Gaballah Inas Fawzy, Helal Sawsan Farouk, Mourad Basma Hussein
a Occupational and Environmental Medicine Department, Faculty of Medicine , Cairo University , Cairo , Egypt.
Int J Occup Environ Health. 2017 Apr;23(2):120-127. doi: 10.1080/10773525.2018.1428265. Epub 2018 Jan 23.
Wood dust is known to be a human carcinogen, with a considerable risk of lung cancer. The increased cancer risk is likely induced through its genotoxic effects resulting from oxidative DNA damage. This study aimed at assessing the genotoxicity of wood dust and demonstrating the role of sputum PCR as a screening tool for early prediction of lung cancer among wood workers. The study was carried out in the carpentry section of a modernized factory involved with the manufacture of wooden furniture in Greater Cairo, Egypt. Environmental assessment of respirable wood dust concentrations was done. Frequency of chromosomal aberrations (CA%) and sister chromatid exchanges (SCE%) in peripheral blood lymphocytes (PBL) was assessed and comet assays were performed in samples from among the study population (n = 86). Levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzymes were measured. The polymerase chain reaction (PCR) was used to study hypermethylation of p16 and ̸or O-methylguanine-DNA methyltransferase (MGMT) gene promoters in sputum DNA. The concentrations of respirable wood dust exceeded the Egyptian and international permissible limits with highest levels generated by sawing operations. Laboratory investigations revealed statistically significantly higher frequencies of CA and SCE as well as increased comet tail length associated with significant decrement in the levels of SOD and GPx among exposed group. A statistically significant elevation in the extent of hypermethylation was detected for the p16 and MGMT gene promoters in the sputum DNA of studied wood workers. The study results support the conclusion that prolonged unprotected occupational exposure to wood dust is associated with possible genotoxicity and oxidative stress that might raise the risk for carcinogenesis including lung cancer.
已知木尘是一种人类致癌物，会带来相当大的肺癌风险。癌症风险增加可能是由氧化DNA损伤导致的基因毒性效应所诱发。本研究旨在评估木尘的基因毒性，并证明痰液PCR作为一种筛查工具在早期预测木工肺癌方面的作用。该研究在埃及大开罗一家生产木制家具的现代化工厂的木工车间进行。对可吸入木尘浓度进行了环境评估。评估了外周血淋巴细胞（PBL）中的染色体畸变频率（CA%）和姐妹染色单体交换频率（SCE%），并对研究人群（n = 86）的样本进行了彗星试验。测量了超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）的水平。采用聚合酶链反应（PCR）研究痰液DNA中p16和/或O-甲基鸟嘌呤-DNA甲基转移酶（MGMT）基因启动子的高甲基化情况。可吸入木尘浓度超过了埃及和国际允许限值，锯切作业产生的木尘浓度最高。实验室调查显示，暴露组的CA和SCE频率在统计学上显著更高，彗星尾长增加，同时SOD和GPx水平显著下降。在所研究木工的痰液DNA中，检测到p16和MGMT基因启动子的高甲基化程度在统计学上显著升高。研究结果支持以下结论：长期无防护的职业性接触木尘与可能的基因毒性和氧化应激有关，这可能会增加包括肺癌在内的致癌风险。
