The Impact of the Deepwater Horizon Oil Spill upon Lung Health—Mouse Model-Based RNA-Seq Analyses

Abstract

We used a transcriptomic approach to interrogate the effects of a saline-accommodated fraction from the Macondo 252 well (MC252) oil and Corexit dispersants on lung tissue. Wild-type C57BL/6 male and female mice were exposed on days 0, 7 and 13 by oropharyngeal aspiration to saline accommodated fractions (SAF) of crude oil from the Macondo (MC252) well, Corexit 9500, Corexit 9527, 9500+oil and 9527+oil or a saline solution as the vehicle control. These treatments did not cause overt toxicity, with the exception of the Corexit exposures which caused brief weight loss after the first exposure. On day 14, total RNA was isolated from the left lung for RNA-seq analyses. KEGG-pathway-based differential expression revealed that Corexit 9527 elicited the strongest changes involving the upregulation of 19 KEGG pathways (FDR < 0.10), followed by Corexit 9500 with the upregulation of seven pathways (FDR < 0.10). As an important signature, pathways related to a response to DNA damage (e.g., p53 signaling and mismatch repair) dominate those upregulated by Corexit 9527 and Corexit 9500. In addition, pro-inflammatory pathways (e.g., cytokine-cytokine receptor interaction, IL-17 signaling pathway and TNF signaling pathways) were upregulated selectively in oil-treated male mice. Surprisingly, oil + dispersant combinations caused lesser effects than the individual treatments at the transcriptomic level. Overall, these findings support potential genotoxicity, inflammation and cell death due to dispersant or oil exposures. Similar exposures to lung tumor bearing K-RasLA1 mice provided evidence for tumor promotion by oil and Corexit dispersant treatments. Our mouse RNA-seq analyses may be relevant to the pulmonary health hazards of MC252 oil and dispersants experienced in exposed populations.

Pollution, Inflammation, and Vaccines: A Complex Crosstalk

“…Inflammation is also driven by other mechanisms: in the case of the gut, fibroblasts and epithelial cells are the activators of the immune system after exposure to pollution, through direct production of inflammatory cytokines (particularly TGF-β, IL-10, IL-17), but also changing the expression of toll-like receptors (TLRs) and surface proteins [ 40 ]. Petrol, which interestingly is a key pollutant for the gut, is also known to activate directly IL-17, TNF, and other cytokines, similarly to pesticides [ 41 ].…”

Combined Effects of Elevated Temperature and Crude Oil Pollution on Oxidative Stress and Apoptosis in Sea Cucumber (Apostichopus japonicus, Selenka)

“…More recently, with the ever-increasing global production and consumption of crude oil, oil pollution derived from harbors, shipping, and offshore drilling could severely threaten marine ecological system and marine economy [ 14 , 15 , 16 ]. For instance, in July 2010, approximately 1500 t of crude oil was spilled from the Xingang Port of Dalian (China) into the Yellow Sea, leading to significant economic losses in the marine aquaculture industry in Liaoning Province, especially in sea cucumber culture [ 2 ].…”