Humans can come into contact with chlorine gas during short-term, high-level exposures due to traffic or rail accidents, spills, or other disasters. By contrast, workplace and public (swimming pools, etc.) exposures are more frequently long-term, low-level exposures, occasionally punctuated by unintentional transient increases. Acute exposures can result in symptoms of acute airway obstruction including wheezing, cough, chest tightness, and/or dyspnea. These findings are fairly nonspecific, and might be present after exposures to a number of inhaled chemical irritants. Clinical signs, including hypoxemia, wheezes, rales, and/or abnormal chest radiographs may be present. More severely affected individuals may suffer acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS). Up to 1% of exposed individuals die. Humidified oxygen and inhaled β-adrenergic agents are appropriate therapies for victims with respiratory symptoms while assessments are underway. Inhaled bicarbonate and systemic or inhaled glucocorticoids also have been reported anecdotally to be beneficial. Chronic sequelae may include increased airways reactivity, which tends to diminish over time. Airways hyperreactivity may be more of a problem among those survivors that are older, have smoked, and/or have pre-existing chronic lung disease. Individuals suffering from irritant-induced asthma (IIA) due to workplace exposures to chlorine also tend to have similar characteristics, such as airways hyperresponsiveness to methacholine, and to be older and to have smoked. Other workplace studies, however, have indicated that workers exposed to chlorine dioxide/sulfur dioxide have tended to have increased risk for chronic bronchitis and/or recurrent wheezing attacks (one or more episodes) but not asthma, while those exposed to ozone have a greater incidence of asthma. Specific biomarkers for acute and chronic exposures to chlorine gas are currently lacking. Animal models for chlorine gas inhalation have demonstrated evidence of oxidative injury and inflammation. Early epithelial injury, airways hyperresponsiveness, and airway remodeling, likely diminishing over time, have been shown. As in humans, ALI/ARDS can occur, becoming more likely when the upper airways are bypassed. Inhalation models of chlorine toxicity provide unique opportunities for testing potential pharmacologic rescue agents.

/pdf/chlorine-gas-inhalation-human-clinical-evidence-of-toxicity-1rah386nup.pdf

Chlorine Gas Inhalation: Human Clinical Evidence of Toxicity and Experience in Animal Models

Myoepithelial Cells of Submucosal Glands Can Function as Reserve Stem Cells to Regenerate Airways after Injury

γδ T cells play a key role in the regulation of inflammatory responses in epithelial tissue, and in adaptive immunity, as γδ T cell deficient mice have a severely impaired capacity to clear lung pathogens. γδ T cells regulate the initial inflammatory response to microbial invasion and thereby protect against tissue injury. Here we examined the response of γδ T cells to lung injury induced by bleomycin, in an effort to study the inflammatory response in the absence of any adaptive immune response to a pathogen. After lung injury by bleomycin, we localized the γδ T cells to the lung lesions. γδ T cells were the predominant source of IL-17 (as detected by flow cytometry and real-time PCR). Moreover, γδ T cell knockout mice showed a significant reduction in cellular infiltration into the airways, reduced expression of IL-6 in the lung, and a significant delay in epithelial repair. Mouse γδ T cells produce IL-17 in response to lung injury and are required for an organized inflammatory response and epithelial repair. The lack of γδ T cells correlates with increased inflammation and fibrosis.

IL-17 Producing γδ T Cells are Required for a Controlled Inflammatory Response after Bleomycin-induced Lung Injury

Objective: To examine the time window between injury and treatment during which nebulized corticosteroid lessens lung injury induced by chlorine gas inhalation. Design: An experimental laboratory study. Setting: Academic research laboratory. Subjects: Twenty-four juvenile female pigs. Interventions: Twenty-four mechanically ventilated pigs were exposed to chlorine gas (400 PPM in air) for 20 min, then divided into four groups (six in each group). Nebulized budesonide (BUD) was given immediately (BUD 0 min), 30 min (BUD 30 min) or 60 min (BUD 60 min) after chlorine gas exposure. Six pigs receiving nebulized saline served as controls. Measurements and main results: Hemodynamics, gas exchange and lung mechanics were evaluated for 5 h after chlorine gas exposure. All animals had an immediate increase in airway and pulmonary artery pressure and a sharp drop of arterial oxygenation. The mean arterial oxygen tension of BUD 0 min and BUD 30 min animals was significantly higher than in the control and the BUD 60 min groups (p<0.001). The recovery of lung compliance in the BUD 0 min and the BUD 30 min groups was significantly more rapid than in the control and the BUD 60 min groups (p<0.001). The pulmonary wet to dry weight ratio was greater in the control group than in the BUD-treated groups (p<0.05). Conclusion: Treatment with inhaled budesonide immediately or 30 min after chlorine gas lung injury had similar positive effects on symptoms and signs of pulmonary injury, whereas treatment delayed for 60 min was less effective.

/pdf/inhaled-budesonide-in-experimental-chlorine-gas-lung-injury-2xdscptxr6.pdf

Inhaled budesonide in experimental chlorine gas lung injury: influence of time interval between injury and treatment.

Inflammation is associated with various pulmonary diseases and contributes to the pathogenesis of acute lung injury. We previously identified a proinflammatory signaling pathway triggered by G protein-coupled receptors (GPCRs) in which stimulation of Gq-coupled GPCRs results in activation of the transcription factor NF-κB. Because damage to the lung causes the release of multiple mediators acting through Gq-coupled GPCRs, this signaling pathway is likely to contribute to inflammatory processes in the injured lung. In an effort to identify novel inhibitors of lung inflammation, the National Institutes of Health Clinical Collection, a library of 446 compounds, was screened for inhibitory activity toward production of IL-8 induced by stimulation of the Gq-coupled tachykinin 1 receptor with substance P in A549 cells. Twenty-eight compounds that significantly inhibited substance P-induced IL-8 production were identified. The most potent inhibitor was triptolide, a diterpenoid compound from Tripterygium wilfordii Hook F, a vine used in traditional Chinese medicine for the treatment of autoimmune diseases. Triptolide inhibited IL-8 production induced by substance P with an IC50 of 2.3 × 10−8 M and inhibited NF-κB activation in response to an agonist of the protease-activated receptor 2 with an IC50 of 1.4 × 10−8 M. Anti-inflammatory effects of triptolide were assessed in vivo using a chlorine gas lung injury model in mice. Triptolide inhibited neutrophilic inflammation and the production of KC (Cxcl1) in the lungs of chlorine-exposed mice. The results demonstrate that triptolide exhibits anti-inflammatory activity in cultured lung cells and in an in vivo model of acute lung injury.

Identification of triptolide, a natural diterpenoid compound, as an inhibitor of lung inflammation

We have examined the effects of chlorine gas inhalation (110 and 140 ppm) on cardiovascular and pulmonary function in nine anaesthetised and mechanically ventilated pigs. Four additional pigs, which were similarly treated but not exposed to gas, served as controls. Severe pulmonary dysfunction developed when the animals were exposed to 100 l of 140 ppm chlorine gas for 10 min. Five of six animals died within 6 h of exposure. This dose induced a rapid drop in arterial oxygen tension (P < 0.001 compared with controls, ANOVA), a biphasic decline in lung compliance (P < 0.001) and a gradual increase in pulmonary vascular resistance (P < 0.001) that eventually caused a significant reduction in cardiac output ( P < 0.05). Microscopic examination showed sloughing of the bronchial epithelium and early infiltration with leukocytes, but largely intact alveoli. The sequence of events and the microscopic appearance suggested that the initial stage of pulmonary dysfunction (the first 1 or 2 h) was the result of mismatching of ventilation and perfusion. This was followed at a later stage by interstitial oedema and migration of immunocompetent cells into the tissue. We conclude that exposure to 100 l of 140 ppm chlorine gas induces a severe stereotypic lung injury with high mortality within 6 h in this anaesthetised animal model. © 1998 John Wiley & Sons, Ltd.

Exposure to chlorine gas : Effects on pulmonary function and morphology in anaesthetised and mechanically ventilated pigs

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Exposure to chlorine gas : Effects on pulmonary function and morphology in anaesthetised and mechanically ventilated pigs