Abstract:With the strengthening of source control of benzene in China, occupational benzene exposure in workplaces has gradually shifted to long-term low-concentration exposure. The chronic toxicity caused by long-term low-concentration occupational benzene exposure, especially hematotoxicity and carcinogenic effects, has become a core concern in the field of occupational health. Benzene is a human carcinogen, and its health hazards and toxicological mechanisms have received much attention. Studies have shown that benzene is metabolized in vivo by cytochrome P450 enzyme system to generate active products such as hydroquinone and benzoquinone, which induce reactive oxygen species (ROS) accumulation and trigger oxidative stress, leading to lipid peroxidation, abnormal protein oxidative regulation, DNA damage, and epigenetic modifications, ultimately mediating chronic toxic effects. This paper systematically reviewed the key mechanisms of oxidative damage caused by long-term low-concentration occupational benzene exposure, such as ferroptosis-mediated lipid peroxidation, p53/nuclear factor-κB pathway oxidative regulation, and DNA oxidative damage repair disfunction, focused on summarizing oxidative stress-related biomarkers such as 8-hydroxydeoxyguanosine, exosomal miR-34a, and heat shock proteins 90α, and summarized the current problem of insufficient specificity of biomarkers for low-concentration exposure. Future research needs to focus on multi-omics combined biomarker development, oxidative damage intervention technology, and wearable monitoring equipment application, so as to provide the evidence for early warning and occupational health protection against low-concentration benzene exposure.
王爱红, 李晓海, 金米聪. 职业性苯暴露氧化损伤机制及其生物标志物研究进展[J]. 预防医学, 2026, 38(2): 149-155.
WANG Aihong, LI Xiaohai, JIN Micong. Research progress of the oxidative damage mechanism and its biomarkers caused by occupational benzene exposure. Preventive Medicine, 2026, 38(2): 149-155.
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