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At least 199 records · Page 11Linked to original sources
PubMed2006

Mustard lung secrets: long term clinicopathological study following mustard gas exposure.

Considering the undefinite nature of lung pathology in patients exposed to sulfur mustard (SM) many years after exposure, we conducted this study to document and quantify lung disease in this setting. In a cross sectional study, we selected 23 patients exposed to SM gas approximately 14 years ago during the Iran-Iraq war (1980-1988). We studied their clinical history, physical examination, pulmonary function test (PFT), high-resolution computed tomography scan (HRCT) of the chest, bronchoscopy, and bronchoalveolar lavage (BAL) sampling, and transbronchial lung biopsies. Other potential causes of lung disease, including smoking of cigarettes, were excluded. All 23 patients were symptomatic with cough, dyspnea, and/or felt tight in the chest. All of them had significant air trapping in HRCT and a marked increase of residual volume in PFT. The most common inflammatory cell in BAL fluid was neutrophil (88%). Of the 23 cases, there was sufficient tissue for detailed evaluation in 22. Histologically, 11 cases showed airway epithelial injury, and nine of the 14 lung biopsies with alveoli had histopathological changes diagnosable as organizing pneumonia (OP) or bronchiolitis obliterans OP (BOOP). Two out of 14 cases showed changes suggestive of OP. Inhalation of SM can lead to persistant and clinically significant lung disease, including bronchial mucosal injury and OP, many years after exposure.

Adult↗
PubMed1975

Mustard gas.

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Animals↗
PubMedDate not supplied

Delayed ocular complications of mustard gas poisoning and the relationship with respiratory and cutaneous complications.

BACKGROUND: This study was aimed to determine the correlation between ocular complications and respiratory or cutaneous complications in a group of 40 Iranian veterans with late complications of sulphur mustard (SM) poisoning. METHODS: Thorough ophthalmologic examination was performed on all severely SM-poisoned veterans in the province of Khorasan, Iran. Spirometric evaluation of pulmonary function, as well as estimation of the burned skin area, was performed for all the patients. The severities of ocular, respiratory and cutaneous complications were classified into four grades in each patient and were compared with each other, using Spearman's rank correlation test. RESULTS: Forty male patients (aged 43.8 +/- 9.8 years) with confirmed SM poisoning were studied 16-20 years after their initial exposure. Common symptoms were recorded as itching (42.5%), burning sensation (37.5%), photophobia (30%) and tearing (27.5%). Abnormal conjunctival and limbal findings were chronic conjunctivitis (17.5%), perilimbal hyperpigmentation (17.5%), vascular tortuosity (15%) and limbal ischaemia (12.5%). Abnormal corneal findings were subepithelial opacity (15%), corneal thinning (15%), diffuse corneal opacity (10%), neovascularization (7.5%) and epithelial defects (5%). A significant positive correlation was found between the severity of ocular and respiratory complications (r = 0.322, P = 0.043). Cutaneous complications revealed no significant correlation with either ocular or respiratory complications. CONCLUSIONS: SM causes delayed destructive lesions in the ocular surface and cornea, leading to progressive visual deterioration and ocular irritation. Late complications of SM poisoning in the eyes, respiratory system and skin are mainly due to SM's local irritant effects.

Adult↗
PubMed2006

Protective effect of ethanolic and water extracts of sea buckthorn (Hippophae rhamnoides L.) against the toxic effects of mustard gas.

Ethanolic extract of H. rhamnoides L. leaf (HL-EOH), water and ethanolic extract of H. rhamnoides fruit (HF-W and HF-EOH), and H. rhamnoides flavone from fruit (HR-flavone) were evaluated against percutaneously administered sulphur mustard (SM), a chemical warfare agent. The animals administered with SM (9.7, 19.3 and 38.7 mg/kg) died at various days depending upon the dose and there was a significant reduction in the body weight. The H. rhamnoides extracts (1 g/kg; 3 doses; po) significantly protected the lethality, with a protective index of 2.4, 1.7, 1.7 and 2.2 for HL-EOH, HF-W, HF-EOH and HR-flavone respectively. Reduced glutathione (GSH) and oxidized glutalthione (GSSG) levels were reduced, and malondialdehyde (MDA) was elevated after percutaneous administration of SM. Oral administration of HL-EOH and HR-flavone significantly protected the body weight loss. Recovery in the levels of GSH, GSSG and MDA were also observed following oral administration of HL-EOH and HR-flavone. All the extracts were non-toxic and the LD50 was more than 5 g/kg. The present study shows that percutaneous administration of SM induces oxidative stress and ethanolic extract of leaf of H. rhamnoides and H. rhamnoides flavone from fruit can significantly protect it.

Animals↗
PubMedDate not supplied

A chick model for the mechanisms of mustard gas neurobehavioral teratogenicity.

The chemical warfare blistering agent, sulfur mustard (SM), is a powerful mutagen and carcinogen. Due to its similarity to the related chemotherapy agents nitrogen mustard (mechlorethamine), it is expected to act as a developmental neurotoxicant. The present study was designed to establish a chick model for the mechanisms of SM on neurobehavioral teratogenicity, free of confounds related to mammalian maternal effects. Chicken eggs were injected with SM at a dose range of 0.0017-17.0 microg/kg of egg, which is below the threshold for dysmorphology, on incubation days (ID) 2 and 7, and then tests were conducted posthatching. Exposure to SM elicited significant deficits in the intermedial part of the hyperstriatum ventrale (IMHV)-related imprinting behavior. Parallel decreases were found in the level of membrane PKCgamma in the IMHV, while eliciting no net change in cytosolic PKCgamma. The chick, thus, provides a suitable model for the rapid evaluation of SM behavioral teratogenicity and elucidation of the mechanisms underlying behavioral anomalies. The results obtained, using a model that controls for confounding maternal effects, may be replicated in the mammalian model and provide the groundwork for studies designed to offset or reverse the SM-induced neurobehavioral defects in both avian and mammals.

Analysis of Variance↗