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首页> 外文期刊>Mutation Research: International Journal on Mutagenesis, Chromosome Breakage and Related Subjects >Children's exposure to environmental pollutants and biomarkers of genetic damage. II. Results of a comprehensive literature search and meta-analysis.
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Children's exposure to environmental pollutants and biomarkers of genetic damage. II. Results of a comprehensive literature search and meta-analysis.

机译:儿童接触环境污染物和遗传标记的生物标志物。二。全面的文献检索和荟萃分析的结果。

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The present review is based on findings from 178 publications retrieved 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-analysis 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 a 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 hemoglobin adducts and CA. The limited number of field studies measuring DNA fragmentation (Comet assay), hypoxanthine-guanine phosphoribosyltransferase (HPRT) and the glycophorinA (GPA) mutation frequency in environmentally exposed children precluded a meaningful evaluation of the usefulness of these assays. Meta-analyses performed in children exposed to ETS and in newborns exposed in utero to their mothers' 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 risks 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 intervention priorities in environmental health.
机译:本综述基于通过对MedLine / PubMed数据库进行长达25年(1980-2004年)的广泛搜索而检索到的178种出版物的发现以及10篇人工鉴定的论文。在经常用于田间研究的细胞遗传学生物标记物中,发现暴露于环境污染物的儿童中染色体畸变(CA)和微核(MN)而不是姐妹染色单体交换(SCE)持续增加。报道脐带血中SCE的研究的荟萃分析显示,暴露和未暴露的新生儿中SCE的水平相似。暴露于空气中的污染物,土壤和饮用水中的污染物,大多数会使儿童的CA升高,并在较小程度上增加儿童的MN水平。通过现场研究测量DNA,白蛋白和血红蛋白加合物,不断报告了暴露于空气中城市污染物的影响。产前(子宫内)和产后暴露(环境烟草烟雾,ETS)与烟草烟雾化合物的发生有关,DNA,血红蛋白加合物和CA的频率增加。在暴露于环境的儿童中,测量DNA片段化(彗星试验),次黄嘌呤-鸟嘌呤磷酸核糖基转移酶(HPRT)和糖尿蛋白A(GPA)突变频率的现场研究数量有限,因此无法对这些试验的有用性进行有意义的评估。对暴露于ETS的儿童和在子宫内暴露于母亲的烟雾的新生儿进行的荟萃分析显示,血红蛋白加合物的水平分别比参照对象高1.3倍和7倍。这些增加与流行病学证据相一致,该流行病学证据表明在儿童时期从未吸烟且未接触过ETS的成年人中,罹患肺癌的风险较高,而吸烟者中罹患肺癌的风险是非吸烟者中的7-15倍。在胎儿中发现的PAH-DNA加合物的水平高于在母体组织中的水平,这表明胎儿对这类普遍存在的环境污染物具有特殊的敏感性。根据这些发现,将来对儿童的研究和生物监测计划将从选择的生物标志物的使用中受益匪浅,这些标志物可以为确定环境卫生干预重点提供生物学依据。

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