Proinflammatory effects and oxidative stress within human bronchial epithelial cells exposed to atmospheric particulate matter (PM(2.5) and PM(>2.5)) collected from Cotonou, Benin

Environ Pollut. 2014 Feb:185:340-51. doi: 10.1016/j.envpol.2013.10.026. Epub 2013 Dec 10.

Abstract

After particulate matter (PM) collection in Cotonou (Benin), a complete physicochemical characterization of PM2.5 and PM>2.5 was led. Then, their adverse health effects were evaluated by using in vitro culture of human lung cells. BEAS-2B (bronchial epithelial cells) were intoxicated during short-term exposure at increasing PM concentrations (1.5-96 μg/cm(2)) to determine global cytotoxicity. Hence, cells were exposed to 3 and 12 μg/cm(2) to investigate the potential biological imbalance generated by PM toxicity. Our findings showed the ability of both PM to induce oxidative stress and to cause inflammatory cytokines/chemokines gene expression and secretion. Furthermore, PM were able to induce gene expression of enzymes involved in the xenobiotic metabolism pathway. Strong correlations between gene expression of metabolizing enzymes, proinflammatory responses and cell cycle alteration were found, as well as between proinflammatory responses and cell viability. Stress oxidant parameters were highly correlated with expression and protein secretion of inflammatory mediators.

Keywords: Benin; Cytotoxicity; Inflammatory response; Oxidative stress; Particulate matter.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Air Pollutants / metabolism
  • Air Pollutants / toxicity*
  • Atmosphere
  • Benin
  • Cell Line
  • Cell Survival
  • Environmental Monitoring
  • Epithelial Cells / drug effects
  • Epithelial Cells / immunology
  • Epithelial Cells / metabolism
  • Humans
  • Lung / drug effects
  • Oxidative Stress
  • Particulate Matter / metabolism
  • Particulate Matter / toxicity*

Substances

  • Air Pollutants
  • Particulate Matter