarkers of exposure as PbB. These predictive models of systemic lead exposure are of differing complexity and utility in diverse exposure settings. Historically, they can be defined as classical compartment models, a hybrid of the compartmental and physiologically based pharmacokinetic (PB-PK) models or the PB-PK model type. 

Lead exposures in the Roman Imperial era sufficient for chronic, multi-generational reproductive and developmental toxicity are supported by data from Nriagu (1983a,b, 1985) and Eisinger (1982) for estimates of lead exposures and likely body lead burdens of Romans of the period, stratified by class. That is, the most severe toxic responses would have been expressed... 

Concentrations of lead in the various environmental media described in this section are presented for extended periods. The available data that meet minimal statistical and measurement criteria generally only extend from the late 1960s/early 1970s to the present. The purposes of a wide temporal look at environmental lead concentrations are several. First, the nature of lead as an accumulating contaminant in the bodies of human populations requires an appreciation of the amounts of environmental lead that existed in past decades. As noted earlier, lead levels in media have been changing, mainly downward, so that current human body lead burdens are only partially quantifiable from current lead intakes into body compartments. Secondly, the use of predictive, biokinetic models of human lead exposures for simulating Ufe-time lead exposures requires knowledge of lead intakes from the earliest periods of life. 

A related qualifier is the extent to which some particular model for some site- or scenario-specific use is flexible for multiple uses by the regulator or risk manager. For example, biokinetic models such as EPA s lEUBK model for children (U.S. EPA, 1994a,b,c) or the O Flaherty PB-PK model for children and adults (O Flaherty, 1995, 1998) theoretically permit assessment of the results of altered land uses, altered population demographics, or impact of lead remedial actions when projecting into future years for body lead burdens indexed by PbB. Such applications should not require recalibration with empirical data for every use. 

Few studies in the earlier literature used pulse pressure (PP) measures (SBP—DBP). As to the exposure biomarkers, those should be more toxicokinetically accurate in capturing both body lead burden and changes in that burden. While bone Pb measurements may have more scatter to their precision, they are more accurate in reflecting the most predictive exposure biomarker, the more important parameter. 

The very low mean PbBs in these women and those men and women in the Muntner et al. (2003) U.S. NHANES III provided good evidence that the relative threshold for Pb nephrotoxic effects with environmental exposures in the general population is an order of magnitude less than was observed in the older occupational Pb literature, 60 pg/dl. Low body lead burdens indexed as chelatable Pb amounts of <80 pg/dl were also found to be a predictor of decreased kidney function (Lin et al., 2006). Taiwanese chronic kidney disease patients (N = 108) without diabetes were assigned to chelation and nonchelation groups. Those patients who were not periodically chelated over a 24-month testing period sustained a mean reduction in GFR of 4.6 ml/min/1.732 m and showed increased serum creatinine. 

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