Evaluation of neutralized Chemical Agent Identification Sets (CAIS) for skin injury with an overview of the vesicant potential of agent degradation products

Olajos, Eugene J.; Olson, Carl; Salem, Harry; Singer, Allen W; Hayes, Timothy L.; Menton, R. G.; Miller, Theodore L.; Rosso, Thomas E.; MacIver, Brian

doi:10.1002/(sici)1099-1263(199811/12)18:6<409::aid-jat515>3.0.co;2-z

Cited by 11 publications

(9 citation statements)

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“…Based on studies of the related vesicant SM, eyes are the most sensitive organ to vesicant exposure with devastating short-and long-term injuries affecting up to 90% of the exposed individuals (9-12). Compared to other vesicants, relatively faster absorption of LEW can cause immediate pain and ocular injury, which can be severe and produce edema of eyelids, inflammation, massive corneal necrosis and blindness (13, 14). Literature reports on animal testing for ocular injuries are limited to the 1940's (15-18), whereby, LEW injuries were characterized by an immediate appearance of edema and blepharospasm, which can be serious with massive necrosis and eventual blindness (15, 18).…”

Section: Introductionmentioning

confidence: 99%

Clinical progression of ocular injury following arsenical vesicant lewisite exposure

Tewari‐Singh

Croutch

Tuttle

et al. 2016

Cutaneous and Ocular Toxicology

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Ocular injury by lewisite (LEW), a potential chemical warfare and terrorist agent, results in edema of eyelids, inflammation, massive corneal necrosis, and blindness. To enable screening of effective therapeutics to treat ocular injury from LEW, useful clinically-relevant endpoints are essential. Hence, we designed an efficient exposure system capable of exposing up to six New-Zealand white rabbits at one time, and assessed LEW vapor-induced progression of clinical ocular lesions mainly in the cornea. The right eye of each rabbit was exposed to LEW (0.2 mg/L) vapor for 2.5, 5.0, 7.5 and 10.0 min and clinical progression of injury was observed for 28 days post-exposure (dose-response study), or exposed to same LEW dose for 2.5 and 7.5 min and clinical progression of injury was observed for up to 56 days post-exposure (time-response study); left eye served as an unexposed control. Increasing LEW exposure caused corneal opacity within 6 h post-exposure, which increased up to 3 days, slightly reduced thereafter till 3 weeks, and again increased thereafter. LEW-induced corneal ulceration peaked at 1 day post-exposure and its increase thereafter was observed in phases. LEW exposure induced neovascularization starting at 7 days which peaked at 22-35 days post-exposure, and remained persistent thereafter. In addition, LEW exposure caused corneal thickness, iris redness, and redness and swelling of the conjunctiva. Together, these findings provide clinical sequelae of ocular injury following LEW exposure and for the first time establish clinically-relevant quantitative endpoints, to enable the further identification of histopathological and molecular events involved in LEW-induced ocular injury.

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Section: Introductionmentioning

confidence: 99%

Clinical progression of ocular injury following arsenical vesicant lewisite exposure

Tewari‐Singh

Croutch

Tuttle

et al. 2016

Cutaneous and Ocular Toxicology

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“…These agents are known to cause both acute toxic effects and long-term medical complications, which are widely investigated [1]. As it was widely reported previously, exposure to mustard gases is associated with development of numerous chronic health problems including chronic neuropathic pain [7], increased susceptibility to cancers [8][9][10][11][12][13][14], defective spermatogenesis [15], ocular injury [16][17][18][19][20][21][22], skin lesions [23][24][25][26][27] and also respiratory disorders [28][29][30][31][32][33][34][35][36][37][38]. Although the best known and the most severe annoying complications of exposure with these agents are those related to respiratory, ocular, and cutaneous systems, however a brief review of the previous reports suggest that mustard agents have also some long-term systemic effects on different organs (such as hematopoitic and productive systems).…”

Section: Introductionmentioning

confidence: 99%

Myocardial perfusion abnormalities in chemical warfare patients intoxicated with mustard gas

Gholamrezanezhad

Saghari

Vakili

et al. 2006

Int J Cardiovasc Imaging

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“…54 Unlike SM, LEW exposure results in an immediate irritation, inflammation of the eyes, and swelling of the eyelids. 3,55 The findings from our recent study for the first time showed clinical sequelae of ocular injury following LEW exposure, including corneal wounding, ulceration, inflammation, neovascularization, corneal thickness, iris redness, and redness and swelling of the conjunctiva, and their progression up to 56 days postexposure. 54 Importantly, LEW exposure in humans is shown to result in swelling and edema, inflammation to the iris and conjunctiva, and corneal damage; 3 the injuries are similar to those observed in the rabbit model in our study, suggesting the relevance of the model developed by us for both mechanistic and efficacy studies in the future.…”

Section: Development Of Vesicant-induced Ocular Injury Modelsmentioning

confidence: 82%

“…Using this consistent and efficient exposure system, we successfully carried out LEW exposures and established clinically relevant end points in a dose‐ and time‐response study . Unlike SM, LEW exposure results in an immediate irritation, inflammation of the eyes, and swelling of the eyelids . The findings from our recent study for the first time showed clinical sequelae of ocular injury following LEW exposure, including corneal wounding, ulceration, inflammation, neovascularization, corneal thickness, iris redness, and redness and swelling of the conjunctiva, and their progression up to 56 days postexposure .…”

Section: Development Of Vesicant‐induced Ocular Injury Modelsmentioning

confidence: 91%

Corneal toxicity induced by vesicating agents and effective treatment options

Goswami

Tewari‐Singh

Agarwal

2016

Annals of the New York Academy of Sciences

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The vesicating agents sulfur mustard (SM) and lewisite (LEW) are potent chemical warfare agents that primarily cause damage to the ocular, skin, and respiratory systems. However, ocular tissue is the most sensitive organ, and vesicant exposure results in a biphasic injury response, including photophobia, corneal lesions, corneal edema, ulceration, and neovascularization, and may cause loss of vision. There are several reports on ocular injury from exposure to SM, which has been frequently used in warfare. However, there are very few reports on ocular injury by LEW, which indicate that injury symptoms appear instantly after exposure and faster than SM. In spite of extensive research efforts, effective therapies for vesicant-induced ocular injuries, mainly to the most affected corneal tissue, are not available. Hence, we have established primary human corneal epithelial (HCE) cells and rabbit corneal organ culture models with the SM analog nitrogen mustard (NM), which have helped to test the efficacy of potential therapeutic agents. These agents will then be further evaluated against in vivo SM- and LEW-induced corneal injury models, which will assist in the development of potential broad-spectrum therapies against vesicant-induced ocular injuries.

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Evaluation of neutralized Chemical Agent Identification Sets (CAIS) for skin injury with an overview of the vesicant potential of agent degradation products

Cited by 11 publications

References 0 publications

Clinical progression of ocular injury following arsenical vesicant lewisite exposure

Clinical progression of ocular injury following arsenical vesicant lewisite exposure

Myocardial perfusion abnormalities in chemical warfare patients intoxicated with mustard gas

Corneal toxicity induced by vesicating agents and effective treatment options

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