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izvor podataka: crosbi

Children's exposure to environmental pollutants and biomarkers of genetic damage (CROSBI ID 116434)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Neri, Monica ; Ugolini, Donatella ; Bonassi Stefano ; Fucic Aleksandra ; Holland, Nina ; Knudsen, Lisbeth ; Sram, Radim ; Ceppi, Marcello ; Bocchini Vittorio ; Merlo Domenico Franco Children's exposure to environmental pollutants and biomarkers of genetic damage // Mutation research. Reviews in mutation research, 590 (2005), 1; 1-37-x

Podaci o odgovornosti

Neri, Monica ; Ugolini, Donatella ; Bonassi Stefano ; Fucic Aleksandra ; Holland, Nina ; Knudsen, Lisbeth ; Sram, Radim ; Ceppi, Marcello ; Bocchini Vittorio ; Merlo Domenico Franco

engleski

Children's exposure to environmental pollutants and biomarkers of genetic damage

The present review is based on findings from 178 publications retrived through an extensive search of the MedLine/PubMed database for a 25 years time period (1980-2004) and 10 manually identified papers.Among the cytogenetic biomarkers that are frequently used in field studies, chromosome aberrations (CA) and micronuclei (MN) but not sister chromatid exchanges (SCE) were found consistently increased in children exposed to environmental pollutants. Meta-analyses of the studies reporting SCE in cord blood showed similar levels of SCE in exposed and in non-exposed newborns. Exposure to airborne pollutants, soil and drinking water contaminants. mostly increased CA and, to lesser extent, MN levels in children. The effect of exposure to airborne urban pollutants was consistently reported by field studies measuring DNA, albumin and hemoglobin adducts. Prenatal (in utero) and postnatal exposure (environmental tobacco smoke, ETS) to tobacco smoke compounds were associated with increased frequencies of DNA and hematoglobin adducts and CA. The limited number of field studies measuring DNA fragmentation (comet assay) hypoxanthine-guanine phosphoribosyltransferase (HPRT) and the glycophorin A (GPA) mutation frequency in environmentally exposed children precluded a meaningful evaluation of the usefulness of these assay. Meta-analyses performed in children exposed to ETS and in newborns exposed in utero to their mother's smoke showed 1.3 and 7 times higher levels of hemoglobin adducts compared to referent subjects, respectively. These increases are consistent with the epidemiological evidence of higher lung cancer risk reported in adults who had never smoked and were exposed to ETS during childhood and with 7-15 times higher lung cancer risks reported in smokers than in non-smokers. Higher levels of PAH-DNA adducts were found in fetal than in maternal tissue, suggesting a specific susceptibility of the fetus to this class of ubiquitous environmental pollutants. According to these findings, future research and biomonitoring programs on children would greatly benefit from the inclusion of selected biomarkers that could provide biologically based evidence for the identification of intervantion priorities in environmental health.

child wlfare; environmental pollution; biological markers; DNA damage; review; meta-analyses; molecular epidemiology

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Podaci o izdanju

590 (1)

2005.

1-37-x

objavljeno

1383-5742

Povezanost rada

Biologija

Indeksiranost