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as there is no treatment that can reverse the symptoms once 9. Steinritz D, Stiepling E, Rudolf KD, et al. Medical documen-
the chronic phase has been reached. 35 tation, bioanalytical evidence of an accidental human expo-
sure to sulfur mustard and general therapy recommendations.
Malignancy and Teratogenesis Toxicol Lett. 2016;244:112–120.
Sulfur mustard is a known carcinogen. Studies examining 10. Kehe K, Thiermann H, Balszuweit F, et al. Acute effects of
former workers involved in the production of mustard gas sulfur mustard injury–Munich experiences. Toxicology. 2009;
demonstrate higher rates of respiratory tract malignancies. 36,37 263(1):3–8.
While chronic exposure, such as occurred in chemical war- 11. Haines DD, Fox SC. Acute and long-term impact of chemical
fare workers, demonstrates a clear relationship between ex- weapons: lessons from the Iran-Iraq War. Forensic Sci Rev.
2014;26(2):97–114.
posure and malignancy, studies of acute exposure have been 12. Chemical casualties. Vesicants (blister agents). J R Army Med
less conclusive. There are several small, underpowered studies Corps. 2002;148(4):358–370.
that have attempted to infer that acute exposure to mustard is 13. Balali-Mood M, Hefazi M. Comparison of early and late
associated with malignancy. 38-40 However, large epidemiologic toxic effects of sulfur mustard in Iranian veterans. Basic Clin
studies have been less conclusive. 41,42 Despite these findings, Pharmacol Toxicol. 2006;99(4):273–282.
it is prudent to ensure that victims of mustard gas exposure 14. Hejazi S, Soroush M, Moradi A, et al. Skin manifestations
receive routine screening for malignancies. in sulfur mustard exposed victims with ophthalmologic com-
plications: association between early and late phase. Toxicol
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posed individuals. In particular, the rates of congenital malfor- 15. Eisenkraft A, Falk A. The possible role of intravenous lipid
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mations and respiratory disorders are 2–4 times higher among ing. Toxicol Rep. 2016;3:202–210.
populations exposed to mustard. Additionally, rates of fetal 16. Yue L, Zhang Y, Chen J, et al. Distribution of DNA adducts
43
44
demise are higher in exposed populations. These findings and corresponding tissue damage of Sprague-Dawley rats
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beyond the lives of the exposed alone. Toxicol. 2015;28(3):534–40.
17. Rahmani H, Javadi I, Shirali S. Respiratory complications due
Disclaimer to sulfur mustard exposure. Int J Curr Res Aca Rev. 2016;
The views expressed herein are those of the authors and do 4(6):143–149.
not reflect the official policy or position of the US Army Med- 18. Otter J, Dawood A, D’Orazio J. Sulfur mustard exposure
ical Department, Department of the Army, Department of De- from dredged artillery shell in a commercial clammer. Clin
Pract Cases Emerg Med. 2017;1(4):283–286.
fense, or the US Government. 19. Rajavi Z, Safi S, Javadi MA, et al. Clinical practice guidelines
for prevention, diagnosis and management of early and de-
Disclosure layed-onset ocular injuries due mustard gas exposure. J Oph-
The authors have nothing to disclose. thalmic Vis Res. 2017;12(1):65–80.
20. Tuorinsky SD (Ed). Medical Aspects of Chemical Warfare.
Funding Washington, DC: Borden Institute; 2008.
The authors have no source of funding to report. 21. Initial care of ocular injuries and adnexal injuries by non-
ophthalmologists at Role 1, Role 2, and non-ophthalmologic
Author Contributions Role 3 facilities. Joint Theater Trauma System Clinical Prac-
tice Guideline; 2014.
The review was designed was SMP, JFP, JBW, and TPP. Review 22. Javadi MA. Mustard gas induced ocular injuries. J Ophthal-
of literature and drafting of the manuscript was performed by mic Vis Res. 2017;12(1):1–2.
GAW, SMP, JFP, JBW, and TPP. Revision of the manuscript 23. Ghanei M, Harandi AA. Long term consequences from expo-
was performed by SMP and TPP. All authors read and ap- sure to sulfur mustard: a review. Inhal Toxicol. 2007;19(5):
proved the final manuscript. 451–456.
24. Saber H, Saburi A, Ghanei M. Clinical and paraclinical guide-
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