Ambient particulate matter (PM2.5): physicochemical characterization and metabolic activation of the organic fraction in human lung epithelial cells (A549)

Environ Res. 2007 Oct;105(2):212-23. doi: 10.1016/j.envres.2007.03.001. Epub 2007 Apr 25.

Abstract

To contribute to complete the knowledge of the underlying mechanisms of action involved in air pollution particulate matter (PM)-induced cytotoxicity, an aerosol was collected in Dunkerque, a French seaside City heavily industrialized. In this work, we focused our attention on its physical and chemical characteristics, its cytotoxicity, and its role in the induction of the volatile organic compound (VOC) and/or polycyclic aromatic hydrocarbon (PAH)-metabolizing enzymes in human lung epithelial cells (A549). Size distribution showed that 92.15% of the collected PM were PM2.5 and the specific surface area was 1 m2/g. Inorganic (i.e. Fe, Al, Ca, Na, K, Mg, Pb, etc.) and organic (i.e. VOC, PAH, etc.) chemicals were found in collected PM, revealing that much of them derived from wind-borne dust from the industrial complex and the heavy motor vehicle traffic. The thermal desorption study indicated that organic chemicals were not only adsorbed onto the surface but also highly incrusted in the structure of PM. The lethal concentrations at 10% and 50% of collected PM were 23.72 microg/mL (or 6.33microg/cm2) and 118.60 microg/mL (or 31.63 microg/cm2), respectively. The VOC and/or PAH-coated onto PM induced significant increases in mRNA expressions of cytochrome P450 (cyp) 1a1, cyp2e1, cyp2f1, nadph quinone oxydo-reductase-1, and glutathione s-transferase-pi 1, versus controls. Hence, we concluded that the metabolic activation of the very low doses of VOC and/or PAH-coated onto the inorganic condensation nuclei from Dunkerque City's PM is one of the underlying mechanisms of action closely involved in its cytotoxicity in human lung epithelial cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Air Pollutants / analysis*
  • Air Pollutants / toxicity*
  • Cell Line
  • Cell Survival / drug effects
  • Cytochrome P-450 Enzyme System / genetics
  • Epithelial Cells / cytology
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism
  • Epoxide Hydrolases / genetics
  • France
  • Gene Expression Regulation, Enzymologic / drug effects*
  • Glutathione Transferase / genetics
  • Humans
  • Lung / cytology
  • NAD(P)H Dehydrogenase (Quinone) / genetics
  • Organic Chemicals / analysis
  • Particle Size
  • Particulate Matter / analysis*
  • Particulate Matter / toxicity*
  • RNA, Messenger / metabolism

Substances

  • Air Pollutants
  • Organic Chemicals
  • Particulate Matter
  • RNA, Messenger
  • Cytochrome P-450 Enzyme System
  • NAD(P)H Dehydrogenase (Quinone)
  • NQO1 protein, human
  • Glutathione Transferase
  • Epoxide Hydrolases