The first Persian Gulf War, known as Operation Desert Storm, was an offensive that followed the August 1990 Iraqi invasion of Kuwait and was led by US and coalition troops in January 1991. The war was over on February 28, 1991, and an official cease-fire was signed in April 1991. The last US troops who participated in the ground war returned home on June 13, 1991. In all, about 697,000 US troops had been deployed to the Persian Gulf during the conflict. That war resulted in few injuries and deaths among coalition forces, but returning veterans soon began to report numerous health problems that they believed were associated with their service in the gulf. Those veterans were not exposed to blast but were potentially exposed to numerous biologic and chemical agents, including vaccinations and other prophylactic medications, nerve agents, depleted uranium, pesticides, solvents, combusted and uncombusted fuels, dust exposure, and burning waste.
On October 7, 2001, the United States began combat operations in Afghanistan in response to the September 11, 2001, terrorist attacks. The war in Afghanistan is also referred to as Operation Enduring Freedom (OEF). On March 20, 2003, the United States became engaged in military operations in Iraq. The Iraq War, also referred to as Operation Iraqi Freedom (OIF), and OEF have been fundamentally different from the first Gulf War in the number of troops deployed, in multiple deployments, in its duration, in the type of warfare, and in the numbers of deaths and injuries, particularly brain injuries. On September 1, 2010, OIF was renamed Operation New Dawn (OND) (Secretary of Defense Memorandum, February 17, 2010). As of September 2013, those wars have resulted in the
deployment of about 2.2 million troops; there have been 2,266 US fatalities in OEF and 4,489 in OIF and OND. The numbers of wounded US troops exceed 19,250 in Afghanistan and 32,000 in Iraq (DOD, 2013). In addition to deaths and morbidity, the operations have unforeseen consequences for military personnel that are not yet fully understood.
In 1998, in response to the growing concerns of ill Gulf War veterans, Congress passed two laws: Public Law (PL) 105-277, the Persian Gulf War Veterans Act, and PL 105-368, the Veterans Programs Enhancement Act. Those laws directed the secretary of veterans affairs to enter into a contract with the National Academy of Sciences (NAS) to review and evaluate the scientific and medical literature regarding associations between illness and exposure to toxic agents, environmental or wartime hazards, and preventive medicines or vaccines related to Gulf War service and to consider the NAS conclusions when making decisions about compensation. The study was assigned to the Institute of Medicine (IOM), and several volumes have been published.1 Several of the volumes address the concerns of not only the 1991 Gulf War veterans but also the veterans of the Iraq and Afghanistan wars.
The legislation did not preclude an IOM recommendation or a Department of Veterans Affairs (VA) request for additional studies, particularly as subjects of concern arise. For example, VA’s request that the IOM consider whether there is an increased risk of amyotrophic lateral sclerosis in all veteran populations resulted in the report Amyotrophic Lateral Sclerosis in Veterans (IOM, 2006a); an examination of all health effects in veterans deployed to the 1991 Persian Gulf War irrespective of specific exposures resulted in Gulf War and Health, Volume 4: Health Effects of Serving in the Gulf War (IOM, 2006b); and a VA request regarding the long-term effects of traumatic brain injury (TBI) resulted in Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury (IOM, 2009). The present volume grew out of discussions with VA over concern about blast injuries and the potential long-term effects of being in a blast.
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1Gulf War and Health, Volume 1: Depleted Uranium, Pyridostigmine Bromide, Sarin, Vaccines (IOM, 2000); Gulf War and Health, Volume 2: Insecticides and Solvents (IOM, 2003); Gulf War and Health, Volume 3: Fuels, Combustion Products, and Propellants (IOM, 2005); Gulf War and Health, Volume 4: Health Effects of Serving in the Gulf War (IOM, 2006); Gulf War and Health, Volume 5: Infectious Diseases (IOM, 2006); Gulf War and Health, Volume 6: Physiologic, Psychologic, and Psychosocial Effects of Deployment-Related Stress (IOM, 2008); Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury (IOM, 2009); and Gulf War and Health, Volume 8: Update of Health Effects of Serving in the Gulf War (IOM, 2010).
The wars in Iraq and Afghanistan have become known for the enemy’s reliance on improvised explosive devices (IEDs) (Champion et al., 2009; Ritenour et al., 2010). It has been estimated that explosive weaponry accounts for about 75% of all US military casualties (Belmont et al., 2010, 2012). Explosive incidents involving IEDs are a worldwide problem. In 2012, the number of terrorist attacks worldwide involving IEDs, including military combat, was 2,451; 2,634 people were killed and 6,601 wounded (CEDAT, 2013).
It is not possible to know precisely the number of military personnel who served in the Iraq and Afghanistan wars and were exposed to blast. However, data that can serve as a surrogate for blast exposure are available and provide a rough estimate of blast-exposed personnel.
A substantial portion of blast exposure during the Iraq and Afghanistan wars comes from IEDs. Since 2001, about 1,380 OEF service members have been killed in action and 11,312 wounded in action because of IEDs. From March 2003 to November 2011, about 2,207 OIF and OND service members have been killed in action and 21,743 wounded in action because of IEDs (DMDC, 2013; iCasualties, 2013). There were limitations in extrapolating those data to overall blast exposure of military personnel of the Iraq and Afghanistan wars. Those numbers refer only to service members who have been killed or wounded in action. The number of service members exposed to blast in the combat environment is probably much higher.
Another means of estimating the number of blast-exposed military personnel is to use data on numbers of personnel who have received TBIs, particularly mild TBIs. Mild TBIs account for nearly 77% of TBIs (187,539 of the total of 244,217 service members who received TBIs) in personnel serving in the Iraq and Afghanistan wars (IOM, 2013). The major cause of TBI in the Iraq and Afghanistan wars is exposure to blast, often from IEDs. Again, this information provides only a rough estimate of blast exposure, and it is probable that the actual number of service members exposed is much higher.
There are five mechanisms by which injuries can occur after exposure to blast. Primary injury is the direct result of spallation, implosion, or inertia; these injuries are caused as a sole consequence of the shock wave–body interaction. Their effects are concentrated on regions where there is an air or fluid interface with tissue (Wolf et al., 2009). For example, a combination of implosion and spallation forces may cause an air embolus to enter a capillary as a blast wave travels through blood and into a capillary where spalling disrupts the endothelium and implosion causes compressed air to expand (Ho, 2002; Wolf et al., 2009). Organ systems that have greater air–tissue interfaces are more susceptible to primary blast injuries. Auditory
injury is the most common, occurring at 35 kilopascal (kPa), compared with pulmonary or intestinal injury, which occurs at 75–100 kPa (Wolf et al., 2009). Overpressure may also affect the central nervous, musculoskeletal, visual, and cardiovascular systems. And a blast wave may cause a systemic shock that subsides in minutes or hours (Wolf et al., 2009). Secondary injury is caused by debris that is displaced by a blast wave or blown by the blast wind. A combination of penetrating or blunt injuries may result, including bruises and lacerations. Fragments or shrapnel may create small puncture wounds. Because fragments travel further than a blast wave, secondary injuries are more common than primary injuries (Wolf et al., 2009). Tertiary injury results from the physical displacement of a person by a blast wave or blast wind. A person who is pushed or blown may suffer a variety of injuries, such as head trauma or fractures. Injuries associated with falling buildings—such as head trauma, traumatic asphyxiation, and crush injuries—are considered tertiary injuries (Wolf et al., 2009). Quartenary injuries, or miscellaneous injuries, include all other injuries directly caused by a blast but not classified by another mechanism. These injuries may be burns, toxic-substance exposures, and psychologic trauma (Wolf et al., 2009). Quinary injuries are illnesses or diseases that result from chemical, biologic, or radiologic substances released by a bomb (Cernak and Noble-Haeusslein, 2010; Plurad, 2011). Chapter 3 describes the mechanisms of blast injury in greater detail.
The charge to the present IOM committee was to examine the strength of the evidence of an association between being exposed to blast and potential long-term health effects. The committee also was asked to make recommendations for future research on the topic. Specifically, the statement of work notes that the IOM
shall comprehensively review, evaluate, and summarize the available scientific and medical literature associated with the multisystem response to blast exposures and subsequent acute and long-term health consequences among Gulf War veterans.
In making determinations, the committee shall consider
a. The strength of scientific evidence, the replicability of results, the statistical significance of results, and the appropriateness of the scientific methods used to detect the association;
b. In any case where there is evidence of an apparent association, whether there is reasonable confidence that the apparent association is not due to chance, bias, or confounding;
c. The increased risk of illness among human or animal populations exposed to blast injuries;
d. Whether a plausible biological mechanism or other evidence of a causal relationship exists between exposure to blast and long-term systemic adverse health effects;
e. Whether type of blast (for example, shaped blast wave vs diffuse) is associated with injury pattern; and
f. Whether improvements in collective and personal blast protection are associated with diminished blast injury.
In evaluating the long-term health effects of blast exposures among Gulf War Veterans, the committee should look broadly for relevant information. Information sources to pursue could include but are not limited to
a. Published peer-reviewed literature related to blast injuries among the 1991 Gulf War Veteran population;
b. Published peer-reviewed literature related to blast injuries among OEF (Operation Enduring Freedom), OIF (Operation Iraqi Freedom), New Dawn active-duty service members and veterans, and other conflicts as appropriate;
c. Published peer-reviewed literature related to blast injuries among similar populations such as allied military personnel; and
d. Published peer-reviewed literature related to blast injuries in other populations.
HOW THE COMMITTEE APPROACHED ITS CHARGE
The committee was charged with conducting a review of the scientific literature on the association between blast and long-term health effects. The charge did not specify the type of blast injury—primary, secondary, tertiary, quaternary, and quinary—and, therefore, the committee did not attempt to limit its review to any mechanism of blast injury. In fact, many of the studies reviewed by the committee, particularly epidemiologic studies, did not specify the mechanism of exposure (that is, the reported exposure was to blast generally). Chapter 3 includes a detailed description of the types of blast injury. The review included all relevant studies of blast in any population (military, occupational, and other) and health outcomes. The committee reviewed all papers that provided information about blast and health outcomes. By examining the full array of evidence of health outcomes in different populations, the committee answered the question, Can sustaining a blast be associated with a specific health outcome? It should be remembered that an association between a blast and a health outcome does not mean that all cases of the outcome are related to the blast; in fact, such direct correspondence is the exception rather than the rule in studies of health outcomes in large populations (IOM, 1994).
The committee reviewed more than 12,800 titles and abstracts of scien-
tific and medical articles related to blast and health outcomes. It reviewed the full text of about 400 peer-reviewed journal articles, many of which are described in the present report. The staff performed several searches in 2012 and 2013 in an effort to keep current with the literature.
The details of the committee’s approach to its charge, the literature-search strategy, the types of studies that were reviewed, the committee’s inclusion criteria, and categories of association are described in Chapter 2.
Chapter 2 summarizes the committee’s methods for approaching its charge and details of its literature search. A model of possible long-term consequences of exposure to blast is described. Animal models of blast and experimental data are discussed in Chapter 3. Chapter 4 contains the committee’s evaluation of the array of human health effects caused by exposure to blast. It also presents the pros and cons of blast protection and the use of body armor. Finally, Chapter 5 presents the committee’s recommendations. Biographic information on the committee members is included in an appendix.
Belmont, P. J., A. J. Schoenfeld, and G. Goodman. 2010. Epidemiology of combat wounds in Operation Iraqi Freedom and Operation Enduring Freedom: Orthopaedic burden of disease. Journal of Surgical Orthopaedic Advances 19(1):2-7.
Belmont, P. J., Jr., B. J. McCriskin, R. N. Sieg, R. Burks, and A. J. Schoenfeld. 2012. Combat wounds in Iraq and Afghanistan from 2005 to 2009. Journal of Trauma and Acute Care Surgery 73(1):3-12.
CEDAT (Centre of Excellence Defence Against Terrorism). 2013. Annual Terrorism Report 2012. Turkey: NATO.
Cernak, I., and L. J. Noble-Haeusslein. 2010. Traumatic brain injury: An overview of pathobiology with emphasis on military populations. Journal of Cerebral Blood Flow and Metabolism 30(2):255-266.
Champion, H. R., J. B. Holcomb, and L. A. Young. 2009. Injuries from explosions: Physics, biophysics, pathology, and required research focus. Journal of Trauma: Injury, Infection, & Critical Care 66(5):1468-1477.
DMDC (Defense Manpower Data Center). 2013. Global War on Terrorism Casualties by Reason. http://siadapp.dmdc.osd.mil/personnel/CASUALTY/gwot_reason.pdf (accessed September 1, 2013).
DOD (Department of Defense). 2013. US Department of Defense Casualty Status. http://www.defense.gov/news/casualty.pdf (accessed June 18, 2013).
Ho, A. M. H. 2002. A simple conceptual model of primary pulmonary blast injury. Medical Hypotheses 59(5):611-613.
iCasualties. 2013. OEF Fatalities. http://icasualties.org/oef (accessed September 5, 2013).
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IOM. 2006a. Amyotrophic Lateral Sclerosis in Veterans. Washington, DC: The National Academies Press.
IOM. 2006b. Gulf War and Health, Volume 4: Health Effects of Serving in the Gulf War. Washington, DC: The National Academies Press.
IOM. 2009. Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury. Washington, DC: The National Academies Press.
IOM. 2013. Returning Home from Iraq and Afghanistan: Assessment of Readjustment Needs of Veterans, Service Members, and Their Families. Washington, DC: The National Academies Press.
Plurad, D. S. 2011. Blast injury. Military Medicine 176(3):276-282.
Ritenour, A. E., L. H. Blackbourne, J. F. Kelly, D. F. McLaughlin, L. A. Pearse, J. B. Holcomb, and C. E. Wade. 2010. Incidence of primary blast injury in US military overseas contingency operations: A retrospective study. Annals of Surgery 251(6):1140-1144.
Wolf, S. J., V. S. Bebarta, C. J. Bonnett, P. T. Pons, and S. V. Cantrill. 2009. Blast injuries. Lancet 374(9687):405-415.
