Kasperczyk Edyta, Tarhonska Kateryna, Jablonska Ewa
Department of Translational Research, Nofer Institute of Occupational Medicine, 91-348 Lodz, Poland.
Laboratory of Molecular Markers and Biostatistics, Department of Chemical Safety, Nofer Institute of Occupational Medicine, 91-348 Lodz, Poland.
J Clin Med. 2025 Jun 25;14(13):4492. doi: 10.3390/jcm14134492.
: There is substantial evidence supporting the role of genetic alterations in chemically induced carcinogenesis. We analyzed the existing literature to gather data on genetic alterations linked to human carcinogens and their possible connection to genotoxic outcomes. The review emphasizes carcinogenic substances and occupational exposures identified as "carcinogenic to humans". In particular, we searched for studies describing genotoxic alterations linked to agents and occupational exposures for which the International Agency for Research on Cancer has found sufficient evidence of an association with bladder cancer. : The review was carried out in compliance with the PRISMA standards. A comprehensive search of the PubMed database was conducted to identify studies published through March 2024. : We identified 60 studies that evaluated genetic alterations for 16 carcinogenic agents and occupations (such as aluminum production, 4-aminobiphenyl, auramine production, benzidine, chlornaphazine, cyclophosphamide, firefighters, magenta production, 2-naphthylamine, opium consumption, ortho-toluidine, painters, the rubber manufacturing industry, infection, X-radiation, gamma-radiation) in healthy humans. : The genotoxic effects of chemical agents in healthy individuals have been well studied and characterized. Additionally, this review presents numerous studies concerning occupational exposure but not exclusively. Genotoxicity assessments have mainly been conducted on biological materials such as blood, peripheral blood lymphocytes, urine, and buccal epithelial cells. The most frequently examined genotoxic effects were DNA damage, chromosomal abnormalities, and micronuclei. Standardized data to clearly define a dose-response relationship for predicting delayed health effects are still lacking.
有大量证据支持基因改变在化学诱导致癌过程中的作用。我们分析了现有文献，以收集与人类致癌物相关的基因改变数据及其与遗传毒性结果的可能联系。该综述强调被确定为“对人类致癌”的致癌物质和职业暴露。特别是，我们搜索了描述与国际癌症研究机构已发现有充分证据表明与膀胱癌有关联的化学物质和职业暴露相关的遗传毒性改变的研究。
该综述按照PRISMA标准进行。对PubMed数据库进行了全面搜索，以识别截至2024年3月发表的研究。
我们确定了60项评估16种致癌物质和职业（如铝生产、4-氨基联苯、金胺生产、联苯胺、氯萘嗪、环磷酰胺、消防员、品红生产、2-萘胺、鸦片消费、邻甲苯胺、油漆工、橡胶制造业、感染、X射线、γ射线）在健康人类中基因改变的研究。
化学物质对健康个体的遗传毒性作用已得到充分研究和表征。此外，本综述介绍了许多关于职业暴露的研究，但不仅限于此。遗传毒性评估主要针对血液、外周血淋巴细胞、尿液和颊黏膜上皮细胞等生物材料进行。最常检测的遗传毒性效应是DNA损伤、染色体异常和微核。仍然缺乏明确界定剂量反应关系以预测延迟健康影响的标准化数据。
