+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      Study of Lead Exposure from Automobile Exhaust as a Risk for Nephrotoxicity among Traffic Policemen

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Background: Traffic policemen are the most exposed population to lead (Pb) from automobile exhaust. There has been increasing concern about the possible harmful effects of Pb from automobile exhaust on health of traffic policemen. However, no such study was concerned with the impact of Pb exposure on renal function among them. Therefore, we aimed to study the effect of Pb exposure from automobile exhaust on renal integrity among traffic policemen. Methods: Markers of tubular damage [urinary excretion of β<sub>2</sub>-microglobulin (β<sub>2</sub>M), N-acetyl-β- D-glucosaminidase (NAG), alkaline phosphatase (ALP) and γ-glutamyl transferase (γ-GT)], a marker of glomerular injury (albuminuria), and markers of glomerular filtration [serum creatinine, serum β<sub>2</sub>M and blood urea nitrogen (BUN)] were determined in 43 traffic policemen (Pb-exposed group) and 52 matched healthy persons (control group). Pb levels in blood, urine, hair and nails were determined in the two groups as exposure indices of Pb. Results: The results obtained show that the Pb-exposed group had higher Pb levels in blood, urine, hair and nails than the controls. Among the Pb-exposed group, Pb levels in blood, hair and nails showed significant and positive correlations with the duration of exposure to Pb which is measured as the duration of employment. Among the studied markers of kidney damage, urinary excretion of NAG and albumin were significantly higher in the Pb-exposed group than in the controls. Urinary excretion of NAG was positively correlated with duration of exposure, blood Pb and nail Pb. Urinary albumin was positively correlated with duration of exposure, blood Pb and hair Pb. The other markers of kidney damage were neither elevated nor correlated with exposure indices of Pb. Conclusion: Traffic policemen are liable to Pb toxicity, and the determination of Pb in blood, hair and nails are good markers of such toxicity. In these exposure conditions, kidney damage is possible. Such damage is both tubular and glomerular in nature and can be documented by determination of the urinary excretion of NAG and albumin.

          Related collections

          Most cited references 4

          • Record: found
          • Abstract: found
          • Article: not found

          Mechanisms of lead and cadmium nephrotoxicity.

           R.A. Goyer (1989)
          Exposure to lead results in accumulation in proximal renal tubular lining cells in the form of morphologically discernible inclusion bodies which are lead-protein complexes. Acute nephrotoxicity consists of proximal tubular dysfunction and can be reversed by treatment with chelating agents. Chronic lead nephrotoxicity consists of interstitial fibrosis and progressive nephron loss, azotaemia and renal failure. Potential complications of lead nephropathy include gout and hypertension. Cadmium accumulates in renal tubular lining cells bound to metallothionein, a small protein containing 30% cystine. Metallothionein protects against nephrotoxicity by binding cadmium in a nontoxic form. Renal tubular dysfunction and chronic interstitial fibrosis occur when cadmium levels in the renal cortex exceed the critical concentration of about 200 micrograms/g. Recommendations are made for specific research needs.
            • Record: found
            • Abstract: not found
            • Article: not found

            Use of gel filtration in the assay of urinary enzymes

             M. Werner,  D Maruhn,  M Atoba (1969)
              • Record: found
              • Abstract: not found
              • Article: not found

              Lead nephrotoxicity and associated disorders: biochemical mechanisms


                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                August 2001
                13 August 2001
                : 21
                : 4
                : 274-279
                aClinical Chemistry Laboratory, bDepartment of Nephrology, Urology and Nephrology Center, and cDepartment of Chemistry, Faculty of Science-Mansoura University, Mansoura, Egypt
                46261 Am J Nephrol 2001;21:274–279
                © 2001 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 8, References: 30, Pages: 6
                Self URI (application/pdf):
                Clinical Study


                Comment on this article