PDF(Pubmed)
Abstract：
Epigenetic marks have been proposed as early changes, at the subcellular level, in disease development. To find more specific biomarkers of effect in occupational exposures to toxicants, DNA methylation studies in peripheral blood cells have been performed. The goal of this review is to summarize and contrast findings about DNA methylation in blood cells from workers exposed to toxicants.
A literature search was performed using PubMed and Web of Science. After first screening, we discarded all studies performed in vitro and in experimental animals, as well as those performed in other cell types other than peripheral blood cells. Results: 116 original research papers met the established criteria, published from 2007 to 2022. The most frequent investigated exposures/labor group were for benzene (18.9%) polycyclic aromatic hydrocarbons (15.5%), particulate matter (10.3%), lead (8.6%), pesticides (7.7%), radiation (4.3%), volatile organic compound mixtures (4.3%), welding fumes (3.4%) chromium (2.5%), toluene (2.5%), firefighters (2.5%), coal (1.7%), hairdressers (1.7%), nanoparticles (1.7%), vinyl chloride (1.7%), and others. Few longitudinal studies have been performed, as well as few of them have explored mitochondrial DNA methylation. Methylation platforms have evolved from analysis in repetitive elements (global methylation), gene-specific promoter methylation, to epigenome-wide studies. The most reported observations were global hypomethylation as well as promoter hypermethylation in exposed groups compared to controls, while methylation at DNA repair/oncogenes genes were the most studied; studies from genome-wide studies detect differentially methylated regions, which could be either hypo or hypermethylated.
Some evidence from longitudinal studies suggest that modifications observed in cross-sectional designs may be transitory; then, we cannot say that DNA methylation changes are predictive of disease development due to those exposures.
Due to the heterogeneity in the genes studied, and scarcity of longitudinal studies, we are far away from considering DNA methylation changes as biomarkers of effect in occupational exposures, and nor can we establish a clear functional or pathological correlate for those epigenetic modifications associated with the studied exposures.
A literature search was performed using PubMed and Web of Science. After first screening, we discarded all studies performed in vitro and in experimental animals, as well as those performed in other cell types other than peripheral blood cells. Results: 116 original research papers met the established criteria, published from 2007 to 2022. The most frequent investigated exposures/labor group were for benzene (18.9%) polycyclic aromatic hydrocarbons (15.5%), particulate matter (10.3%), lead (8.6%), pesticides (7.7%), radiation (4.3%), volatile organic compound mixtures (4.3%), welding fumes (3.4%) chromium (2.5%), toluene (2.5%), firefighters (2.5%), coal (1.7%), hairdressers (1.7%), nanoparticles (1.7%), vinyl chloride (1.7%), and others. Few longitudinal studies have been performed, as well as few of them have explored mitochondrial DNA methylation. Methylation platforms have evolved from analysis in repetitive elements (global methylation), gene-specific promoter methylation, to epigenome-wide studies. The most reported observations were global hypomethylation as well as promoter hypermethylation in exposed groups compared to controls, while methylation at DNA repair/oncogenes genes were the most studied; studies from genome-wide studies detect differentially methylated regions, which could be either hypo or hypermethylated.
Some evidence from longitudinal studies suggest that modifications observed in cross-sectional designs may be transitory; then, we cannot say that DNA methylation changes are predictive of disease development due to those exposures.
Due to the heterogeneity in the genes studied, and scarcity of longitudinal studies, we are far away from considering DNA methylation changes as biomarkers of effect in occupational exposures, and nor can we establish a clear functional or pathological correlate for those epigenetic modifications associated with the studied exposures.
摘要：
未经评估：表观遗传标记已被提议为早期更改，在亚细胞水平，在疾病发展中。为了找到更具体的生物标志物对职业暴露于毒物的影响，已经进行了外周血细胞中的DNA甲基化研究。这篇综述的目的是总结和对比有关暴露于有毒物质的工人的血细胞中DNA甲基化的发现。
UNASSIGNED：使用PubMed和WebofScience进行了文献检索。经过第一次筛选,我们放弃了所有在体外和实验动物中进行的研究，以及在外周血细胞以外的其他细胞类型中进行的那些。结果：116篇原创研究论文符合既定标准，2007年至2022年出版。最常见的暴露/劳动群体是苯（18.9％）多环芳烃（15.5％），颗粒物(10.3%)，铅(8.6%),农药(7.7%)，辐射(4.3%)，挥发性有机化合物混合物(4.3%)，焊接烟气(3.4%)铬(2.5%)，甲苯(2.5%),消防员(2.5%),煤炭(1.7%)，美发师(1.7%)，纳米颗粒(1.7%)，氯乙烯(1.7%)，和其他人。很少进行纵向研究，以及很少有人探索线粒体DNA甲基化。甲基化平台已经从重复元件（全局甲基化）的分析演变而来，基因特异性启动子甲基化，全表观基因组研究。报道最多的观察结果是与对照组相比，暴露组的整体低甲基化以及启动子高甲基化。而DNA修复/癌基因的甲基化研究最多；全基因组研究检测差异甲基化区域，可能是低甲基化或高甲基化。
未经评估：纵向研究的一些证据表明，在横截面设计中观察到的修改可能是暂时的；然后，我们不能说DNA甲基化改变是疾病发展的预测由于这些暴露。
UNASSIGNED：由于所研究基因的异质性，缺乏纵向研究，我们还远未将DNA甲基化变化视为职业暴露影响的生物标志物，我们也不能为那些与所研究的暴露相关的表观遗传修饰建立明确的功能或病理相关性。
UNASSIGNED：使用PubMed和WebofScience进行了文献检索。经过第一次筛选,我们放弃了所有在体外和实验动物中进行的研究，以及在外周血细胞以外的其他细胞类型中进行的那些。结果：116篇原创研究论文符合既定标准，2007年至2022年出版。最常见的暴露/劳动群体是苯（18.9％）多环芳烃（15.5％），颗粒物(10.3%)，铅(8.6%),农药(7.7%)，辐射(4.3%)，挥发性有机化合物混合物(4.3%)，焊接烟气(3.4%)铬(2.5%)，甲苯(2.5%),消防员(2.5%),煤炭(1.7%)，美发师(1.7%)，纳米颗粒(1.7%)，氯乙烯(1.7%)，和其他人。很少进行纵向研究，以及很少有人探索线粒体DNA甲基化。甲基化平台已经从重复元件（全局甲基化）的分析演变而来，基因特异性启动子甲基化，全表观基因组研究。报道最多的观察结果是与对照组相比，暴露组的整体低甲基化以及启动子高甲基化。而DNA修复/癌基因的甲基化研究最多；全基因组研究检测差异甲基化区域，可能是低甲基化或高甲基化。
未经评估：纵向研究的一些证据表明，在横截面设计中观察到的修改可能是暂时的；然后，我们不能说DNA甲基化改变是疾病发展的预测由于这些暴露。
UNASSIGNED：由于所研究基因的异质性，缺乏纵向研究，我们还远未将DNA甲基化变化视为职业暴露影响的生物标志物，我们也不能为那些与所研究的暴露相关的表观遗传修饰建立明确的功能或病理相关性。
