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Sulfur Mustard (sulfur + mustard)
Selected AbstractsRegulation of 1-,, 25-Dihydroxyvitamin D3 on Interleukin-6 and Interleukin-8 Induced by Sulfur Mustard (HD) on Human Skin Cells,BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 5 2003Carmen M. Arroyo Stimulation of human skin fibroblasts with sulfur mustard (10,4 M for 24 hr at 37°) resulted in approximately a 5 times increase in the secretion of interleukin-6 and over a 10 times increase for interleukin-8, which was inhibited by 1-,, 25 (OH)2D3, at ,10,9 M. 1-,, 25 (OH)2D3 also suppressed interleukin-8 secretion by 5 times and interleukin-6 by 4 times on sulfur mustard-stimulated human epidermal keratinocytes at concentrations , 10,9 M. The effect of 1-,, 25 (OH)2D3 was dose-dependent for the suppression of interleukin-6 and interleukin-8 induced by sulfur mustard on human skin fibroblasts/human epidermal keratinocytes, apparent at nanomolar concentrations. Our results indicate that the suppression of these inflammatory mediators by 1-,, 25 (OH)2D3 is dependent on the source of the primary cultures, cell densities, and kinetics of pretreatments. In contrast to the inhibition of cytokine/chemokine production, cell proliferation was enhanced by almost 1.7 times on treated human epidermal keratinocytes with 1-,, 25 (OH)2D3 (1×10,9 M) after sulfur mustard-stimulation (10,4 M for 24 hr at 37°C). The observed enhancement diversified based on cell density, and kinetics of pretreatment with a maximal synergism (s) observed at 1×10,9 M. Photomicrographs show typical signs of cellular degeneration caused by sulfur mustard such as chromatin condensation. The observed cellular degeneration was lessened when human epidermal keratinocytes were treated with 1-,, 25 (OH)2D3 (2×10,9 M). 1-,, 25(OH)2D3 could be an alternative treatment for cutaneous inflammation disorders caused by sulfur mustard because we have demonstrated its ability to suppress inflammatory mediators and enhanced cell proliferation in human skin cells stimulated with sulfur mustard. [source] Evaluation of analogues of DRDE-07 as prophylactic agents against the lethality and toxicity of sulfur mustard administered through percutaneous routeJOURNAL OF APPLIED TOXICOLOGY, Issue 2 2006A. S. Kulkarni Abstract Sulfur mustard (SM), chemically bis (2-chloroethyl) sulfide is a bifunctional alkylating agent that causes serious blisters on contact with human skin. Although several antidotes have been reported for the systemic toxicity of SM in experimental animals none of them are approved so far and decontamination of SM immediately by physical or chemical means is recommended as the best protection. Two compounds amifostine [S-2(3-aminopropylamino) ethyl phosphorothioate] and DRDE-07 [S-2(2-aminoethylamino) ethyl phenyl sulfide] gave very good protection as an oral prophylactic agent against SM the in mouse model, but in the rat model the protection was only moderate. In the search for more effective and less toxic compounds, a number of analogues of DRDE-07 were synthesised and their protective efficacy was evaluated in mouse and rat models. The LD50 of S-aryl substitution was between 1 and 2 g kg,1 and S-alkyl substitution was more than 2 g kg,1. In the mouse model, DRDE-07, DRDE-10, DRDE-21, DRDE-30 and DRDE-35 gave about 20 fold protection, and DRDE-23 and DRDE-38 gave less protection of 4.8 and 9.0 fold respectively, against percutaneously administered SM. In the rat model, DRDE-07, DRDE-09, DRDE-10 and DRDE-21 gave about two fold protection. Percutaneously administered SM (19.33 mg kg,1) significantly depleted the hepatic GSH content in mice. Pretreatment with DRDE-21 significantly elevated the levels. A 4.4 fold increase in % DNA fragmentation was observed 7 days after SM administration (19.33 mg kg,1) in mice. Pretreatment with DRDE-07, DRDE-09, DRDE-10, DRDE-21, DRDE-30 and DRDE-35 significantly protected the mice from SM induced DNA damage. The histopathological lesions in liver and spleen induced by percutaneously administered SM was reduced by pretreatment with DRDE-07, DRDE-09, DRDE-10 and DRDE-21. These analogues may prove as prototypes for the designing of more effective prophylactic drug for SM. Copyright © 2006 John Wiley & Sons, Ltd. [source] Use of methyl salicylate as a simulant to predict the percutaneous absorption of sulfur mustardJOURNAL OF APPLIED TOXICOLOGY, Issue 2 2001Jim E. Riviere Abstract Exposure to chemical vesicants such as sulfur mustard (HD) continues to be a threat to military forces requiring protectant strategies to exposure to be evaluated. Methyl salicylate (MS) has historically been the simulant of choice to assess HD exposure. The purpose of this study was to compare the percutaneous absorption and skin deposition of MS to HD in the isolated perfused porcine skin flap (IPPSF). The HD data were obtained from a previously published study in this model wherein 400 ,g cm,2 of ]14C[-MS or ]14C[-HD in ethanol were topically applied to 16 IPPSFs and experiments were terminated at 2, 4 or 8 h. Perfusate was collected at increasing time intervals throughout perfusion. Radioactivity was determined in perfusate and skin samples. Perfusate flux profiles were fitted to a bi-exponential model Y(t) = A(e, , e,) and the area under the curve (AUC), peak flux and time to peak flux were determined. Sulfur mustard had more pronounced and rapid initial flux parameters (P < 0.05). The AUCs determined from observed and model-predicted parameters were not statistically different, although the mean HD AUC was 40,50% greater than MS. The HD skin and fat levels were up to twice those seen with MS, but had lower stratum corneum and residual skin surface concentrations (P < 0.05). Compared with other chemicals studied in this model, HD and MS cutaneous disposition were very similar, supporting the use of MS as a dermal simulant for HD exposure. Copyright © 2001 John Wiley & Sons, Ltd. [source] Sulfur mustard induced cytokine production and cell death: Investigating the potential roles of the p38, p53, and NF-,B signaling pathways with RNA interference,JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 3 2010Albert L. Ruff Abstract Cutaneous and ocular injuries caused by sulfur mustard (SM; bis-(2-chloroethyl) sulfide) are characterized by severe inflammation and death of exposed cells. Given the known roles of p38MAPK and NF-,B in inflammatory cytokine production, and the known roles of NF-,B and p53 in cell fate, these pathways are of particular interest in the study of SM injury. In this study, we utilized inhibitory RNA (RNAi) targeted against p38,, the p50 subunit of NF-,B, or p53 to characterize their role in SM-induced inflammation and cell death in normal human epidermal keratinocytes (NHEK). Analysis of culture supernatant from 200 ,M SM-exposed cells showed that inflammatory cytokine production was inhibited by p38, RNAi but not by NF-,B p50 RNAi. These findings further support a critical role for p38 in SM-induced inflammatory cytokine production in NHEK and suggest that NF-,B may not play a role in the SM-induced inflammatory response of this cell type. Inhibition of NF-,B by p50 RNAi did, however, partially inhibit SM-induced cell death, suggesting a role for NF-,B in SM-induced apoptosis or necrosis. Interestingly, inhibition of p53 by RNAi potentiated SM-induced cell death, suggesting that the role of p53 in SM injury, may be complex and not simply prodeath. © 2010 Wiley Periodicals, Inc. J Biochem Mol Toxicol 24:155,164, 2010; Published online inWiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20321 [source] Shift of oxidants and antioxidants levels in rats as a reaction to exposure to sulfur mustardJOURNAL OF APPLIED TOXICOLOGY, Issue 8 2009Miroslav Pohanka Abstract Antixodants as well as oxidants levels were investigated in plasma of rats exposed to sulfur mustard in doses of 0 (control), 5, 20 and 80 mg kg,1 body weight. Cyclic voltammetry performed on screen-printed strips with platinum working electrode used as a tool for assaying oxidant and antioxidant levels. We found significant shifts in both examined analytes. A dose of sulfur mustard of 5 mg kg,1 body weight caused only a small change in oxidant and antioxidant levels when compared with the control group. A dose of 20 mg kg,1 body weight provided a significant increase in antioxidants as well oxidants; however, the ratio of both was similar to that in the control group. The most surprising facts were found when the highest dose of 80 mg kg,1 body weight of sulfur mustard was applied. While antioxidants were significantly increased, oxidants were decreased on an extensive scale. Copyright © 2009 John Wiley & Sons, Ltd. [source] Evaluation of analogues of DRDE-07 as prophylactic agents against the lethality and toxicity of sulfur mustard administered through percutaneous routeJOURNAL OF APPLIED TOXICOLOGY, Issue 2 2006A. S. Kulkarni Abstract Sulfur mustard (SM), chemically bis (2-chloroethyl) sulfide is a bifunctional alkylating agent that causes serious blisters on contact with human skin. Although several antidotes have been reported for the systemic toxicity of SM in experimental animals none of them are approved so far and decontamination of SM immediately by physical or chemical means is recommended as the best protection. Two compounds amifostine [S-2(3-aminopropylamino) ethyl phosphorothioate] and DRDE-07 [S-2(2-aminoethylamino) ethyl phenyl sulfide] gave very good protection as an oral prophylactic agent against SM the in mouse model, but in the rat model the protection was only moderate. In the search for more effective and less toxic compounds, a number of analogues of DRDE-07 were synthesised and their protective efficacy was evaluated in mouse and rat models. The LD50 of S-aryl substitution was between 1 and 2 g kg,1 and S-alkyl substitution was more than 2 g kg,1. In the mouse model, DRDE-07, DRDE-10, DRDE-21, DRDE-30 and DRDE-35 gave about 20 fold protection, and DRDE-23 and DRDE-38 gave less protection of 4.8 and 9.0 fold respectively, against percutaneously administered SM. In the rat model, DRDE-07, DRDE-09, DRDE-10 and DRDE-21 gave about two fold protection. Percutaneously administered SM (19.33 mg kg,1) significantly depleted the hepatic GSH content in mice. Pretreatment with DRDE-21 significantly elevated the levels. A 4.4 fold increase in % DNA fragmentation was observed 7 days after SM administration (19.33 mg kg,1) in mice. Pretreatment with DRDE-07, DRDE-09, DRDE-10, DRDE-21, DRDE-30 and DRDE-35 significantly protected the mice from SM induced DNA damage. The histopathological lesions in liver and spleen induced by percutaneously administered SM was reduced by pretreatment with DRDE-07, DRDE-09, DRDE-10 and DRDE-21. These analogues may prove as prototypes for the designing of more effective prophylactic drug for SM. Copyright © 2006 John Wiley & Sons, Ltd. [source] Attenuation of half sulfur mustard gas-induced acute lung injury in ratsJOURNAL OF APPLIED TOXICOLOGY, Issue 2 2006Shannon D. McClintock Abstract Airway instillation into rats of 2-chloroethyl ethyl sulfide (CEES), the half molecule of sulfur mustard compound, results in acute lung injury, as measured by the leak of plasma albumin into the lung. Morphologically, early changes in the lung include alveolar hemorrhage and fibrin deposition and the influx of neutrophils. Following lung contact with CEES, progressive accumulation of collagen occurred in the lung, followed by parenchymal collapse. The co-instillation with CEES of liposomes containing pegylated (PEG)-catalase (CAT), PEG-superoxide dismutase (SOD), or the combination, greatly attenuated the development of lung injury. Likewise, the co-instillation of liposomes containing the reducing agents, N-acetylcysteine (NAC), glutathione (GSH), or resveratrol (RES), significantly reduced acute lung injury. The combination of complement depletion and airway instillation of liposomes containing anti-oxidant compounds maximally attenuated CEES-induced lung injury by nearly 80%. Delayed airway instillation of anti-oxidant-containing liposomes (containing NAC or GSH, or the combination) significantly diminished lung injury even when instillation was delayed as long as 1 h after lung exposure to CEES. These data indicate that CEES-induced injury of rat lungs can be substantially diminished by the presence of reducing agents or anti-oxidant enzymes delivered via liposomes. Copyright © 2005 John Wiley & Sons, Ltd. [source] Putative role of proteolysis and in,ammatory response in the toxicity of nerve and blister chemical warfare agents: implications for multi-threat medical countermeasures,JOURNAL OF APPLIED TOXICOLOGY, Issue 3 2003F. M. Cowan Abstract Despite the contrasts in chemistry and toxicity, for blister and nerve chemical warfare agents there may be some analogous proteolytic and in,ammatory mediators and pathological pathways that can be pharmacological targets for a single-drug multi-threat medical countermeasure. The dermal,epidermal separation caused by proteases and bullous diseases compared with that observed following exposure to the blister agent sulfur mustard (2,2,-dichlorodiethyl sul,de) has fostered the hypothesis that sulfur mustard vesication involves proteolysis and in,ammation. In conjunction with the paramount toxicological event of cholinergic crisis that causes acute toxicity and precipitates neuronal degeneration, both anaphylactoid reactions and pathological proteolytic activity have been reported in nerve-agent-intoxicated animals. Two classes of drugs already have demonstrated multi-threat activity for both nerve and blister agents. Serine protease inhibitors can prolong the survival of animals intoxicated with the nerve agent soman and can also protect against vesication caused by the blister agent sulfur mustard. Poly (ADP-ribose) polymerase (PARP) inhibitors can reduce both soman-induced neuronal degeneration and sulfur-mustard-induced epidermal necrosis. Protease and PARP inhibitors, like many of the other countermeasures for blister and nerve agents, have potent primary or secondary anti-in,ammatory pharmacology. Accordingly, we hypothesize that drugs with anti-in,ammatory actions against either nerve or blister agent might also display multi-threat ef,cacy for the in,ammatory pathogenesis of both classes of chemical warfare agent. Published in 2003 by John Wiley & Sons, Ltd. [source] Kojic acid reduces the cytotoxic effects of sulfur mustard on cultures containing human melanoma cells in vitroJOURNAL OF APPLIED TOXICOLOGY, Issue 6 2001C. N. Smith Abstract In vivo experiments have shown that melanocytes are more sensitive than keratinocytes to the cytotoxic effects of sulfur mustard when it is applied topically to pig skin.1 It has been hypothesized that this is caused by the uncoupling of the melanogenic pathway by depletion of cellular glutathione, resulting in the uncontrolled production of cytotoxic quinone free-radical species by tyrosinase.2. In the present study, the feasibility of blocking the melanogenic pathway as a means of reducing the cytotoxicity of sulfur mustard was evaluated using kojic acid. Kojic acid is a topically applied depigmenting agent that exerts its effect by acting as a slow-binding, competitive inhibitor of tyrosinase.3 Preincubation of G361 pigmented melanoma cells and mixed cultures of G361 cells and SVK keratinocytes with 2.5 mM kojic acid resulted in significant increases in the viability of these cultures as determined by neutral red (NR) and gentian violet (GV) dye binding assays for up to 48 h following exposure to 50 µM sulfur mustard. The highest levels of protection were seen in the G361 cultures, with a 26.8% increase in culture viability (NR assay) compared with the sulfur-mustard-only controls at 24 h. Preincubation of SVK cells alone with kojic acid resulted in lower increases in viability (2.5% at 24 h by the NR assay). Inhibition of the melanogenic pathway reduces the sensitivity of cultures containing pigment cells to sulfur mustard. © Crown copyright 2001. Reproduced with the permission of Her Majesty's Stationery Office. Published by John Wiley & Sons, Ltd. [source] Use of methyl salicylate as a simulant to predict the percutaneous absorption of sulfur mustardJOURNAL OF APPLIED TOXICOLOGY, Issue 2 2001Jim E. Riviere Abstract Exposure to chemical vesicants such as sulfur mustard (HD) continues to be a threat to military forces requiring protectant strategies to exposure to be evaluated. Methyl salicylate (MS) has historically been the simulant of choice to assess HD exposure. The purpose of this study was to compare the percutaneous absorption and skin deposition of MS to HD in the isolated perfused porcine skin flap (IPPSF). The HD data were obtained from a previously published study in this model wherein 400 ,g cm,2 of ]14C[-MS or ]14C[-HD in ethanol were topically applied to 16 IPPSFs and experiments were terminated at 2, 4 or 8 h. Perfusate was collected at increasing time intervals throughout perfusion. Radioactivity was determined in perfusate and skin samples. Perfusate flux profiles were fitted to a bi-exponential model Y(t) = A(e, , e,) and the area under the curve (AUC), peak flux and time to peak flux were determined. Sulfur mustard had more pronounced and rapid initial flux parameters (P < 0.05). The AUCs determined from observed and model-predicted parameters were not statistically different, although the mean HD AUC was 40,50% greater than MS. The HD skin and fat levels were up to twice those seen with MS, but had lower stratum corneum and residual skin surface concentrations (P < 0.05). Compared with other chemicals studied in this model, HD and MS cutaneous disposition were very similar, supporting the use of MS as a dermal simulant for HD exposure. Copyright © 2001 John Wiley & Sons, Ltd. [source] Sulfur mustard induced cytokine production and cell death: Investigating the potential roles of the p38, p53, and NF-,B signaling pathways with RNA interference,JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 3 2010Albert L. Ruff Abstract Cutaneous and ocular injuries caused by sulfur mustard (SM; bis-(2-chloroethyl) sulfide) are characterized by severe inflammation and death of exposed cells. Given the known roles of p38MAPK and NF-,B in inflammatory cytokine production, and the known roles of NF-,B and p53 in cell fate, these pathways are of particular interest in the study of SM injury. In this study, we utilized inhibitory RNA (RNAi) targeted against p38,, the p50 subunit of NF-,B, or p53 to characterize their role in SM-induced inflammation and cell death in normal human epidermal keratinocytes (NHEK). Analysis of culture supernatant from 200 ,M SM-exposed cells showed that inflammatory cytokine production was inhibited by p38, RNAi but not by NF-,B p50 RNAi. These findings further support a critical role for p38 in SM-induced inflammatory cytokine production in NHEK and suggest that NF-,B may not play a role in the SM-induced inflammatory response of this cell type. Inhibition of NF-,B by p50 RNAi did, however, partially inhibit SM-induced cell death, suggesting a role for NF-,B in SM-induced apoptosis or necrosis. Interestingly, inhibition of p53 by RNAi potentiated SM-induced cell death, suggesting that the role of p53 in SM injury, may be complex and not simply prodeath. © 2010 Wiley Periodicals, Inc. J Biochem Mol Toxicol 24:155,164, 2010; Published online inWiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20321 [source] Upregulation of gamma-2 laminin-332 in the mouse ear vesicant wound model,JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 3 2009Yoke-Chen Chang Abstract Epithelial cell migration during wound healing is regulated in part by enzymatic processing of laminin-332 (formerly LN-5), a heterodimer formed from ,, ,, and , polypeptide chains. Under static conditions, laminin-332 is secreted into the extracellular matrix as a proform and has two chains processed to smaller forms, allowing it to anchor epithelial cells to the basement membrane of the dermis. During incisional wounding, laminin ,2 chains in particular are processed to smaller sizes and function to promote epithelial sheet migration over the wound bed. The present study examines whether this same function occurs following chemical injury. The mouse ear vesicant model (MEVM) was used to follow the pathology in the ear and test whether processed laminin-332 enhances epithelial cell migration. Skin biopsies of sulfur mustard (SM) exposed ears for several time points were analyzed by histology, immunohistochemistry, real-time PCR, and Western blot analysis. SM exposure greatly increased mRNA levels for laminin-,2 in comparison to the other two chains. Protein production of laminin-,2 was upregulated, and there was an increase in the processed forms. Protein production was in excess of the amount required to form heterotrimeric laminin-332 and was associated with the migrating epithelial sheet, suggesting a potential role in wound healing for monomeric laminin-,2. © 2009 Wiley Periodicals, Inc. J Biochem Mol Toxicol 23:172,184, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20275 [source] Modulation of sulfur mustard induced cell death in human epidermal keratinocytes using IL-10 and TNF-,,,JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 4 2005Aziz Qabar Abstract We compared the effects of overexpressing a tightly regulated anti-inflammatory cytokine, interleukin 10 (IL-10), and the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-,) on sulfur mustard induced cytotoxicity in human epidermal keratinocytes. Both cytokines were overexpressed when compared with the cells transfected with the empty vector as determined by quantitative ELISA. Cells overexpressing interleukin 10 suppressed the pro-inflammatory cytokines interleukin 8 and interleukin 6 following exposure to 50,300 ,M sulfur mustard. These cells exhibited delayed onset of sulfur mustard induced cell death. On the other hand, cells overexpressing tumor necrosis factor alpha induced a sustained elevation in both interleukin 6 and 8 expression following exposure to 50,300 ,M sulfur mustard. These cells were sensitized to the effects of sulfur mustard that resulted in an increased sulfur mustard induced cell death. Normal human epidermal keartinocytes treated with sulfur mustard exhibited elevated levels of tumor necrosis factor alpha expression and increased activity of nuclear factor kappa B. Gene array data indicated that cells overexpressing interleukin 10 induced several genes that are involved in growth promotion and cell-fate determination. We, therefore, identify IL-10 and TNF-, signal transduction pathways and their components as possible candidates for early therapeutic intervention against sulfur mustard induced cell injury. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:213,225, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20089 [source] Kinetics of adsorption of 2-CEES and HD on impregnated silica nanoparticles under static conditionsAICHE JOURNAL, Issue 5 2009Amit Saxena Abstract Silica nanoparticles of high surface area (887.3 m2/g) were synthesized using aerogel route and, thereafter, impregnated with those reactive chemicals, which have already been proven to be effective against sulfur mustard (HD). Thus, developed adsorbents were tested for their potential by conducting studies on kinetics of adsorption of 2-chloroethylethyl sulfide (2-CEES) and HD under static conditions. Kinetics of adsorption was studied using linear driving force model and Fickian diffusion model. The kinetic parameters such as equilibration constant, equilibration capacity, diffusional exponent, and adsorbate-adsorbent interaction constant were also determined. Trichloroisocyanuric acid impregnated silica nanoparticles (10% w/w) showed the maximum uptake of 2-CEES (1824 mg/g) and HD (1208 mg/g). Values of diffusional exponent indicated the mechanisms to be Fickian and anomalous. Chemical interaction seemed to be another mechanism involved in the toxicant uptake rate. Hydrolysis, dehydrochlorination, and oxidation reactions were found to be the route of degradation of toxicants. © 2009 American Institute of Chemical Engineers AIChE J, 2009 [source] Chemical Agent Simulant Release from Clothing Following Vapor ExposureACADEMIC EMERGENCY MEDICINE, Issue 2 2010Robert J. Feldman MD ACADEMIC EMERGENCY MEDICINE 2010; 17:1,4 © 2010 by the Society for Academic Emergency Medicine Abstract Objectives:, Most ambulatory victims of a terrorist chemical attack will have exposure to vapor only. The study objective was to measure the duration of chemical vapor release from various types of clothing. Methods:, A chemical agent was simulated using methyl salicylate (MeS), which has similar physical properties to sulfur mustard and was the agent used in the U.S. Army's Man-In-Simulant Test (MIST). Vapor concentration was measured with a Smiths Detection Advanced Portable Detector (APD)-2000 unit. The clothing items were exposed to vapor for 1 hour in a sealed cabinet; vapor concentration was measured at the start and end of each exposure. Clothing was then removed and assessed every 5 minutes with the APD-2000, using a uniform sweep pattern, until readings remained 0. Results:, Concentration and duration of vapor release from clothing varied with clothing composition and construction. Lightweight cotton shirts and jeans had the least trapped vapor; down outerwear, the most. Vapor concentration near the clothing often increased for several minutes after the clothing was removed from the contaminated environment. Compression of thick outerwear released additional vapor. Mean times to reach 0 ranged from 7 minutes for jeans to 42 minutes for down jackets. Conclusions:, This simulation model of chemical vapor release demonstrates persistent presence of simulant vapor over time. This implies that chemical vapor may be released from the victims' clothing after they are evacuated from the site of exposure, resulting in additional exposure of victims and emergency responders. Insulated outerwear can release additional vapor when handled. If a patient has just moved to a vapor screening point, immediate assessment before additional vapor can be released from the clothing can lead to a false-negative assessment of contamination. [source] Skin hydration and transepidermal water loss in patients with a history of sulfur mustard contact: a case,control studyJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 8 2009Seyyed Masoud Davoudi Abstract Background,, Skin lesions are among the most common complications of contact with sulfur mustard. Objective,, This study was aimed to measure skin water content and transepidermal water loss (TEWL) in patients with a history of sulfur mustard contact. Methods,, Three hundred ten male participants were included in this study: 87 (28.1%) sulfur mustard,exposed patients with current skin lesions (group 1), 71 (22.9%) sulfur mustard,exposed patients without skin lesions (group 2), 78 (25.2%) patients with dermatitis (group 3) and 74 (23.8%) normal controls (group 4) The water content and TEWL of skin was measured at four different locations of the body: forehead, suprasternal, palm and dorsum of hand. Nonparametric statistical tests (Kruskal,Wallis) were used to compare the four groups, and P < 0.05 was considered statistically significant. Results,, The mean age of participants were 44.0 ± 6.7, 41.9 ± 5.9, 43.8 ± 9.3 and 44.8 ± 8.9 years in groups 1 to 4, respectively (P = 0.146). Xerosis, post-lesional hyperpigmentation and lichenification were significantly more common in either sulfur mustard,exposed participants or non-exposed participants with dermatitis (P < 0.05). Skin hydration was higher in subjects with sulfur mustard contact than in non-injured participants (P < 0.05) in the dorsum and palm of hands and forehead. TEWL was significantly higher in participants only in suprasternal area and dorsum of hand. Conclusion,, Contact with sulfur mustard agent can alter biophysical properties of the skin-especially the function of stratum corneum as a barrier to water loss-several years after exposure. Conflicts of interest None declared. [source] Regulation of 1-,, 25-Dihydroxyvitamin D3 on Interleukin-6 and Interleukin-8 Induced by Sulfur Mustard (HD) on Human Skin Cells,BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 5 2003Carmen M. Arroyo Stimulation of human skin fibroblasts with sulfur mustard (10,4 M for 24 hr at 37°) resulted in approximately a 5 times increase in the secretion of interleukin-6 and over a 10 times increase for interleukin-8, which was inhibited by 1-,, 25 (OH)2D3, at ,10,9 M. 1-,, 25 (OH)2D3 also suppressed interleukin-8 secretion by 5 times and interleukin-6 by 4 times on sulfur mustard-stimulated human epidermal keratinocytes at concentrations , 10,9 M. The effect of 1-,, 25 (OH)2D3 was dose-dependent for the suppression of interleukin-6 and interleukin-8 induced by sulfur mustard on human skin fibroblasts/human epidermal keratinocytes, apparent at nanomolar concentrations. Our results indicate that the suppression of these inflammatory mediators by 1-,, 25 (OH)2D3 is dependent on the source of the primary cultures, cell densities, and kinetics of pretreatments. In contrast to the inhibition of cytokine/chemokine production, cell proliferation was enhanced by almost 1.7 times on treated human epidermal keratinocytes with 1-,, 25 (OH)2D3 (1×10,9 M) after sulfur mustard-stimulation (10,4 M for 24 hr at 37°C). The observed enhancement diversified based on cell density, and kinetics of pretreatment with a maximal synergism (s) observed at 1×10,9 M. Photomicrographs show typical signs of cellular degeneration caused by sulfur mustard such as chromatin condensation. The observed cellular degeneration was lessened when human epidermal keratinocytes were treated with 1-,, 25 (OH)2D3 (2×10,9 M). 1-,, 25(OH)2D3 could be an alternative treatment for cutaneous inflammation disorders caused by sulfur mustard because we have demonstrated its ability to suppress inflammatory mediators and enhanced cell proliferation in human skin cells stimulated with sulfur mustard. [source] Electrospray ionization tandem mass spectral analysis of oxidation products of precursors of sulfur mustardsRAPID COMMUNICATIONS IN MASS SPECTROMETRY, Issue 16 2006Vijay Tak Electrospray ionization tandem mass spectral (ESI-MSn) analysis of thiodiglycol, bis(2-hydroxyethylthio)alkanes (BHETAs) and their mono-, di-, tri-, and tetraoxygenated compounds was carried out to obtain their characteristic spectra for ESI-MS analysis. These compounds are important markers of chemical warfare agents, namely sulfur mustards. ESI-MSn (n,,,3) analysis of a compound by collisionally induced dissociation in an ion trap gives rise to mass spectra that are somewhat similar to electron ionization mass spectra. These ESI-MSn spectra can be used for compound identification. Under ESI-MS and ESI-MS/MS the compounds mostly produced [M+NH4]+, [M+H]+ and [M+HH2O]+ ions. Fragmentations of these even-electron precursors in the ion trap gave rise to characteristic product ions via neutral loss of O2, H2O, C2H4, HCHO, C2H4O, C2H4S, HSC2H4OH and C2H4SO. Fragmentation routes of these compounds are proposed that rationalize the formation of product ions in ESI-MSn analysis. Copyright © 2006 John Wiley & Sons, Ltd. [source] | |||||||||||||