Epidemiology and Community Health Branch, National Heart Lung and Blood Institute, Bethesda, Maryland, USA
Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA.
Occup Environ Med. 2023 May;80(5):260-267. doi: 10.1136/oemed-2022-108719. Epub 2023 Mar 27.
We previously found that occupational exposure to diesel engine exhaust (DEE) was associated with alterations to 19 biomarkers that potentially reflect the mechanisms of carcinogenesis. Whether DEE is associated with biological alterations at concentrations under existing or recommended occupational exposure limits (OELs) is unclear.
In a cross-sectional study of 54 factory workers exposed long-term to DEE and 55 unexposed controls, we reanalysed the 19 previously identified biomarkers. Multivariable linear regression was used to compare biomarker levels between DEE-exposed versus unexposed subjects and to assess elemental carbon (EC) exposure-response relationships, adjusted for age and smoking status. We analysed each biomarker at EC concentrations below the US Mine Safety and Health Administration (MSHA) OEL (<106 µg/m), below the European Union (EU) OEL (<50 µg/m) and below the American Conference of Governmental Industrial Hygienists (ACGIH) recommendation (<20 µg/m).
Below the MSHA OEL, 17 biomarkers were altered between DEE-exposed workers and unexposed controls. Below the EU OEL, DEE-exposed workers had elevated lymphocytes (p=9E-03, false discovery rate (FDR)=0.04), CD4+ count (p=0.02, FDR=0.05), CD8+ count (p=5E-03, FDR=0.03) and miR-92a-3p (p=0.02, FDR=0.05), and nasal turbinate gene expression (first principal component: p=1E-06, FDR=2E-05), as well as decreased C-reactive protein (p=0.02, FDR=0.05), macrophage inflammatory protein-1β (p=0.04, FDR=0.09), miR-423-3p (p=0.04, FDR=0.09) and miR-122-5p (p=2E-03, FDR=0.02). Even at EC concentrations under the ACGIH recommendation, we found some evidence of exposure-response relationships for miR-423-3p (p=0.01, FDR=0.19) and gene expression (p=0.02, FDR=0.19).
DEE exposure under existing or recommended OELs may be associated with biomarkers reflective of cancer-related processes, including inflammatory/immune response.
我们之前发现职业性接触柴油机尾气（DEE）与潜在反映致癌机制的 19 种生物标志物的改变有关。在现有的或推荐的职业暴露限值（OEL）下，DEE 是否与生物改变有关尚不清楚。
在一项对 54 名长期接触 DEE 的工厂工人和 55 名未接触的对照者的横断面研究中，我们重新分析了之前确定的 19 种生物标志物。多变量线性回归用于比较 DEE 暴露组与未暴露组之间的生物标志物水平，并评估元素碳（EC）暴露反应关系，调整年龄和吸烟状况。我们在以下三个 EC 浓度水平分析了每个生物标志物：低于美国矿山安全与健康管理局（MSHA）OEL（<106μg/m）、低于欧盟（EU）OEL（<50μg/m）和低于美国工业卫生学家协会（ACGIH）建议值（<20μg/m）。
在 MSHA OEL 以下，17 种生物标志物在 DEE 暴露组与未暴露对照组之间发生改变。在欧盟 OEL 以下，DEE 暴露组的淋巴细胞升高（p=9E-03，错误发现率（FDR）=0.04）、CD4+计数（p=0.02，FDR=0.05）、CD8+计数（p=5E-03，FDR=0.03）和 miR-92a-3p（p=0.02，FDR=0.05），以及鼻甲骨基因表达（第一主成分：p=1E-06，FDR=2E-05），同时 C-反应蛋白降低（p=0.02，FDR=0.05）、巨噬细胞炎症蛋白-1β（p=0.04，FDR=0.09）、miR-423-3p（p=0.04，FDR=0.09）和 miR-122-5p（p=2E-03，FDR=0.02）。即使在 ACGIH 建议值以下的 EC 浓度下，我们也发现 miR-423-3p（p=0.01，FDR=0.19）和基因表达（p=0.02，FDR=0.19）存在暴露反应关系的一些证据。
在现有的或推荐的 OEL 下，DEE 暴露可能与反映癌症相关过程的生物标志物有关，包括炎症/免疫反应。
