Indian Journal of Clinical Biochemistry

, Volume 27, Issue 1, pp 83–89 | Cite as

Impact of Chronic Lead Exposure on Selected Biological Markers

  • Ambica P. Jangid
  • P. J. JohnEmail author
  • D. Yadav
  • Sandhya Mishra
  • Praveen Sharma
Original Article


Lead poisoning remains a major problem in India due to the lack of awareness of its ill effects among the clinical community. Blood lead, δ-aminolevulinic acid dehydratase (δ-ALAD) and zinc protoporphyrin (ZPP) concentrations are widely used as biomarkers for lead toxicity The present study was designed to determine the impact of chronic lead exposure on selected biological markers. A total of 250 subjects, of both sexes, ranging in age from 20 to 70 years, were recruited. On the basis of BLLs, the subjects were categorized into four groups: Group A (BLL: 0–10 μg/dl), Group B (BLL: 10–20 μg/dl). Group C (BLL: 20–30 μg/dl) and Group D (BLL: 30–40 μg/dl) having BLLs of 3.60 ± 2.71 μg/dl, 15.21 ± 2.65 μg/dl, 26.82 ± 2.53 μg/dl and 36.38 ± 2.83 μg/dl, respectively. Significant changes in biological markers due to elevated BLLs were noted. The relation of BLL and biological markers to demographic characteristics such as sex, habits, diet and substances abuse (smoking effect) were also studied in the present investigation. Males, urban population, non-vegetarians, and smokers had higher blood lead levels. δ-ALAD activity was found to be significantly lower with increased BLL (P < 0.001), while the ZPP level was significantly higher with increased BLL (P < 0.001). Further, BLL showed a negative correlation with δ-ALAD (r = −0.425, P < 0.001, N = 250) and a positive correlations with ZPP (r = 0.669, P < 0.001, N = 250). Chronic lead exposure affects the prooxidant-antioxidant equilibrium leading to cellular oxidative stress.


Blood lead level δ-amino levulinic acid dehydratase Zinc protoporphyrin 


  1. 1.
    Sakai T. Reviews on biochemical markers of lead exposure with special emphasis on heme and nucleotide metabolism. Sangyo Eiseigaku Zasshi. 1995;40:314–7.Google Scholar
  2. 2.
    Somashekaraiah BV, Venkaiah B, Prasad AR. Biochemical diagnosis of occupational exposure to lead toxicity. Bull Environ Contam Toxicol. 1990;44:268–75.PubMedCrossRefGoogle Scholar
  3. 3.
    Phillip AT, Gerson B. Lead poisoning-Part I. Incidence, etiology, and toxicokinetics. Clin Lab Med. 1994;14:423–44.Google Scholar
  4. 4.
    Gurer-Orhan H, Sabir HU, Ozgunes H. Correlation between clinical indicators of lead poisoning and oxidative stress parameters in controls and lead-exposed workers. Toxicology. 2004;195:147–54.PubMedCrossRefGoogle Scholar
  5. 5.
    Fernandez FJ. Micromethod for lead determination in whole blood by atomic absorption, with use of the graphite furnace. Clin Chem. 1975;21:558–61.PubMedGoogle Scholar
  6. 6.
    Wigfield DC, Farrant JP. Assay of delta-aminolaevulinate dehydratase in 10 microlitre blood. Clin Chem. 1981;27(1):100–3.PubMedGoogle Scholar
  7. 7.
    Blumberg WE, Esinger J, Lamola AA, Zuckerman DM. The haematofluorometer. Clin Chem. 1977;23:270–1.PubMedGoogle Scholar
  8. 8.
    CDC (Centers for Disease Control and Prevention). Preventing lead poisoning in young children. Public Health Service, Centers for Disease Control, US Department of Health and Human Services, Atlanta, Georgia. 1991. Accessed 1 Jan 2008.
  9. 9.
    WHO (World Health Organization). International Programme on Chemical Safety (IPCS). Inorganic lead. Environmental health criteria 165. Geneva. 1995. Accessed 21 Apr 2008.
  10. 10.
    Baghurst PA, McMichael AJ, Wigg NR, Vimpani GV, Robertson EF, Roberts RJ, Tong SL. Environmental exposure to lead and children’s intelligence at the age of seven years. New Engl J Med. 1992;327:1279–84.PubMedCrossRefGoogle Scholar
  11. 11.
    Muntner P, Menke A, DeSalvo KB, Rabito FA, Batuman V. Continued decline in blood lead levels among adults in the United States: the National Health and Nutrition Examination Surveys. Arch Intern Med. 2005;165:2155–61.PubMedCrossRefGoogle Scholar
  12. 12.
    Roels HA, Lauwerys RR, Buchet JP, Vrelust MT. Response of free erythrocyte porphyrin and urinary-delta-aminolevulinic acid in men and women moderately exposed to lead. Int Arch Arbeitsmed. 1975;34:97–108.Google Scholar
  13. 13.
    Grandjean P, Lintrup J. Erythrocyte–Zn–protoporphyrin as an indicator of lead exposure. Scand J Clin Lab Invest. 1978;38:669–75.PubMedCrossRefGoogle Scholar
  14. 14.
    Mohammad IK, Mahdi AA, Raviraja A, Najmul I, Iqbal A, Thuppil V. Oxidative stress in painters exposed to low lead levels. Arh Hig Rada Toksikol. 2008;59:161–8.PubMedGoogle Scholar
  15. 15.
    Sprinkle RV. Leaded eye cosmetics: a cultural cause of elevated lead levels in children. J Fam Pract. 1995;40(4):358–62.PubMedGoogle Scholar
  16. 16.
    Sharma DC, Seervi N, Rawtani J. Effect of environmental lead pollution on hemoglobin and erythrocyte ALAD activity. Indian J Physiol Pharmacol. 2000;44(1):117–8.PubMedGoogle Scholar
  17. 17.
    Quinn MJ, Sherlock JC. The correspondence between U.K. ‘action levels’ for lead in blood and in water. Food Addit Contam. 1990;7:387–424.PubMedCrossRefGoogle Scholar
  18. 18.
    WHO (World Health Organization). Lead in drinking water. Background document of WHO guidelines for drinking water quality, Geneva, WHO (WHO/SDE/WSH/03.04/09). 2003.Google Scholar
  19. 19.
    Ahamed M, Verma S, Kumar A, Siddiqui MK. Delta-aminolevulinic acid dehydratase inhibition and oxidative stress in relation to blood lead among urban adolescents. Hum Exp Toxicol. 2006;25(9):547–53.PubMedCrossRefGoogle Scholar
  20. 20.
    Ahamed M, Singh S, Behari JR, Kumar A, Siddiqui MK. Interaction of lead with some essential trace metals in the blood of anemic children from Lucknow. India Clin Chim Acta. 2007;377(1–2):92–7.CrossRefGoogle Scholar
  21. 21.
    Hulea SA, Olinescu R, Nita S, Crocnan D, Kummerow FA. Cigarette smoking causes biochemical changes in blood that are suggestive of oxidative stress: a case-control study. J Environ Pathol Toxicol Oncol. 1995;14(3–4):173–80.Google Scholar
  22. 22.
    Flora SJS, Singh S, Tandon SK. Plumbism among Indian silver jewellery industry workers. J Environ. Sci Health Part A 1990;25A (2):105–113.Google Scholar
  23. 23.
    Farant JP, Wigfeld DC. Biomonitoring lead exposure with delta-aminolevulinate dehydratase (ALA-D) activity ratios. Int Arch Occup Environ Health. 1982;51:15–24.PubMedCrossRefGoogle Scholar
  24. 24.
    Sandhir R, Julka D, Gill KD. Lipoperoxidative damage on lead exposure in rat brain and its implications on membrane bound enzymes. Pharmacol Toxicol. 1994;74:66–71.PubMedCrossRefGoogle Scholar
  25. 25.
    Ahamed M, Verma S, Kumar A, Siddiqui MK. Environmental exposure to lead and its correlation with biochemical indices in children. Sci Total Environ. 2005;346(1–3):48–55.PubMedGoogle Scholar
  26. 26.
    Austrin KH, Bishap DF, Wetmur JG, Kaul BC, Davidow B, Desnick RJ. Aminolevulinic acid dehydratase isozymes and lead toxicity. Ann NY Acad Sci. 1987;514:23–9.CrossRefGoogle Scholar
  27. 27.
    Sakai T, Morita Y. Delta-aminolevulinic acid in plasma or whole blood as a sensitive indicator of lead effects, and its relation to the other heme-related parameters. Int Arch Occup Environ Health. 1996;68:126–32.PubMedGoogle Scholar
  28. 28.
    Bechara EJ. Oxidative stress in acute intermittent porphyria and lead poisoning may be triggered by 5-aminolevulinic acid. Braz J Med Biol Res. 1996;29:841–51.PubMedGoogle Scholar
  29. 29.
    Sakai T. Biomarkers of lead exposers. Ind Health. 2000;38:127–42.PubMedCrossRefGoogle Scholar
  30. 30.
    Chiba M, Shinohara A, Matsushits K, Watanabe H, Inaba Y. Indices of lead exposure in blood, urine of lead exposed workers, concentrations of major, trace elements, activities of SOD, GsH-Px and catalase in their blood. Tohoku J Exp Med. 1996;178:49–62.PubMedCrossRefGoogle Scholar
  31. 31.
    Goyer H, Clarkson TW. Toxic effects of metals. In: Klassen CD, editor. Casarett and Doull’s toxicology. The basic science of poisons. New York: McGraw-Hill; 2001. p. 830.Google Scholar
  32. 32.
    Jin Y, Liao Y, Lu C. Health effects in children aged 3–6 years induced by environmental lead exposure. Ecotoxicol Environ Saf. 2006;63(2):313–7.PubMedCrossRefGoogle Scholar
  33. 33.
    Marcus AH, Schwartz J. Dose-response curves for erythrocyte porphyrin vs. blood lead, effects of iron status. Environ Res. 1987;44:221–7.PubMedCrossRefGoogle Scholar
  34. 34.
    Onalaja VO, Claudio L. Genetic susceptibility to lead poisoning. Environ Health Perspect. 2000;108:23–8.PubMedGoogle Scholar
  35. 35.
    ATSDR (Agency for Toxic Substances and Disease Registry). Toxicological profile for lead. (Draft for Public Comment). Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service. 2007;232. Accessed 1 Jan 2008.

Copyright information

© Association of Clinical Biochemists of India 2011

Authors and Affiliations

  • Ambica P. Jangid
    • 1
  • P. J. John
    • 1
    Email author
  • D. Yadav
    • 3
  • Sandhya Mishra
    • 3
  • Praveen Sharma
    • 2
  1. 1.Environmental Toxicology Laboratory, Department of ZoologyUniversity of RajasthanJaipurIndia
  2. 2.Department of BiochemistryGovernment Medical CollegeKotaIndia
  3. 3.Department of BiochemistryS.M.S. Medical CollegeJaipurIndia

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