Occupational exposure to diesel engine exhaust and serum cytokine levels

Environ Mol Mutagen. 2018 Mar;59(2):144-150. doi: 10.1002/em.22142. Epub 2017 Oct 12.

Abstract

The International Agency for Research on Cancer has classified diesel engine exhaust (DEE) as a human lung carcinogen. Given that inflammation is suspected to be an important underlying mechanism of lung carcinogenesis, we evaluated the relationship between DEE exposure and the inflammatory response using data from a cross-sectional molecular epidemiology study of 41 diesel engine testing workers and 46 unexposed controls. Repeated personal exposure measurements of PM2.5 and other DEE constituents were taken for the diesel engine testing workers before blood collection. Serum levels of six inflammatory biomarkers including interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor (TNF)-α, macrophage inflammatory protein (MIP)-1β, and monocyte chemotactic protein (MCP)-1 were analyzed in all subjects. Compared to unexposed controls, concentrations of MIP-1β were significantly reduced by ∼37% in DEE exposed workers (P < 0.001) and showed a strong decreasing trend with increasing PM2.5 concentrations in all subjects (Ptrend < 0.001) as well as in exposed subjects only (Ptrend = 0.001). Levels of IL-8 and MIP-1β were significantly lower in workers in the highest exposure tertile of PM2.5 (>397 µg/m3 ) compared to unexposed controls. Further, significant inverse exposure-response relationships for IL-8 and MCP-1 were also found in relation to increasing PM2.5 levels among the DEE exposed workers. Given that IL-8, MIP-1β, and MCP-1 are chemokines that play important roles in recruitment of immunocompetent cells for immune defense and tumor cell clearance, the observed lower levels of these markers with increasing PM2.5 exposure may provide insight into the mechanism by which DEE promotes lung cancer. Environ. Mol. Mutagen. 59:144-150, 2018. © 2017 Wiley Periodicals, Inc.

Keywords: diesel engine exhaust; inflammatory biomarkers; molecular epidemiology; occupational exposure.

MeSH terms

  • Air Pollutants, Occupational / toxicity
  • Chemokine CCL2 / blood*
  • Chemokine CCL4 / blood*
  • Cytokines / blood
  • Cytokines / drug effects
  • Female
  • Humans
  • Interleukin-1 / blood
  • Interleukin-6 / blood
  • Interleukin-8 / blood*
  • Lung Neoplasms / blood*
  • Lung Neoplasms / chemically induced
  • Male
  • Tumor Necrosis Factor-alpha / blood
  • Vehicle Emissions / toxicity*

Substances

  • Air Pollutants, Occupational
  • CCL2 protein, human
  • Chemokine CCL2
  • Chemokine CCL4
  • Cytokines
  • Interleukin-1
  • Interleukin-6
  • Interleukin-8
  • Tumor Necrosis Factor-alpha
  • Vehicle Emissions