Background 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.
Methods 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/m3), below the European Union (EU) OEL (<50 µg/m3) and below the American Conference of Governmental Industrial Hygienists (ACGIH) recommendation (<20 µg/m3).
Results 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 (ptrend=0.01, FDR=0.19) and gene expression (ptrend=0.02, FDR=0.19).
Conclusions DEE exposure under existing or recommended OELs may be associated with biomarkers reflective of cancer-related processes, including inflammatory/immune response.
- cross-sectional studies
- biological monitoring
- air pollution, indoor
Data availability statement
Data are available on reasonable request. Data are available on reasonable request at the discretion of the senior authors.
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Contributors Wrote and edited manuscript: all authors. Designed study: QL, NR, RV, DTS. Data analysis: JW, BB, WH, GSD. Data management: WH. Study supervision: DTS, YZ, QL. Exposure assessment: RV, GSD, KM, WH. DTS, YZ, QL are co-supervised authors. Guarantor: JW.
Funding This work is partly supported by National Natural Science Foundation of China (NSFC 91643203; NSFC 81130050) and intramural funding from the National Institutes of Health/National Cancer Institute / Division of Cancer Epidemiology and Genetics (HHSN261201500229P).
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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