Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

NIOSHTIC-2 Publications Search

Search Results

Neurotoxicity following acute inhalation exposure to the oil dispersant COREXIT EC9500A.

Authors
Sriram-K; Lin-GX; Jefferson-AM; Goldsmith-WT; Jackson-M; McKinney-W; Frazer-DG; Robinson-VA; Castranova-V
Source
J Toxicol Environ Health, A 2011 Nov; 74(21):1405-1418
NIOSHTIC No.
20039687
Abstract
Consequent to the 2010 Deepwater Horizon oil spill in the Gulf of Mexico, there is an emergent concern about the short- and long-term adverse health effects of exposure to crude oil, weathered-oil products, and oil dispersants among the workforce employed to contain and clean up the spill. Oil dispersants typically comprise of a mixture of solvents and surfactants that break down floating oil to micrometer-sized droplets within the water column, thus preventing it from reaching the shorelines. As dispersants are generally sprayed from the air, workers are at risk for exposure primarily via inhalation. Such inhaled fractions might potentially permeate or translocate to the brain via olfactory or systemic circulation, producing central nervous system (CNS) abnormalities. To determine whether oil dispersants pose a neurological risk, male Sprague-Dawley rats were exposed by whole-body inhalation exposure to a model oil dispersant, COREXIT EC9500A (CE; approximately 27 mg/m(3) x 5 h/d x 1 d), and various molecular indices of neural dysfunction were evaluated in discrete brain areas, at 1 or 7 d postexposure. Exposure to CE produced partial loss of olfactory marker protein in the olfactory bulb. CE also reduced tyrosine hydroxylase protein content in the striatum. Further, CE altered the levels of various synaptic and neuronal intermediate filament proteins in specific brain areas. Reactive astrogliosis, as evidenced by increased expression of glial fibrillary acidic protein, was observed in the hippocampus and frontal cortex following exposure to CE. Collectively, these findings are suggestive of disruptions in olfactory signal transduction, axonal function, and synaptic vesicle fusion, events that potentially result in an imbalance in neurotransmitter signaling. Whether such acute molecular aberrations might persist and produce chronic neurological deficits remains to be ascertained.
Keywords
Environmental-contamination; Environmental-exposure; Exposure-assessment; Oil-industry; Oils; Crude-oil; Petroleum; Petroleum-industry; Petroleum-oils; Health-hazards; Dispersion; Solvents; Surfactants; Inhalants; Neurological-reactions; Neurological-system; Laboratory-animals; Laboratory-testing; Animal-studies; Animals; Exposure-levels; Exposure-methods; Brain-function; Olfactory-disorders; Neurotransmitters; Proteins; Molecular-structure; Central-nervous-system; Central-nervous-system-disorders; Risk-analysis; Acute-toxicity; Brain-damage
Contact
Krishnan Sriram, PhD, Toxicology and Molecular Biology Branch, Mailstop L-3014, CDC-NIOSH, 1095 Willowdale Road, Morgantown, WV 26505, USA
CODEN
JTEHD6
CAS No.
1338-43-8; 9005-65-6; 9005-70-3; 577-11-7; 29911-28-2; 64742-47-8
Publication Date
20111101
Document Type
Journal Article
Email Address
kos4@cdc.gov
Fiscal Year
2012
NTIS Accession No.
NTIS Price
Identifying No.
B10122011
Issue of Publication
21
ISSN
1528-7394
NIOSH Division
HELD
Priority Area
Manufacturing
Source Name
Journal of Toxicology and Environmental Health, Part A: Current Issues
State
WV
TOP