Environmental lead exposure increases micronuclei in children

Research output: Contribution to journalJournal articleResearchpeer-review

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Environmental lead exposure increases micronuclei in children. / Kapka, Lucyna; Baumgartner, Adolf; Siwińska, Ewa; Knudsen, Lisbeth E.; Anderson, Diana; Mielzyńska, Danuta.

In: Mutagenesis, Vol. 22, No. 3, 2007, p. 201-7.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Kapka, L, Baumgartner, A, Siwińska, E, Knudsen, LE, Anderson, D & Mielzyńska, D 2007, 'Environmental lead exposure increases micronuclei in children', Mutagenesis, vol. 22, no. 3, pp. 201-7. https://doi.org/10.1093/mutage/gem004

APA

Kapka, L., Baumgartner, A., Siwińska, E., Knudsen, L. E., Anderson, D., & Mielzyńska, D. (2007). Environmental lead exposure increases micronuclei in children. Mutagenesis, 22(3), 201-7. https://doi.org/10.1093/mutage/gem004

Vancouver

Kapka L, Baumgartner A, Siwińska E, Knudsen LE, Anderson D, Mielzyńska D. Environmental lead exposure increases micronuclei in children. Mutagenesis. 2007;22(3):201-7. https://doi.org/10.1093/mutage/gem004

Author

Kapka, Lucyna ; Baumgartner, Adolf ; Siwińska, Ewa ; Knudsen, Lisbeth E. ; Anderson, Diana ; Mielzyńska, Danuta. / Environmental lead exposure increases micronuclei in children. In: Mutagenesis. 2007 ; Vol. 22, No. 3. pp. 201-7.

Bibtex

@article{94f6c0f23121434fb9ed00156c31a469,
title = "Environmental lead exposure increases micronuclei in children",
abstract = "The objective of this pilot study was to investigate the contribution of environmental exposures to lead in the development of cytogenetic damage detected as the frequency of micronuclei (MN) in children. The other aim was to apply the MN assay in combination with fluorescence in situ hybridization (FISH) using a pan-centromeric chromosome probe to elucidate the formation mechanism of induced MN. The examined population was composed of 9-year-old children (n = 92), living in the region where non-ferrous ores are extracted and processed. The non-exposed group consisted of 49 children of the same age from an unexposed recreational area. Exposure to lead was assessed by determination of lead concentrations in blood (PbB) by atomic absorption spectrophotometry, whereas the level of selenium (Se) in serum was detected by using graphite furnace atomic-absorption spectrometry. The frequency of MN was determined by the cytokinesis-block MN assay and fluorescence in situ hybridization performed using a specific pan-centromeric probe. Environmental exposure to lead resulted in significantly increased levels of PbB (5.29 +/- 2.09 versus 3.45 +/- 1.20 microg/dl in controls), although the average level was much below the value of the biological exposure limit = 10 microg/dl. A negative correlation between lead in blood and Se in serum concentrations (P = 0.006) was found for the pooled study population. The results showed a significant difference (P < 0.0001) in the level of MN between the exposed and control group (standard MN test: 2.96 +/- 2.36 versus 1.16 +/- 1.28; FISH technique: 3.57 +/- 3.02 versus 1.43 +/- 1.69, respectively). The frequencies of both centromere-positive (C+MN) and centromere-negative (C-MN) micronuclei were significantly increased in exposed children; however, the contribution of C+MN in the total number of MN in peripheral blood lymphocytes of exposed children was significantly higher than in the controls what may suggest a pro-aneugenic effect of the exposure to lead. The results of multiple regression analysis indicated that the exposure to lead was an important factor affecting the increase in MN frequency what was confirmed by significant correlation between the PbB and MN levels. In conclusion, our results suggest that the exposure to lead may be associated with an increased frequency of MN, especially of C+MN; however, the influence of other factors (e.g. vitamins and minerals in the diet) cannot be excluded.",
keywords = "Child, Environmental Exposure, Female, Humans, In Situ Hybridization, Fluorescence, Lead, Male, Micronuclei, Chromosome-Defective, Micronucleus Tests, Pilot Projects, Poland, Regression Analysis, Selenium, Spectrophotometry, Atomic",
author = "Lucyna Kapka and Adolf Baumgartner and Ewa Siwi{\'n}ska and Knudsen, {Lisbeth E.} and Diana Anderson and Danuta Mielzy{\'n}ska",
year = "2007",
doi = "10.1093/mutage/gem004",
language = "English",
volume = "22",
pages = "201--7",
journal = "Mutagenesis",
issn = "0267-8357",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - Environmental lead exposure increases micronuclei in children

AU - Kapka, Lucyna

AU - Baumgartner, Adolf

AU - Siwińska, Ewa

AU - Knudsen, Lisbeth E.

AU - Anderson, Diana

AU - Mielzyńska, Danuta

PY - 2007

Y1 - 2007

N2 - The objective of this pilot study was to investigate the contribution of environmental exposures to lead in the development of cytogenetic damage detected as the frequency of micronuclei (MN) in children. The other aim was to apply the MN assay in combination with fluorescence in situ hybridization (FISH) using a pan-centromeric chromosome probe to elucidate the formation mechanism of induced MN. The examined population was composed of 9-year-old children (n = 92), living in the region where non-ferrous ores are extracted and processed. The non-exposed group consisted of 49 children of the same age from an unexposed recreational area. Exposure to lead was assessed by determination of lead concentrations in blood (PbB) by atomic absorption spectrophotometry, whereas the level of selenium (Se) in serum was detected by using graphite furnace atomic-absorption spectrometry. The frequency of MN was determined by the cytokinesis-block MN assay and fluorescence in situ hybridization performed using a specific pan-centromeric probe. Environmental exposure to lead resulted in significantly increased levels of PbB (5.29 +/- 2.09 versus 3.45 +/- 1.20 microg/dl in controls), although the average level was much below the value of the biological exposure limit = 10 microg/dl. A negative correlation between lead in blood and Se in serum concentrations (P = 0.006) was found for the pooled study population. The results showed a significant difference (P < 0.0001) in the level of MN between the exposed and control group (standard MN test: 2.96 +/- 2.36 versus 1.16 +/- 1.28; FISH technique: 3.57 +/- 3.02 versus 1.43 +/- 1.69, respectively). The frequencies of both centromere-positive (C+MN) and centromere-negative (C-MN) micronuclei were significantly increased in exposed children; however, the contribution of C+MN in the total number of MN in peripheral blood lymphocytes of exposed children was significantly higher than in the controls what may suggest a pro-aneugenic effect of the exposure to lead. The results of multiple regression analysis indicated that the exposure to lead was an important factor affecting the increase in MN frequency what was confirmed by significant correlation between the PbB and MN levels. In conclusion, our results suggest that the exposure to lead may be associated with an increased frequency of MN, especially of C+MN; however, the influence of other factors (e.g. vitamins and minerals in the diet) cannot be excluded.

AB - The objective of this pilot study was to investigate the contribution of environmental exposures to lead in the development of cytogenetic damage detected as the frequency of micronuclei (MN) in children. The other aim was to apply the MN assay in combination with fluorescence in situ hybridization (FISH) using a pan-centromeric chromosome probe to elucidate the formation mechanism of induced MN. The examined population was composed of 9-year-old children (n = 92), living in the region where non-ferrous ores are extracted and processed. The non-exposed group consisted of 49 children of the same age from an unexposed recreational area. Exposure to lead was assessed by determination of lead concentrations in blood (PbB) by atomic absorption spectrophotometry, whereas the level of selenium (Se) in serum was detected by using graphite furnace atomic-absorption spectrometry. The frequency of MN was determined by the cytokinesis-block MN assay and fluorescence in situ hybridization performed using a specific pan-centromeric probe. Environmental exposure to lead resulted in significantly increased levels of PbB (5.29 +/- 2.09 versus 3.45 +/- 1.20 microg/dl in controls), although the average level was much below the value of the biological exposure limit = 10 microg/dl. A negative correlation between lead in blood and Se in serum concentrations (P = 0.006) was found for the pooled study population. The results showed a significant difference (P < 0.0001) in the level of MN between the exposed and control group (standard MN test: 2.96 +/- 2.36 versus 1.16 +/- 1.28; FISH technique: 3.57 +/- 3.02 versus 1.43 +/- 1.69, respectively). The frequencies of both centromere-positive (C+MN) and centromere-negative (C-MN) micronuclei were significantly increased in exposed children; however, the contribution of C+MN in the total number of MN in peripheral blood lymphocytes of exposed children was significantly higher than in the controls what may suggest a pro-aneugenic effect of the exposure to lead. The results of multiple regression analysis indicated that the exposure to lead was an important factor affecting the increase in MN frequency what was confirmed by significant correlation between the PbB and MN levels. In conclusion, our results suggest that the exposure to lead may be associated with an increased frequency of MN, especially of C+MN; however, the influence of other factors (e.g. vitamins and minerals in the diet) cannot be excluded.

KW - Child

KW - Environmental Exposure

KW - Female

KW - Humans

KW - In Situ Hybridization, Fluorescence

KW - Lead

KW - Male

KW - Micronuclei, Chromosome-Defective

KW - Micronucleus Tests

KW - Pilot Projects

KW - Poland

KW - Regression Analysis

KW - Selenium

KW - Spectrophotometry, Atomic

U2 - 10.1093/mutage/gem004

DO - 10.1093/mutage/gem004

M3 - Journal article

C2 - 17311805

VL - 22

SP - 201

EP - 207

JO - Mutagenesis

JF - Mutagenesis

SN - 0267-8357

IS - 3

ER -

ID: 137758381