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Review
.2022;34(13-14):412-432.
doi: 10.1080/08958378.2022.2147257. Epub 2022 Nov 17.

A review of chemical warfare agents linked to respiratory and neurological effects experienced in Gulf War Illness

Affiliations
Review

A review of chemical warfare agents linked to respiratory and neurological effects experienced in Gulf War Illness

Angela Cruz-Hernandez et al. Inhal Toxicol.2022.

Abstract

Over 40% of veterans from the Persian Gulf War (GW) (1990-1991) suffer from Gulf War Illness (GWI). Thirty years since the GW, the exposure and mechanism contributing to GWI remain unclear. One possible exposure that has been attributed to GWI are chemical warfare agents (CWAs). While there are treatments for isolated symptoms of GWI, the number of respiratory and cognitive/neurological issues continues to rise with minimum treatment options. This issue does not only affect veterans of the GW, importantly these chronic multisymptom illnesses (CMIs) are also growing amongst veterans who have served in the Afghanistan-Iraq war. What both wars have in common are their regions and inhaled exposures. In this review, we will describe the CWA exposures, such as sarin, cyclosarin, and mustard gas in both wars and discuss the various respiratory and neurocognitive issues experienced by veterans. We will bridge the respiratory and neurological symptoms experienced to the various potential mechanisms described for each CWA provided with the most up-to-date models and hypotheses.

Keywords: CEES; Chemical warfare agents; Gulf War Illness; chronic multisymptom illness; cyclosarin; neurological effects; nitrogen mustard; organophosphorus compounds; respiratory; sarin; sulfur mustard.

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Figures

Figure 1.
Figure 1.. Overview of SM exposure.
Inhalation to SM has been attributed to lung and brain injury. After exposure to SM, soldiers and civilians develop respiratory complications, such as asthma-like pathologies, chronic bronchitis, and pulmonary fibrosis. While the lungs are known for their susceptibility to SM toxicity, the brain’s effects remain primarily unknown. Figure created withbiorender.com
Figure 2.
Figure 2.. Overview of Proposed Mechanisms of Toxicity for Sulfur Mustard.
(A) SM can cause apoptosis via the FAS/FASL pathway. (B) SM alkylates DNA, RNA, and proteins. DNA alkylation leads to single and double-strand breaks, which leads to the activation of PARP. Overactivation of PARP leads to NAD+ depletion and necrosis. While RNA and protein alkylation don’t lead directly to cell death, lack of antioxidants increases intracellular Ca2+ and alters cell morphology. (C) SM’s damage and toxicity causes epithelial damage leading to a robust inflammatory response through macrophages, neutrophils, and mast cells. (D) SM causes mitochondrial dysfunction, immune cell accumulation (macrophage and neutrophils), leading to a respiratory burst of reactive oxygen species (ROS), nitric oxide (NO), and necrotic cell death. Figure created withbiorender.com
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References

    1. Institute of Medicine Committee on Gulf, W. & Health: Health Effects of Serving in the Gulf War, U. in Gulf War and Health: Volume 8: Update of Health Effects of Serving in the Gulf War (National Academies Press (US)Copyright 2010 by the National Academy of Sciences. All rights reserved., 2010).
    1. Murphy FM Gulf war syndrome. BMJ 318, 274–275, doi:10.1136/bmj.318.7179.274 (1999). - DOI - PMC - PubMed
    1. Kaimal G & Dieterich-Hartwell R Grappling with Gulf War Illness: Perspectives of Gulf War Providers. Int J Environ Res Public Health 17, doi:10.3390/ijerph17228574 (2020). - DOI - PMC - PubMed
    1. Maule AL et al. Meta-analysis of self-reported health symptoms in 1990–1991 Gulf War and Gulf War-era veterans. BMJ Open 8, e016086, doi:10.1136/bmjopen-2017-016086 (2018). - DOI - PMC - PubMed
    1. Affairs, U. S. D. o. V. Gulf War Illnesses linked to Southwest Asia service, <https://www.va.gov/disability/eligibility/hazardous-materials-exposure/g...> (2021).

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