Scientists believe nasal and respiratory irritation caused by desert sand storms and oil field fires during Operation Desert Storm, may have weakened the nose/brain barrier and allowed depleted uranium to enter the central nervous system of soldiers in the field resulting in slowly developing neurotoxic responses.
Preliminary investigations with depleted uranium shrapnel have shown that the brain is one of the target organs for deposition of depleted uranium dissolved from shrapnel. The follow-up medical exams of 29 Gulf War veterans with retained DU shrapnel have shown subtle neurocognitive losses that show a statistical relationship between uranium levels and performance on computerized tests of performance efficiency (McDiarmid et al., 2000).
During Operation Desert Storm, American M1A1, M1, and M60 tanks and British Challenger tanks fired thousands of large caliber depleted uranium armor penetrators. American A-10 and AV-8B aircraft shot hundreds of thousands of small caliber depleted uranium rounds. In addition, one-third of the American tanks used in the war were equipped with DU armor.
The extensive use of depleted uranium during the war could have resulted in substantial inhalation exposure. Although depleted uranium is considered toxic to the kidney because of its properties as a heavy metal, recent data have linked systemic exposure to depleted uranium to neurotoxic effects as well (Pellmar et al, 1999 a,b; McDiarmid et al, 2000).
Following the Gulf War, veterans began to report a variety of symptoms that have become known “Gulf War Illness.” Given the complexity of environmental exposures that occurred during the war, the level of stress involved in battlefield situations and the presence of several potentially toxic agents, the most practical assumption is to believe that Gulf War illness is the result of several factors acting in synergy. But in addition to being possible, the proposed causes must be unique to the Gulf War, as similar symptoms had not been observed prior to that operation.
The exposure to depleted uranium combined with the exposure to extensive combustion products from oil fires and blowing sand from the desert environment, however, is unique and the extent of exposure to respiratory irritants during this war was probably greater than in previous wars.
This combination of respiratory irritants could result in a sensitization or alteration of the response to other toxic chemicals such as depleted uranium. Irritation of the respiratory tract could result in increased amounts of depleted uranium being taken in, creating more intense responses. It could also result in uranium reaching other targets in the body, such as the brain, which could produce a different pattern of responses.
Personnel have emphasized that air quality during the war was a major difficulty due not only to the high levels of dust generated from blowing desert sands, but also to the extensive oil field fires that contributed extensive hydrocarbon smoke plumes.
Therefore, the occurrence of the first potentially substantial inhalation exposures to DU during the Gulf War and the occurrence of an illness which includes a high frequency of symptoms of neurologic origin suggests that the relationship of DU exposures to these symptoms deserves additional attention. The presence of coexposures likely to result in inflammation of the upper respiratory tract provides a plausible mechanism for enhancing the entry of inhaled DU directly to the Central Nervous System through weakening of the nose-brain barrier.
Scientists working on this study will investigate the potential for inhaled DU aerosols to penetrate the nose-brain barrier in conditions modeling Gulf War exposures. They will examine whether it can then spread within the Central Nervous System and result in slowly developing neurotoxic responses.
Hypotheses:
I. Inhalation of uranium aerosols during the Gulf War from combustion of DU-containing weapons resulted in CNS deposition and subsequent neurodegeneration in a subset of those exposed.
II. Transient conditions such as inflammation will compromise the olfactory epithelium (nose/brain barrier) and enhance the entry of uranium and the subsequent development of neurodegeneration.
III: Markers of neurodegeneration will be correlated with the concentration and pattern of deposition of uranium within the CNS following inhalation exposure.
IV: The degree and time-course of neurodegeneration will be dose and exposure duration dependent.
Technical Objectives:
To determine whether uranium enters the CNS via penetration of the nose-brain barrier using exposure atmospheres that model environmental exposures encountered in the Gulf war.
To determine whether uranium uptake into the CNS causes progressive neurodegeneration with increasing time post-exposure.
To examine potential alterations in susceptibility as a result of nasal inflammation which was likely to occur in soldiers during the war as a result of high concentrations of blowing sand and smoke from oil-field fires.
Inhalation data will be cross referenced to data arising from DU implant studies and to determine whether the more commonly associated nephrotoxic and pulmonary effects occur at levels where CNS deposition and/or toxicity occur.
The results obtained from the studies should provide a realistic assessment of the neurotoxic, nephrotoxic and pulmonary effects posed by inhalation of uranium oxide aerosols during the Gulf war.
This will better enable DOD to assess potentially toxic effects resulting from the deployment of uranium containing weapons and equipment in battlefield conditions. Inclusion of tantalum oxide controls will provide a more complete information base for consideration of these factors in future weapons design initiatives.
Lovelace Respiratory Research Institute
2425 Ridgecrest Drive SE
Albuquerque, NM 87108
(505) 348-9400
