Mutagenicity and oxidative damage induced by an organic extract of the particulate emissions from a simulation of the deepwater horizon surface oil burns

作者：DeMarini David M^*; Warren Sarah H; Lavrich Katelyn; Flen Alexis; Aurell Johanna; Mitchell William; Greenwell Dale; Preston William; Schmid Judith E; Linak William P; Hays Michael D; Samet James M; Gullett Brian K

来源：Environmental and Molecular Mutagenesis, 2017, 58(3): 162-171.

DOI：10.1002/em.22085

• oil-burn emissions
• mutagenicity
• oxidative damage
• Salmonella
• mitochondrial respiration
• extracellular flux analysis

Emissions from oil fires associated with the Deepwater Horizon explosion and oil discharge that began on April 20, 2010 in the Gulf of Mexico were analyzed chemically to only a limited extent at the time but were shown to induce oxidative damage in vitro and in mice. To extend this work, we burned oil floating on sea water and performed extensive chemical analyses of the emissions (Gullett et al., Marine Pollut Bull, in press, ). Here, we examine the ability of a dichloromethane extract of the particulate material with an aerodynamic size2.5 mu m (PM2.5) from those emissions to induce oxidative damage in human lung cells in vitro and mutagenicity in 6 strains of Salmonella. The extract had a percentage of extractable organic material (EOM) of 7.0% and increased expression of the heme oxygenase (HMOX1) gene in BEAS-2B cells after exposure for 4 hr at 20 mu g of EOM/ml. However, the extract did not alter mitochondrial respiration rate as measured by extracellular flux analysis. The extract was most mutagenic in TA100 +S9, indicative of a role for polycyclic aromatic hydrocarbons (PAHs), reflective of the high concentrations of PAHs in the emissions (1 g/kg of oil consumed). The extract had a mutagenicity emission factor of 1.8 +/- 0.1 x 10(5) revertants/megajoule(thermal) in TA98 +S9, which was greater than that of diesel exhaust and within an order of magnitude of open burning of wood and plastic. Thus, organics from PM2.5 of burning oil can induce oxidative responses in human airway epithelial cells and are highly mutagenic. Environ. Mol. Mutagen. 58:162-171, 2017.

• 出版日期2017-4