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The author reflects on the evolving definition of lead poisoning. He mentions that lead poisoning has been acknowledged for very long years, but still remains as an environmental and occupational hazard around the world. The author cites the chelation therapy as the often recommended to remove lead from the body, however, negative balance occurs naturally over weeks.

Suggests that the racial differences in blood lead levels and the incidence of hypertensive renal disease may be mediated, in part, by dietary calcium. Information on the second National Health and Nutrition Examination Survey.

The Finnish Institute of Occupational Health (FIOH) has received support from the World Health Organization (WHO) and the International Labor Office (ILO) to publish the African Newsletter on Occupational Health and Safety. The African Newsletter on Occupational Health and Safety should not be a medium for industry propaganda, or the source of misinformation among the workers of Africa. Instead, FIOH should provide the same level of scientific information in Africa that it does in Finland and other developed countries.

Background: Occupational exposure to lead and solvents has declined steadily over the past 20 years, however, construction workers continue to be exposed to these neurotoxicants. The purpose of this study was to investigate the cognitive effects of chronic occupational exposure to lead and solvents., Method: Based on K-XRF of tibial bone lead and occupational history of solvent exposure, subjects were classified into four exposure groups: lead (N = 40), solvent (N = 39), lead/solvent (N = 45), and control (N = 33). All subjects completed tests to assess concentration, motor skills, memory, and mood., Results: Relative to controls, the lead, solvent, and lead/solvent groups performed significantly more poorly on a test of verbal memory, while the lead and lead/solvent groups were slower than the solvent and control groups on a task of processing speed. Bone lead was a significant predictor of information processing speed and latency of response while solvent exposure was a significant predictor of verbal learning and memory., Conclusions: Bone lead was associated with slower speed of processing while exposure to lead and/or solvents reduced efficiency of verbal learning., (Copyright 2003 Wiley-Liss, Inc.)

Using modern technology, minute quantities of LMWP, prostanoids, growth factors, intra-renal and extra-renal enzymes can be measured in urine. Excretory patterns that are characteristic for site and mechanism of renal injury often can be found. It is possible to recognise urinary biomarker patterns that suggest the putative environmental nephrotoxin. Our own studies performed in subjects with low level occupational and environmental exposures in New Jersey confirm the pattern specificity and threshold effects for Cr, Hg and Pb. In addition, we have been able to show that increased NAG and IAP excretion following Pb exposure correlates with current (blood Pb) but not with the cumulative Pb burden (bone Pb). The relatively specific characteristic patterns of biomarker excretion are lost as renal failure progresses. Moreover, renal injury that results in tubular proteinuria may not progress to renal failure. Nevertheless, urine biomarkers can help to establish acceptable levels and identify the need for long term surveillance to ascertain when clinical renal disease may result.

Occupational renal diseases provide models for understanding environmental renal diseases. Kidney damage in a few workers induced by heavy exposure to identifiable toxins indicates what to expect among the large population exposed to low levels of toxins dispersed in the larger environment. Occupational and environmental renal diseases present a unique opportunity for primary prevention as well as the diagnostic challenge of long latency and multifactorial etiology. The occupational and environmental toxins that cause chronic renal disease include the heavy metals (Pb, Cd, Hg, As, Cr, U), organic compounds sometimes referred to as solvents, silica, and beryllium. Toxins encountered as medicinal agents such as germanium, gold, and aluminum will not be considered. This review will update major contributions to the subject which have appeared over the past half decade.

Certain chromium compounds are known to be nephrotoxic, but renal damage from long-term environmental or occupational exposure to chromium has not been documented. To detect possible preclinical renal damage, we tested the urine of 55 lifelong residents of an area contaminated with chromium landfill. The levels of four proteins were determined in urine samples: (1) human intestinal alkaline phosphatase, (2) tissue nonspecific alkaline phosphatase, (3) N-acetyl-beta-D-glucosaminidase, and (4) microalbumin. No elevated levels of proteins were found, and there were no significant correlations between urine protein and urine chromium concentrations. We concluded that long-term environmental exposure to chromium dust did not lead to tubular proteinuria.

We used in vivo tibial K-x-ray fluorescence for clinical evaluation of bone lead stores in 31 patients suspected of excessive lead absorption. Four clinical situations were examined: (1) postchelation therapy, (2) renal failure, (3) home exposure, and (4) occupational exposure. K-x-ray fluorescence assisted in determining the magnitude of body lead stores in patients with known excessive lead exposure. Serial measurements revealed a reduction in bone lead that occurred over the years, during which there was an absence of continued exposure; this reduction occurred more rapidly during chelation therapy. Sustained high bone lead levels following chelation therapy in two children were consistent with elevated lead stores from prior pica. In a patient with renal failure, K-x-ray fluorescence demonstrated massive lead stores at a time when chelation testing was not possible. In other cases, bone lead levels indicated the possible contribution of lead nephropathy to renal diseases of other etiologies. In individuals exposed to lead during home renovations, K-x-ray fluorescence provided reassurance that past exposure did not result in elevated body lead stores decades later. In the occupational setting, K-x-ray fluorescence documented cumulative lead stores in workers whose exposures varied in intensity and duration. The examples discussed here show how physicians can use K-x-ray fluorescence to deal with practical questions of patient management. As the test becomes more generally available, its safety, specificity, and simplicity should make it an important alternative to cumbersome chelation tests and potentially misleading blood lead measurements.

As toxic pollution spreads throughout New Jersey, the environment induces illness and the fear of illness in an ever-increasing population. The questions to ask physicians and residents of New Jersey are: Who will share the burden? What is the cost of this burden?

The chelating agent, CaNa2EDTA, has proven useful for both the diagnosis and treatment of lead poisoning. The EDTA lead-mobilization test has demonstrated the presence of excessive body lead stores when blood concentrations were "normal." The EDTA lead-mobilization test is, however, impractical because it requires injections and timed urine collections. Bone lead measured in biopsy specimens by atomic absorption spectroscopy shows a good correlation with chelatable lead. Over 95% of the body stores of lead are retained in bone with a biological half-life approximating two decades. The half-life of lead in blood, on the other hand, approximates one month. Bone, therefore, provides a good estimate of cumulative lead absorption. In vivo tibial K x-ray fluorescence (XRF) is a safe, specific and reliable technique for the non-invasive measurement of elevated bone lead concentrations. K XRF measures lead to a depth of about 2 cm in cortical bone and is largely independent of geometric factors because lead is measured relative to bone calcium. In vivo tibial K XRF can therefore replace the EDTA lead-mobilization test and bone biopsies for assessing body lead stores and for following the efficacy and endpoint of deleading during chelation therapy.

Environmental toxicants, including those from industrial sources, represent potentially preventable causes of chronic kidney disease. The etiology of chronic renal failure of recognized occupational origin (other than malignancies) is reviewed, including that for heavy metals, organic solvents, beryllium, and silicon.

The separation of occupational and environmental disease from the mainstream of medical practice has deep roots in the culture of the profession. Medical practice centered on individual patient care as nineteenth-century science yielded the therapeutic triumphs of the twentieth century. Social issues seemed remote to medical practitioners as the rewards of scientifically based therapies upstaged the unglamorous aspects of preventive medicine. Public health was left to politicians and bureaucrats. Victorian ambivalence toward the less successful members of society reinforced the isolation of medicine from public policy. As a consequence, physicians are largely ignored in contemporary debates about environmental hazards, to the detriment of both society and the profession.

The similarity of lead and cadmium nephropathy to Balkan endemic nephropathy warrants careful reevaluation of the possibility that these nephrotoxic metals contribute to the production of the endemic renal disease. Low-level environmental exposure may result in a relationship between the concentration of the metals in tissue storage sites and biological fluids that differs from that encountered after occupational exposure. Urine and blood concentrations may therefore be inadequate measures of exposure. Lead is accumulated in the skeleton and cadmium in the liver and kidneys with biological half lives approximating a decade. Non-invasive in vivo x-ray fluorescence or neutron activation analysis can therefore be used to measure cumulative tissue stores. Multiple regression analysis of epidemiologic data could reveal the relative contribution of causal factors, including lead and cadmium, and help to distinguish Balkan endemic nephropathy from other renal diseases using rigorous diagnostic criteria. As long as Balkan endemic nephropathy remains a diagnosis of exclusion, the accuracy of the diagnosis of other renal disease determines the reliability of identification of the endemic disease.

In the past, lead poisoning was recognized when classical symptoms of acute intoxication were present and the blood lead was elevated. The (ethylenediamine tetracetatic acid (EDTA) test is presently the most reliable method for detecting excessive lead stores. We used the EDTA lead mobilization test to demonstrate excessive past lead absorption as a cause of renal disease in lead workers and in both gouty and hypertensive patients with renal failure. These studies show that lead nephropathy occurs in the absence of acute intoxication and that occult poisoning often goes unrecognized because of inappropriate diagnostic criteria.

Hypertension of unknown cause is generally termed "essential." Because hypertension has long been considered a possible complication of lead poisoning and the EDTA lead-mobilization test has proved to be a sensitive indicator of excessive body stores of lead, we used this test to evaluate cumulative past lead absorption in 48 men diagnosed as having essential hypertension. Patients who had hypertension with reduced renal function (i.e., serum creatinine level greater than 1.5 mg per deciliter [133 mumols per liter]) had significantly larger amounts of mobilizable lead than did patients who had hypertension without renal impairment. The increase in mobilizable lead was not due to the renal disease itself, since 22 control patients without a history of essential hypertension but with comparable renal impairment from known causes excreted significantly less lead chelate during the three-day test. These data suggest that lead may have an etiologic role in the renal disease of some patients usually designated as having "essential" hypertension.

Deposition of calcium oxalate is responsible for the pathologic manifestations of oxalosis and may contribute to multiorgan dysfunction in uremia and to the progression of renal damage after renal failure is established. We have developed a rat model of oxalosis using a single intravenous injection of sodium oxalate, 0.3 mmol./kg. body weight, in rats. Polarized light microscopy and section freeze-dry autoradiography were used to identify 14C-oxalate within the renal parenchyma and in extrarenal organs. 14C-oxalate crystals under three mu in length were identified within one min. of injection in proximal tubule lumens. Section freeze-dry autoradiography showed occasional minute crystals within glomeruli, heart, lung and liver at one hr. In contrast to concentrative cellular uptake demonstrated in rat renal cortical slices in vitro, intracellular accumulation of 14C-oxalate could not be detected in vivo. Within the first 24 hr., renal oxalate retention reached a maximum of 25 +/- 4 per cent of the injected dose/gm. kidney compared to a maximum of only 7 +/- 3 per cent/gm. kidney after intraperitoneal administration. Although less than one per cent dose/gm. kidney remained after one week, crystal fragments were scattered throughout the cortex and medulla, often surrounded by foci of interstitial nephritis. The retention of crystals in kidney and other body organs following i.v. oxalate provides a model of oxalosis which stimulates pathophysiologic events in a variety of clinical situations characterized by transiently or persistently elevated serum oxalate.

An adult presenting with anemia and seizures was found to have lead poisoning. Chelation therapy undertaken before the source of exposure was known was accompanied by clinical improvement. Recurrence of an excessive body lead burden despite chelation led to the discovery of pica for lead-contaminated garden soil. Lead nephropathy progressed when the geophagia was resumed.