Dispersant Used in Gulf Oil Spill Causes Injuries to Humans and Aquatic Animals

New research from investigators at the University of Alabama at Birmingham suggests that Corexit EC9500A, an oil-dispersal agent widely used in the Gulf of Mexico following the Deepwater Horizon oil spill, contributes to damage to epithelium cells within the lungs of humans and gills of marine creatures. The study also identifies an enzyme that is expressed in epithelial cells across species that has protective properties against Corexit-induced damage.

The investigators say that finding a way to boost or enhance that enzyme, heme oxygenase-1 or HO-1, could prevent lung damage in cases of exposure to oil dispersal agents in future. The study, published in PLOS ONE on April 2, 2015, looked at epithelium cells — the cells lining the airways of humans and the gills of certain marine species, in particular zebrafish and blue crabs.

The Deepwater Horizon spill, which began April 20, 2010, involved 205.8 million gallons of crude oil that spilled from a well head blow-out during the next three months. A dispersant, Corexit EC9500A, was used to degrade and break down the oil. A total of 1.84 million gallons of chemical dispersant was sprayed on the water or applied below the surface of the water.

“There were some 48,000 workers involved in the cleanup operations, and it is possible that workers were exposed to Corexit via inhalation,” said Veena Antony, M.D., professor in the Division of Pulmonary, Allergy and Critical Care Medicine and senior author of the paper. “Cough, shortness of breath and sputum production were among symptoms expressed by workers.”

The epithelium is a thin layer of cells that provides a continuous, critical and a highly regulated barrier to environmental insults. Inflammation of these cells can lead to a loss of integrity of the epithelium, causing an increase in permeability across the airway. Swelling of the airway with a corresponding reduction in airflow also can occur.

Sustained damage to this tissue also may lead to an inflammatory response in the epithelium, leading to obstruction of the airways in humans with exacerbation of pre-existing respiratory diseases such as asthma.The study findings suggest that Corexit exposure caused oxidative stress to epithelium cells, leading to a breakdown in their ability to function as a barrier. The exposure also increased the frequency of apoptosis, or programmed cell death.“The evidence that Corexit causes structural and functional abnormalities in airway tissue includes dispersant-induced cell detachment, edema, contraction in cell diameter and increased permeability,” Antony said.

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