Level of DNA damage in lead-exposed workers.
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Institute of Occupational Medicine and Environmental Health, Laboratory of Genetic Toxicology, Sosnowiec, Poland
Medical University of Silesia, Department of Biochemistry, Katowice, Poland
Institute of Agricultural Medicine, Independent Laboratory of Molecular Biology, Lublin, Poland
University of Information Technology and Management, Department of Public Health, Rzeszów, Poland
Corresponding author
Elżbieta Olewińska   

Laboratory of Genetic Toxicology, Institute of Occupational Medicine and Environmental Health, Sosnowiec, Poland
Ann Agric Environ Med. 2010;17(2):231-236
Lead plays a significant role in modern industry. This metal is related to a broad range of physiological, biochemical and behavioural dysfunctions. The genotoxic effects of lead have been studied both in animals and humans in in vitro systems but results were contradictory. The aim of this study was to investigate the association between DNA damage and occupational exposure to lead in workers. The study population consisted of 62 employees of metalworks exposed to lead in the southern region of Poland. The control group consisted of 26 office workers with no history of occupational exposure to lead. The concentration of lead (PbB) and zincprotoporphyrin (ZPP) in blood samples were measured. The DNA damage was analyzed in blood lymphocytes using alkaline comet assay. The level of DNA damage was determined as the percentage of DNA in the tail, tail length and tail moment. The lead exposure indicators were significantly higher in lead exposed group: PbB about 8.5 times and ZPP 3.3 times. Also, the percentage of DNA in the tail (60.3 ± 14 vs. 37.1 ± 17.6), comet tail length (86.9 ± 15.49 vs. 73.8 ± 19.12) and TM (57.8 ± 17.82 vs. 33.2 ± 19.13) were significantly higher in the study group when compared with the controls; however, the difference between the subgroups was only 5-10%. Years of lead exposure positively correlated with all comet assay parameters (R = 0.21-0.41). Both mean and current PbB and ZPP were correlated with tail DNA % and TM (R = 0.32; R = 0.33; R = 0.24; R = 0.26 and R = 0.34; R = 0.33; R = 0.28 and R = 0.28, respectively). This study shows that occupational exposure to lead is associated with DNA damage and confirmed that comet assay is a rapid, sensitive method suitable for biomonitoring studies.
ATSDR: Toxicological Profile for Lead. U.S. Departament of Heath and Human Services. Public Health Service. Agency for Toxic Substances and Disease Registry, 2007.
Bilban M: Influence of the work environment in a Pb-Zn mine on the incidence of cytogenetic damage in miners. Am J Ind Med 1998, 34, 455–463.
Botta C, Iarmarcovai G, Chaspoul F, Sari-Minodier I, Pompili J, Orsiere T, Bergé-Lefranc JL, Botta A, Gallice P, De Méo M: Assessment of occupational exposure to welding fumes by inductively coupled plasma-mass spectroscopy and by the alkaline comet assay. Environ Mol Mutagen 2006, 47, 284–295.
Cebulska-Wasilewska A, Panek A, Zabinski Z, Moszczyński P, Au WW: Occupational exposure to mercury on genotoxicity and DNA repair. Mutat Res 2005, 586, 102–114.
Chen Z, Lou J, Chen S, Zheng W, Wu W, Jin L, Deng H, He J: Evaluating the genotoxic effects of workers exposed to lead using micronucleus assay, comet assay and TCR gene mutation test. Toxicology 2006, 223, 219–226.
Collins AR: The comet assay for DNA damage and repair. Principles, applications, and limitations. Mol Biotechnol 2004, 26, 249–261.
Danadevi K, Rozati R, Saleha-Banu B, Hanumanth Rao P, Grover P: DNA damage in workers exposed to lead using comet assay. Toxicology 2003, 187, 183–193.
DeBoeck M, Lardau S, Buchet JP, Kirsch-Volders M, Lison D: Absence of significant genotoxicity in lymphocytes and urine from workers exposed to moderate levels of cobalt-containing dust: a cross-sectional study. Environ Mol Mutagen 2000, 36, 151–160.
de Laat WL, Jaspers NGJ, Hoeijmakers JHJ: Molecular mechanism of nucleotide excision repair. Genes Dev 1999, 13, 768–785.
Dušinská M, Collins AR: The comet assay in human biomonitoring: gene-environment interactions. Mutagenesis 2008, 23, 191–205.
Dušinská M, Ficek A, Horská A, Rašlová K, Petrovská H, Vallová B, Drlicková M, Wood SG, Štupáková A, Gasparovič J, Bobek P, Nagyová A, Kováčiková Z, Blažíek P, Liegebel U, Collins AR: Glutathione Stransferase polymorphisms influence the level of oxidative DNA damage and antioxidant protection in humans. Mutat Res 2001, 482, 47–55.
Final Report on Carcinogens Background Document for Lead and Lead Compounds, 2003. Available from:
Fracasso ME, Perbellini L, Solda S, Talamini G, Franceschetti P: Lead induced DNA strand breaks in lymphocytes of exposed workers: role of reactive oxygen species and protein kinase C. Mutat Res 2002, 515, 159–169.
Hoffman H, Hogel J, Speit G: The effect of smoking on DNA effects in the comet assay: a metaanalysis. Mutagenesis 2005, 20, 455–466.
Huang XP, Feng ZY, Zhai WL, Xu JH: Chromosomal aberrations and sister chromatid exchanges in workers exposed to lead. Biomed Environ Sci 1988, 1, 382–387.
IARC: Overall evaluations of carcinogenicity: an updating of IARC monographs. In: Proceedings of the IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, Vol. 1–42, Suppl. 7, 230–232. International Agency for Research on Cancer, Lyon 1987.
Kassie F, Parzefall W, Knasmuller S: Single cell gel electrophoresis assay: a new technique for human biomonitoring studies. Mutat Res 2000, 463, 13–31.
Liao W, McNutt MA, Zhu WG: The comet assay: a sensitive method for detecting DNA damage in individual cells. Methods 2009, 48, 46–53.
Moller P, Knudsen LE, Loft S, Wallin H: The comet assay as a rapid test in biomonitoring occupational exposure to DNA-damaging agents and effect of confounding factors. Cancer Epidemiol Biomarkers Prev 2000, 9, 1005–1015.
Nilsen H, Krokan HE: Base excision repair in a network of defence and tolerance. Carcinogenesis 2001, 22, 987–998.
Onalaja AO, Claudio L: Genetic susceptibility to lead poisoning. Environ Health Perspect 2000, 108, 23–28.
Palus J, Rydzynski K, Dziubaltowska E, Wyszynska K, Natarajan AT, Nilsson R: Genotoxic effects of occupational exposure to lead and cadmium. Mutat Res 2003, 540, 19–28.
Piperakis SM, Visvardis E-E, Sagnou M, Tassiou AM: Effects of smoking and aging on oxidative DNA damage of human lymphocytes. Carcinogenesis 1998, 19, 695–698.
Restrepo HG, Sicard D, Torres MM: DNA damage and repair in cells of lead exposed people. Am J Ind Med 2000, 38, 330–334.
Sakai T: Biomarkers of lead exposure. Ind Health 2000, 38, 127–142.
Singh NP, McCoy MT, Tice RR, Schneider EL: A simple technique for quantification of low levels of DNA damage in individual cells. Exp Cell Res 1988, 175, 184–191.
Srám RJ. Effect of glutathione S-transferase M1 polymorphisms on biomarkers of exposure and effects. Environ Health Perspect 1998, 106, 231–239.
Steinmetz-Beck A, Szahidewicz-Krupska E, Beck B, Poręba R, Andrzejak R: Genotoksyczny efekt przewlekłej ekspozycji na ołów w teście kometkowym. Med Pr 2005, 56, 295–302.
Stęplewski Z:Children’s lead poisoning in the industrial upper Silesian Region of Poland. Zdr Publ 2010, 120, 14–18.
Vaglenov A, Carbonell E, Marcos R: Biomonitoring of workers exposed to lead. Genotoxic effects, its modulation by polyvitamin treatment and evaluation of induced radioresistance. Mutat Res 1998, 418, 79–92.
Valverde M, Fortoul TI, Díaz-Barriga F, Mejía J, del Castillo ER: Genotoxicity induced in CD-1 mice by inhaled lead: differential organ response. Mutagenesis 2002, 17, 55–61.
Valverde M, Ostrosky-Wegman P, Rojas E, Fortoul TI, Meneses F, Ramirez M, Diaz-Barriga F, Cebrian M: The application of single cell gel electrophoresis or comet assay to human monitoring studies. Salud Publica Mex 1999, 41, 109–113.
Valverde M, Rojas E: Environmental and occupational biomonitoring using the comet assay. Mutat Res 2009, 681, 93–109.
Wetmur JG, Lehnert G, Desnick RJ: The delta-aminolevulinate dehydratase polymorphism: higher blood lead levels in lead workers and environmentally exposed children with the 1-2 and 2-2 isozymes. Environ Res 1991, 56, 109–119.
Ye XB, Fu H, Zhu JL, Ni WM, Lu YW, Kuang XY, Yang SL, Shu BX: A study on oxidative stress in lead-exposed workers. J Toxicol Environ Health 1999, 57, 161–172.
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