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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. [ABSTRACT FROM AUTHOR]

To develop a novel inhalation exposure system capable of delivering a controlled inhaled HD dose through an endotracheal tube to anesthetized rats to investigate the lung pathophysiology and evaluate potential medical countermeasures. Target HD vapor exposures were generated by a temperature-controlled vapor generator, while concentration was monitored near real-time by gas chromatography. Animal breathing parameters were monitored real-time by in-line EMKA/SciReq pulmonary analysis system. Individual exposures were halted when the target inhaled doses were achieved. Animals were observed daily for clinical observations and lethality with scheduled termination at 28 days post-exposure. Upon scheduled or unscheduled death, animals underwent a gross necropsy and lung and trachea were collected for histopathology. Controlled HD concentrations ranged from 60 to 320 mg/m3. Delivered inhaled doses range from 0.3 to 3.20 mg/kg with administered doses within 3% of the target. The 28-day inhaled LD50 is 0.80 mg/kg (95% CI = 0.42–1.18 mg/kg). Post exposure respiratory abnormalities were observed across all dose levels though the higher dose levels had earlier onset and higher frequency of occurrence. Histopathologic alterations were not qualitatively altered in accordance with dose but instead showed a relationship to an animals' time of death, with early deaths demonstrating acute damage and later deaths displaying signs of repair. This novel exposure system administers targeted HD inhaled doses to generate a small animal model that can be used to evaluate physiological toxicities of inhaled HD on the lungs and for evaluation of potential medical countermeasure treatments. [ABSTRACT FROM AUTHOR]

Background: Sulfur mustard (SM), also known as mustard gas, was first widely used in the Iraq–Iran. After SM exposure, the most prominent clinical signs are the development of extensive non-healing skin wounds and pulmonary signs, persisting over long time. Since the most frequent complications in SM-intoxicated patients are respiratory and dermatologic lesions, and with respect to the important role of endothelial progenitor cells (EPCs) in the pathophysiology of these lesion, we conducted this study to recognize the potential effects of SM on biological features of EPCs in patients exposed with this gas. Methods: In this study, 30 patients with the history of SM exposure during the Iran–Iraq war (1984–1988), 27 patients with pulmonary signs with no history of SM exposure and 20 healthy participants were included. Cell population and function of EPCs were assessed 4 years post-exposure. For this purpose, circulating EPCs (cEPCs) were harvested and cultivated, then the biological features of these cells, including migratory, proliferative, and tubulogenic activities were analyzed. We also measured serum antioxidants levels and mRNA levels of some proangiogenic factors in EPCs from SM-intoxicated patients. Results: Our results showed lesser number of cEPCs in patients exposed with SM, which was associated with decreased proliferative, migratory, and tubulogenic activity of these cells. Also, we found the lesser serum activity of SOD, GPX and MDA in the SM group than in the healthy control group. Conclusions: SM exposure resulted in decreased proliferation and migration of EPCs, which was associated with decreased tubule formation and angiogenic factors. [ABSTRACT FROM AUTHOR]

Sulfur mustard (SM) is a mutagenic compound that targets various organs. Although it causes a wide range of abnormalities, cellular and molecular mechanisms of its action are not-well-understood. Oxidation of DNA, proteins, lipids, as well as depletion of cellular nicotinamide adenine dinucleotide (NAD), antioxidants and increase of intracellular calcium are the hypothesized mechanisms of its action at the acute phase of injury. In this review, the proteome analysis of SM toxicity has been considered. We selected articles that considered proteomics analysis of SM toxicity with two-dimensional gel electrophoresis (2DE) followed by mass spectrometry. Our search yielded nine related articles, four original in vitro and five human studies. The results of these studies have revealed a change in expression pattern of various proteins such as haptoglobin, amyloid A1, surfactant proteins, S100 proteins, apolipoprotein, Vit D binding protein, transferrin, alpha 1 antitrypsin, protein disulfide isomerase and antioxidant enzymes in patients who were exposed to SM about 30 years ago. Most of these proteins are up- or down-regulated in response to excessive production of reactive oxygen species (ROS) and oxidative stress (OS). There is a tight link between the expression pattern of these proteins with accumulation of leukocytes, inflammatory conditions, antioxidant depletion, mitochondrial deficiency, as well as increased expression or activity of several proteases such as caspases and matrix metalloproteinases (MMPs). Therefore, excessive production of ROS and OS along with chronic inflammatory may be the long-term toxic effects of SM following acute exposure. [ABSTRACT FROM AUTHOR]

Context: Sulfur mustard (SM) as a cytotoxic and blistering agent can alkylate a variety of cellular components, causing the incidence of ongoing oxidative stress. Objective: The present study was conducted to assess oxidative stress index (OSI) in SM-exposed veterans with long-term pulmonary complications. Methods: Participants consisted of 289 SM-exposed individuals with pulmonary complications (classified into three groups: mild, moderate and severe) and 66 healthy individuals as the control group. Enzymatic and non-enzymatic antioxidant and also trace elements were measured in the study groups. Moreover, some of oxidative stress indicators consist of malondialdehyde (MDA), protein carbonyl (CO), total antioxidant (TA) and total peroxide (TPX) were measured and then OSI was calculated. Results: Glutathione-S-transferase (GST) activity and vitamin C (Vit C) were significantly decreased in SM-exposed patients as compared with controls. Besides, Cu level and Cu/Zn ratio in SM-exposed veterans showed a significant correlation with the severity of the diseases. Serum TPX was significantly increased in SM-exposed individuals, as a result of which the OSI was slightly higher in them than controls. This can be considered as an indicative for oxidative stress in SM-exposed patients. Conclusion: This study suggests a particular role for TPX, Cu, Vit C and GST in SM-induced pulmonary complications. Therefore, a special attention should be paid to these factors in designing therapeutic protocols, which can reduce the progression risk of the disease. [ABSTRACT FROM AUTHOR]

Context: Sulfur mustard (SM) and lewisite are vesicant chemical warfare agents that can cause skin blistering and chronic lung complications. During 1929–1945, a Japanese factory produced poisonous gases, which included SM, lewisite and other chemical weapons. The aim of this study was to investigate the chest computed tomography (CT) findings among long-term survivors who worked at this factory. Methods: During 2009–2012, we evaluated chest CT findings from 346 long-term survivors who worked at the poison gas factory. Skin lesions were used as an indicator of significant exposure to vesicant agents. Results: Among the 346 individuals, 53 (15%) individuals experienced skin lesions while working at the factory, and chest CT revealed abnormal findings in 179 individuals (52%). Emphysema was the most common CT finding and was observed in 75 individuals (22%), while honeycombing was observed in 8 individuals (2%). Emphysema and honeycombing were more prevalent among individuals with skin lesions, compared to individuals without skin lesions. Multivariate analyses revealed significant associations between the presence of emphysema and skin lesions (p = 0.008). Among individuals who never smoked, individuals with skin lesions (n = 26) exhibited a significantly higher rate of emphysema, compared to individuals without skin lesions (n = 200) (35% versus 7%, respectively;p < 0.001). Conclusion: Among the long-term survivors who worked at the poison gas factory, a history of skin lesions was associated with the presence of emphysema, even among never smokers, which suggests that emphysema might be a long-term complication of exposure to chemical warfare agents. [ABSTRACT FROM PUBLISHER]

Context: Previous research has found relationships between sulfur mustard (SM) toxicity and its adverse effects. Objective: SM is highly toxic to the respiratory system, leading to hacking cough, rhinorrheachest tightness, acute pharyngitis and laryngitis, chronic bronchitis and lung fibrosis. In this review, based on the scientific literature, we provide an updated summary of information on SM exposures and their differences with asthma and COPD. Method: Information of this review was obtained by searching Medline/PubMed, ScienceDirect, Scopus, Google Scholar, ISI Web of Knowledge and Chemical Abstracts. Results: SM exposure can decrease pulmonary function tests (PFTs) values. In addition, inflammatory cell accumulation in the respiratory tract and increased expression of some pro-inflammatory cytokines including tumor necrosis factor-α (TNFα), IL-1a, IL-1β, and reactive oxygen radicals due to SM exposure have been shown. Matrix metalloproteinase (MMP) which degrade extracellular matrix proteins, contributing to inflammatory cell recruitment, tissue injury and fibrosis are also up-regulated in the lung after SM exposure. In the lung, SM exposure also can cause serious pathological changes including airway inflammation, parenchymal tissue destruction and airway obstruction which can lead to asthma or chronic obstructive pulmonary disease (COPD). Following SM poisoning, DNA damage, apoptosis and autophagy are observed in the lung along with the increased expression of activated caspases and DNA repair enzymes. Conclusion: In the present article, respiratory symptoms, changes in PFTs, lung pathology and lung inflammation due to SM exposure and the similarities and differences between them and those observed in asthma and COPD were reviewed. [ABSTRACT FROM AUTHOR]

Mustard lung is a major pulmonary complication in individuals exposed to sulfur mustard (SM) gas during the Iran–Iraq war. It shares common pathological and clinical features with some chronic inflammatory lung disorders, particularly chronic obstructive pulmonary disease (COPD). Airway remodeling, which is one of the main causes of lung dysfunction and the dominant phenomenon of chronic pulmonary diseases, is seen in the mustard lung. Among all mediators involved in the remodeling process, the transforming growth factor (TGF)-β plays a pivotal role in lung fibrosis and consequently in the airway remodeling. Regarding the high levels of this mediator detected in mustard lung patients, in the present study, we have discussed the possible roles of TGF-β in airway remodeling (including epithelial layer damage, subepithelial fibrosis and angiogenesis). Finally, based on TGF-β targeting, we have reviewed new airway remodeling therapeutic approaches. [ABSTRACT FROM AUTHOR]

Context: Sulfur mustard (SM), with extensive nucleophilic and alkylating properties, was employed during the Iran–Iraq war by Iraqi forces. The most critical complications attributed to SM are related to dangerous pulmonary disorders collectively known as “mustard lung”. The symptoms gradually emerge over a long period, becoming chronic, and are dependent on time and the amount of exposed SM. Because of the unknown and complex nature of the disease, no differential diagnostic method or absolute treatment strategy has been formally developed. Objective: The aim of our study was to determine the expression pattern of the microRNAs (miRNAs) miR-92a and miR-20a in the serum of patients with mustard lung along with that of normal individuals. miRNAs have been shown to possess stable persistence in biofluids like plasma and serum and are considered non-aggressive biomarkers helpful for diagnosis and treatment of many diseases. Materials and methods: A highly sensitive approach called stem-loop real-time quantitative polymerase chain reaction was employed to study the expression of miRNAs.Results:The expression of miR-92a and miR-20a was significantly down-regulated in the serum of patients with mustard lung compared to the control group. Discussion: Down-regulation of miR-92a and miR-20a may be due to chronic epigenetic alterations after SM exposure, which finally leads to changes in vital cellular processes such as differentiation, proliferation and so forth. Conclusion: Our findings may provide a differential diagnostic method that is effective for diagnosing lung diseases caused by SM exposure. Additionally, these miRNAs may be regarded as probable targets for treatment of lung injuries. [ABSTRACT FROM PUBLISHER]

Sulfur mustard (SM) is a potent alkylating agent that targets several organs, especially lung tissue. Although pathological effects of SM have been widely considered, molecular and cellular mechanisms for these pathologies are not well understood, yet. General cellular and molecular events such as inflammation, DNA damage, cell membrane disintegrity, apoptosis and cell death were observed either in in vitro or in vivo models exposed to SM. However, it is not obvious that which specific molecules and signaling pathways are relevant to the pathogenesis of mustard lung. Oxidative stress (OS) and antioxidants depletion induced by SM seem to be one of these factors. SM can trigger several molecular and cellular pathways linked to oxidative stress and inflammation that can cause cell necrosis and apoptosis as well as loss of tissue structure and function. Identification of these signaling pathways and molecules gives us valuable information regarding the toxic mechanisms of SM on injured tissues and the way for developing a better clinical approach. In this review we aimed to discuss the proposed cellular and molecular mechanisms of SM on pulmonary damage, the importance of oxidative stress and the mechanisms by which SM induces OS and antioxidants depletion along with research on antioxidant therapy as a suitable antidote. [ABSTRACT FROM AUTHOR]

Context: Sulfur mustard exposure, as the most widely used chemical weapon, can lead to acute and long-term pulmonary complications via various pathways, such as triggering an imbalance between the oxidant and antioxidant system. Currently, there is no validated antidote, chemoprophylaxis and curative modality for pulmonary toxicities secondary to sulfur mustard exposure. Objective: The aim of this literature review is to collect available experimental and clinical data on the efficacy of N-acetylcysteine (NAC), as a prominent antioxidant agent, in the prevention and/or treatment of sulfur mustard-induced acute and chronic pulmonary toxicities. Methods: A literature search was performed by the relevant keywords like ' N-acetyl cysteine', 'Sulfur mustard' and 'Lung injury' in databases such as Scopus, Medline, Embase and ISI Web of Knowledge. No time limitation was considered. Nineteen articles were selected for review. Results: A number of in vitro and experimental studies concluded that oral, intravenous, intraperitoneal and intra-tracheal administration of NAC is effective in the management of sulfur mustard-induced acute lung injury, in a time-dependent manner, via direct scavenging, inhibition of oxidative stress, inflammatory responses and apoptosis. In addition, oral NAC alone (1200 or 1800 mg/day for 4 months) or at a dose 600 mg/day for 6 months in combination with clarithromycin (500 mg/day) have led to improvements of clinical and paraclinical pulmonary parameters of patients with bronchiolitis obliterans due to sulfur mustard, through undetermined mechanisms. Conclusion: Despite limitations of relevant experimental and clinical studies, NAC can be considered as a candidate agent for prevention and/or treatment of sulfur mustard-induced acute lung injuries, as well as its long-term pulmonary toxicities, especially bronchiolitis obliterans. [ABSTRACT FROM AUTHOR]

It is well documented that inhalation of sulfur mustard (SM) causes injury to the respiratory system. Many Iranian civilians and war veterans are suffering from late respiratory complications of SM exposure. Recent studies have shown that bronchiolitis obliterans (BO) is the major cause of respiratory complications following SM exposure. In this review, we focus on the clinical, pulmonary, radiological, immunological and pathological manifestations in SM-induced BO with intent to provide a practical, clinical and paraclinical guideline for diagnosis and step-wise workup of these patients, which may be used to manage similar lung injuries induced by other similar inhaled toxins. [ABSTRACT FROM AUTHOR]

Sulfur mustard (SM), a potent chemical weapon agent, was used by Iraqi forces against Iranian in the Iraq--Iran war (1981--1989). Chronic obstructive pulmonary disease (COPD) is a late toxic pulmonary consequence after SM exposure. The COPD observed in these patients is unique (described as Mustard Lung) and to some extent different from COPD resulted from other well-known causes. Several mechanisms have been hypothesized to contribute to the pathogenesis of COPD including oxidative stress, disruption of the balance between apoptosis and replenishment, proteinase-antiproteinase imbalance and inflammation. However, it is not obvious which of these pathways are relevant to the pathogenesis of mustard lung. In this paper, we reviewed studies addressing the pathogenicity of mustard lung, and reduced some recent ambiguities in this field. There is ample evidence in favor of crucial role of both oxidative stress and apoptosis as two known mechanisms that are more involved in pathogenesis of mustard lung comparing to COPD. However, according to available evidences there are no such considerable data supporting neither proteolytic activity nor inflammation mechanism as the main underlying pathogenesis in Mustard Lung. [ABSTRACT FROM AUTHOR]

Pulmonary complications of sulfur mustard (SM) range from mild respiratory symptoms to even severe bronchial stenosis. In the present study, the protective effect of vitamin E on tracheal responsiveness (TR) and lung inflammation of SM-exposed guinea pigs were examined. Guinea pigs were exposed to ethanol (control group), 40 mg/m3 inhaled SM and ethanol vehicle (sulfur mustard exposed (SME) group), SME treated with vitamin E (SME ++ E), SME with dexamethasone (SME ++ D) and both drugs (SME ++ E ++ D), ( n == 8 for each group). TR to methacholine, total and differential white blood cell (WBC) count of lung lavage and serum cytokines were evaluated 14 days post-exposure. TR, WBC, interleukin 4 (IL-4), interferon gamma (INF-γγ), eosinophil, and monocyte levels in SME guinea pigs were significantly higher, but lymphocyte was lower than those of controls ( P < 0.05 to P < 0.001). TR, IL-4, and eosinophil levels in SME ++ E, SME ++ D and SME ++ E ++ D, INF-γγ in SME ++ E and SME ++ E ++ D and WBC in SME ++ E were significantly decreased compared to that of the SME group ( P < 0.01 to P < 0.001). In addition, the TR of SME ++ D ++ E was significantly higher than that of SME ++ E ( P < 0.01) and SME ++ D ( P < 0.05) groups. The results showed a preventive effect of vitamin E, dexamethasone and their combination on TR and lung inflammation in SME guinea pigs. [ABSTRACT FROM AUTHOR]

Context: Inhalation of sulfur mustard (HD) vapor can cause life-threatening lung injury for which there is no specific treatment. A reproducible, characterized in vivo model is required to investigate novel therapies targeting HD-induced lung injury. Materials and methods: Anesthetized, spontaneously breathing large white pigs (∼50 kg) were exposed directly to the lung to HD vapor at 60, 100, or 150 µg/kg, or to air, for ∼10 min, and monitored for 6 h. Cardiovascular and respiratory parameters were recorded. Blood and bronchoalveolar lavage fluid (BALF) were collected to allow blood gas analysis, hematology, and to assay for lung inflammatory cells and mediators. Urine was collected and analyzed for HD metabolites. Histopathology samples were taken postmortem (PM). Results: Air-exposed animals maintained normal lung physiology whilst lying supine and spontaneously breathing. There was a statistically significant increase in shunt fraction across all three HD-exposed groups when compared with air controls at 3-6 h post-exposure. Animals were increasingly hypoxemic with respiratory acidosis. The monosulfoxide β-lyase metabolite of HD (1-methylsulfinyl-2-[2(methylthio)ethylsulfonyl)ethane], MSMTESE), was detected in urine from 2 h post-exposure. Pathological examination revealed necrosis and erosion of the tracheal epithelium in medium and high HD-exposed groups. Conclusion: These findings are consistent with those seen in the early stages of acute lung injury (ALI). [ABSTRACT FROM AUTHOR]

The Iraqi government used a range of chemical weapons, including blistering and nerve agents, against Iraqi Kurdish civilians in the 1980s. Few data exist about the long-term respiratory consequences of this exposure. In this study, Kurdish subjects with a history of exposure to chemical weapons were invited to attend a clinical assessment, including a review of their history, physical examination, and a high-resolution computed tomography (CT) of the thorax. Blistering at the time of exposure was used to define significant exposure to mustard gas. Results were compared between two groups of blistering and nonblistering. Four hundred seventy-nine subjects were studied; 45.7% male and 54.3% female. The mean age and standard deviation (mean ± SD) of the cases was 43.1 ± 13.7. Spirometry was abnormal in 15.2% of subjects and air trapping was present on CT scan in 46.6% and did not differ between patients with ( n = 278) or without a history of blistering. Respiratory symptoms, including dyspnea, cough, and sputum production, were more common in subjects with a history of blistering (all p < .005) and blistering was also associated with a lower forced expiratory volume in one second (FEV1) ( p < .0001). Severe complications were most common in subjects from Halabja who also made up the majority of participants. These results show that objective abnormalities are common in people with symptoms attributed to prior exposure to chemical agent. Blistering at the time of exposure was associated with more respiratory symptoms and worse lung function, but not with CT appearances. The high proportion of severe cases in comparison to reports from Iran may reflect the historical absence of effective early treatment, including strategies to reduce prolonged early exposure in this population. [ABSTRACT FROM AUTHOR]

Dyspnea is the hallmark symptom of some respiratory diseases such as chronic obstructive pulmonary disease and bronchiolitis and is a major reason for which these patients seek medical attention. We performed a randomized triple-blind controlled crossover clinical trial in which we compared the efficacy of inhaled furosemide (4 ml equal to 40 mg in 10 min) with placebo (4 ml of 0.9% saline solution) in 41 mustard gas-exposed patients. Dyspnea index, visual analog scale (VAS), and pulmonary function test results were obtained before and 4 h after treatments. Results showed that both furosemide and placebo significantly decreased VAS and dyspnea index and increased FEV1, FVC, and FEV1/FVC, while there was no difference between the two drugs in these effects (p values .23, .61, .81, .36, and .27, respectively). Our results failed to address the previously reported effects of inhaled furosemide on dyspnea. In fact, we suggest that patients with a previous exposure to sulfur mustard, in which chronic bronchitis and bronchiolitis are the most suggested underlying mechanisms, may not benefit from furosemide to alleviate their dyspnea. [ABSTRACT FROM AUTHOR]

Chemical warfare agents (CWA) including sulfur mustard (SM) were commonly used in Iran-Iraq war. Respiratory problems are the greatest cause of long-term disability among people who had combat exposure to SM. High-resolution computed tomography (HRCT) has been accepted as the imaging modality of choice in these patients. We used expiratory HRCT findings in comparison to inspiratory HRCT for demonstration of pulmonary damage in these patients. HRCT in deep inspiration as well as full expiration was performed in 473 patients with a history of chemical gas exposure during the war and the results were compared. The study was prospective during 1 yr. Of 473 patients, 366 (77.38%) showed normal HRCT in deep inspiration; however, on corresponding expiratory cuts, 263 (71.86%) had abnormalities. The most frequent abnormal finding in expiration was patchy air trapping (77.77%). We conclude that exposure to SM causes pulmonary complications resulting in disability in the affected patients; however, HRCT in inspiration is normal in most of the affected patients. Expiratory HRCT showed patchy air trapping as the most common finding, which is suggestive of small air way diseases such as bronchiolitis obliterans; therefore it is recommended to do HRCT both in deep inspiration and full expiration in patients with a history of CWA exposure. [ABSTRACT FROM AUTHOR]

We examined the role of two regimens of combination inhaler therapy on amount of reversibility of chronic lung complications in mustard gas exposed patients. In a phase III, prospective, randomized clinical trial, 105 participants received either combination form of fluticasone propionate and salmetrol, 500/100 μ g daily (group 1; n = 52) or beclomethasone, 1000 μ g daily, and salbutamol inhaler, 800 μg daily (group 2; n = 53) for 12 wk. Pulmonary function test (PFT) indices and respiratory symptoms (including dyspnea, night awakening due to dyspnea and cough) were assessed at baseline and in each visit. Thirty-six patients in group 1 and 30 patients in group 2 completed study course. Both medication regimes increased pretreatment forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), FEV1/FVC%, and peak expiratory force (PEF) by the end of 12 wk. It seems that these improvements are more constant in group 1 than in group 2. Reversibility, that is, 10% increase of FEV1 in the second month was seen for 27% of patients in the group 1 and for 7% in the group 2. VAS scores have decreased in two groups during treatment period (p = .003) and after follow-up period it remained sustained in group 1 alone. Inhaled corticosteroids and long-acting β 2-agonists are effective in treatment of patients with chronic bronchiolitis following exposure to sulfur mustard. However, a medium dose of fluticasone/salmeterol has the same effect on the airways reversibility, rather than a very high dose of beclomethasone with only the short-acting beta-agonist. [ABSTRACT FROM AUTHOR]

Mustard gas (HD) was a widely used chemical warfare agent during World War I and more recently in the Iraq–Iran war (1980–1988). To date, dramatically, 45,000 Iranians are suffering from late respiratory complications due to MG exposure. This review covers two decades of researches on latent pulmonary effects of MG. Findings from clinical manifestations, pathologic examinations, laboratory data, lung function tests, and radiological evaluations are reviewed. From this review we are able to provide a suitable practical plan for workup and management of patients in this setting. [ABSTRACT FROM AUTHOR]

Mustard gas or sulfur mustard (SM) is an alkylating chemical warfare agent that was widely used during the World War I and in the Iran-Iraq conflict. We aimed to study late toxic effects of SM on the respiratory system of severely intoxicated Iranian veterans. Respiratory examination, spirometry, arterial blood gas (ABG) analysis, and high resolution computed tomograpghy (HRCT) of the chest were performed on all severely SM-poisoned veterans in the province of Khorasan, Iran. HRCT abnormalities were classified into four grades based on the number of lung lobes involved. ABG and spirometric results were compared with each other, as well as, with the severity grades of HRCT abnormalities, using Spearman's rank correlation test. Forty male subjects with confirmed SM poisoning 16 to 20 years ago, were studied. Main respiratory complications were diagnosed as chronic obstructive pulmonary disease (COPD) (35%), bronchiectasis (32.5%), asthma (25%), large airway narrowing (15%), pulmonary fibrosis (7.5%), and simple chronic bronchitis (5%) patients. While there was a significant correlation (p 2 . We concluded that SM-induced respiratory complications tend to progress over the years. While spirometry is a valuable diagnostic tool for evaluation of pulmonary impairment during regular follow-ups, ABG and HRCT are more objective and should be more considered for evaluation of the severity and for diagnosis of the respiratory complications. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Incidence of cancer in Iranian sulfur mustard exposed veterans: a long-term follow-up cohort study" by Mohammad Reza Zafarghandi and colleagues in a 2013 issue.