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Markers of early renal changes induced by industrial pollutants. II. Application to workers exposed to lead

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TLDR
The recent recommendation by the American Conference of Governmental Industrial Hygienists (ACGIH) of 5 micrograms Cd/g creatinine in urine as the biological exposure limit for occupational exposure to Cd appears justified, although for most of the effects occurring around this threshold the link with the subsequent development of overt Cd nephropathy is not established.
Abstract
The present study has been carried out in the framework of a collaborative research project on the development of new markers of nephrotoxicity. A battery of more than 20 potential indicators of renal changes has been applied to 50 workers exposed to lead (Pb) and 50 control subjects. After application of selection criteria 41 exposed and 41 control workers were eventually retained for the final statistical analysis. The average blood Pb concentration of exposed workers was 480 micrograms/l and their mean duration of exposure was 14 years. The battery of tests included parameters capable of detecting functional deficits (for example, urinary proteins of low or high molecular weight), biochemical alterations (for example, urinary eicosanoids, glycosaminoglycans, sialic acid) or cell damage (for example, urinary tubular antigens or enzymes) at different sites of the nephron or the kidney. The most outstanding effect found in workers exposed to Pb was an interference with the renal synthesis of eicosanoids, resulting in lower urinary excretion of 6-keto-PGF1 alpha and an enhanced excretion of thromboxane (TXB2). The health significance of these biochemical alterations, detectable at low exposure to Pb is unknown. As they were not associated with any sign of renal dysfunction, they may represent reversible biochemical effects or only contribute to the degradation of the renal function from the onset of clinical Pb nephropathy. The urinary excretion of some tubular antigens was also positively associated with duration of exposure to Pb. Another effect of Pb that might deserve further study is a significant increase in urinary sialic acid concentration.

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References
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Journal ArticleDOI

Renal effects of cadmium body burden of the general population

TL;DR: Five variables (urinary excretion of retinol-binding protein, N-acetyl-beta-glucosaminidase, beta 2-microglobulin, aminoacids, and calcium) were significantly associated with the urinaryexcretion of cadmium (as a marker of cad mium body burden), suggesting the presence of tubular dysfunction.
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Cadmium and health: A toxicological and epidemiological appraisal Volume II: Effects and response

TL;DR: In this article, the authors discuss the following: Respiratory effects. Renal effects. Carcinogenic and genetic effects. Critical organs, critical concentrations, and whole body Dose-Response Relationships.
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Cold Urticaria: Release into the Circulation of Histamine and Eosinophil Chemotactic Factor of Anaphylaxis during Cold Challenge

TL;DR: This initial observation of release of eosinophil chemotactic factor of anaphylaxis in vivo along with histamine assigns the mast cell a central role in cold urticaria.
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The clinical significance of inhibition of renal prostaglandin synthesis

TL;DR: The purpose of this editorial review is to analyze the physiologic significance of renal prostaglandin synthesis and the pathophysiologic consequences of inhibition of prostag landin production through the use of nonsteroidal anti-inflammatory drugs.
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In vivo measurement of liver and kidney cadmium in workers exposed to this metal: Its significance with respect to cadmium in blood and urine

TL;DR: It has been found that kidney dysfunction is likely to develop in workers with CdL between 30 and 60 ppm and that almost all the Cd workers above 60 ppm evidence renal dysfunction, and there exists a range of critical CdKc levels, i.e., approximately from 160 to 285 ppm.
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