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Mutagenicity and Oxidative Damage Induced by an Organic Extract of the Particulate Emissions from a Simulation of the Deepwater Horizon Surface Oil Burns
Citation:
DeMarini, D., S. Warren, K. Lavrich, A. Flen, J. Aurell, Bill Mitchell, D. Greenwell, B. Preston, Judy Schmid, Bill Linak, M. Hays, J. Samet, B. Gullett, AND I. Lambert. Mutagenicity and Oxidative Damage Induced by an Organic Extract of the Particulate Emissions from a Simulation of the Deepwater Horizon Surface Oil Burns. ENVIRONMENTAL AND MOLECULAR MUTAGENESIS. John Wiley & Sons, Inc, Hoboken, NJ, 58(3):162-171, (2017).
Impact/Purpose:
At the time of the BP Deepwater Horizon oil spill and explosion, which killed 11 men and discharged millions of barrels of oil into the Gulf of Mexico in April 2010, only one toxicology study was done on those emissions, and it showed that the emissions could induce oxidative stress. To fill this data gap, the U.S. EPA, as part of the commitment made by the Agency as a trustee under the Natural Resource Damage Assessment (NRDA) was funded by the National Pollution Funds Center of the U.S. Coast Guard to perform the study described in this paper. The companion paper by Brian K. Gullett, describes the generation of the oil-burn emissions and the collection and chemical analyses of those emissions. Here we have evaluated the emissions for their ability to induce mutations in bacteria and oxidative damage in human lung cells in culture. The results show that the emissions from burning oil are quite toxic and could have contributed to some of the damage to natural resources in the Gulf area at the time of the event, including lung damage as a contributor to the death of many marine mammals such as dolphins.
Description:
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, 2017). Here, we examine the ability of a dichloromethane extract of the particulate material with an aerodynamic size ≤ 2.5 µm (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 µg 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 × 105 revertants/megajoulethermal 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. © 2017 Wiley Periodicals, Inc.
