Inhalation of Uranium Oxide Aerosois: CNS Deposition, Neurotoxicity, and Role in Gulf War Illness
Abstract
This study investigates the potential for inhaled uranium oxide (UO) aerosols to penetrate the nose-brain barrier, directly enter the central nervous system (CNS), distribute within the CNS, and result in slowly developing neurotoxicity. Inhalation exposures to depleted uranium (DU) may have occurred during the GW in several scenarios of varying duration and airborne uranium concentration. Nasal inflammation could alter sensitivity to uranium uptake. Nephrotoxic and pulmonary effects are evaluated to determine whether CNS effects can occur at lower thresholds than nephrotoxic effects. In year 4, we focused on analysis of tissues following long-term (30 days), moderate dose (1 mg/m3) uranium inhalation, with or without induced nasal inflammation. Brain uptake was only seen in a subset of rats (2 of 12) and only in the olfactory bulb. Similarly, rats re-exposed to long-term, low dose uranium in combination with induced nasal damage also showed a limited uranium uptake (3 of 24 rats). Histological evaluation of olfactory bulbs revealed an increased astrogliosis and an upregulation of tyrosine hydroxylase (a marker for dopaminergic neurons) 180 days after uranium inhalation. No loss of large spinal motor neurons was seen at the same timepoint. Uranium-associated kidney pathology was not notable at this exposure regimen, but alveolar macrophage hyperplasia and particle inclusion were uniform and persistent, apparent even at 180 days post 30 day exposure.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2005
- Accession Number
- ADA454899
Entities
People
- Fletcher F. Hahn
- Graham Bench
- Johnnye L. Lewis
Organizations
- University of New Mexico