Department of Cytogenetics and Immunology, National Institute of Chemical Safety, H-1097, Nagyvárad tér 2., Budapest, Hungary.
Mutat Res. 2010 Apr 30;698(1-2):11-7. doi: 10.1016/j.mrgentox.2010.02.015. Epub 2010 Mar 1.
Peripheral blood lymphocytes (PBL) of 37 formaldehyde-exposed women from four pathology departments in Hungary were investigated to collect data on the effects of occupational exposures to formaldehyde and to find a possible relationship between in vivo formaldehyde-induced apoptosis and genotoxic effects. The subjects were divided into two groups: 16 donors exposed to formaldehyde together with various organic solvents, and 21 subjects exposed mainly to formaldehyde. The results were compared with 37 controls (all women) without known occupational exposure. Ambient air concentrations of formaldehyde were measured in three work places, and ranged from 0.23 to 1.21mg/m(3) (mean 0.9mg/m(3)). Measures of genotoxicity included the determination of the frequencies of chromosomal aberrations (CA), sister-chromatid exchange (SCE), HPRT mutations (variant frequency, VF) and the measurement of UV-induced unscheduled DNA-repair synthesis (UDS). The percentages of premature centromere division (PCD) and of cells with a high frequency of SCE (HF/SCE) were also scored. Apoptosis and cell proliferation were determined by flow cytometry. In both formaldehyde-exposed groups, the apoptotic activity and the CA levels in PBLs were significantly higher than in controls. The CA were mostly breaks of the chromatid type. In the second group, which was mainly exposed to formaldehyde, CA were slightly lower in comparison with the group exposed to formaldehyde and solvents, which may be attributed to a different rate of elimination of damaged lymphocytes as a consequence of formaldehyde-induced apoptotic activity. In the second group, a significant decrease of VF and a non-significant increase in HF/SCE were found compared with the control and the other group. In conclusion, the results demonstrate that exposure to formaldehyde induces apoptosis and CA, indicating an excess cancer risk among subjects occupationally exposed to formaldehyde. The results also emphasize the importance of the measurement of occupational air pollutants, such as formaldehyde, in order to avoid genotoxic effects in the workers.
对来自匈牙利四个病理学部门的 37 名接触甲醛的女性外周血淋巴细胞(PBL)进行了调查,以收集职业暴露于甲醛的影响数据,并寻找体内甲醛诱导的细胞凋亡与遗传毒性效应之间可能存在的关系。研究对象分为两组:16 名接触甲醛和各种有机溶剂的捐献者,以及 21 名主要接触甲醛的受试者。将结果与 37 名无已知职业暴露的对照者(均为女性)进行比较。在三个工作场所测量了环境空气中的甲醛浓度,范围从 0.23 到 1.21mg/m3(平均值为 0.9mg/m3)。遗传毒性测量包括染色体畸变(CA)频率、姐妹染色单体交换(SCE)、HPRT 突变(变体频率,VF)的测定和紫外线诱导的非计划性 DNA 修复合成(UDS)的测量。也对过早着丝粒分裂(PCD)的百分比和具有高 SCE 频率的细胞(HF/SCE)的百分比进行了评分。通过流式细胞术测定细胞凋亡和细胞增殖。在两个暴露于甲醛的组中,PBL 的细胞凋亡活性和 CA 水平明显高于对照组。CA 主要是染色单体类型的断裂。在第二个主要暴露于甲醛的组中,与暴露于甲醛和溶剂的组相比,CA 略低,这可能归因于由于甲醛诱导的细胞凋亡活性而导致受损淋巴细胞的消除率不同。在第二组中,与对照组和另一组相比,VF 显著降低,HF/SCE 非显著增加。总之,结果表明,暴露于甲醛会诱导细胞凋亡和 CA,表明职业暴露于甲醛的受试者患癌症的风险增加。结果还强调了测量职业空气污染物(如甲醛)的重要性,以避免工人的遗传毒性效应。