Chlorine gas inhalation: human clinical evidence of toxicity and experience in animal models.
Chlorine gas inhalation: human clinical evidence of toxicity and experience in animal models.
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DOI：
10.1513/pats.201001-008sm
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发表时间：
2010-07-01
期刊：
影响因子：
--
通讯作者：
Martin, James G
中科院分区：
文献类型：
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作者：
White, Carl W;Martin, James G
由于交通或铁路事故、泄漏或其他灾难，人类可能在短期、高水平暴露期间接触氯气。相比之下，工作场所和公共场所(游泳池等)暴露更多的是长期的、低水平的暴露，偶尔会被无意的一过性增加所打断。急性暴露可导致急性呼吸道阻塞的症状，包括喘息、咳嗽、胸闷和/或呼吸困难。这些发现相当不具特异性，可能是在接触了一些吸入的化学刺激物后出现的。可能出现临床症状，包括低氧血症、喘息、罗音和/或胸片异常。受影响更严重的人可能会患上急性肺损伤(ALI)和/或急性呼吸窘迫综合征(ARDS)。高达1%的接触者死亡。对于有呼吸道症状的患者，湿化氧气和吸入β-肾上腺素能药物是合适的治疗方法，目前正在进行评估。吸入碳酸氢盐和全身或吸入糖皮质激素也有坊间报道是有益的。慢性后遗症可能包括呼吸道反应性增强，随着时间的推移，这种反应性往往会减弱。在那些年龄较大、吸烟和/或既往患有慢性肺部疾病的幸存者中，呼吸道高反应性可能是一个更大的问题。因工作场所接触氯而患上刺激性哮喘(IIA)的人也往往有类似的特征，如呼吸道对乙酰甲胆碱过敏，年龄较大和吸烟。然而，其他工作场所的研究表明，接触二氧化氯/二氧化硫的工人患慢性支气管炎和/或反复喘息发作(一次或多次)的风险往往增加，但不会增加哮喘的风险，而接触臭氧的工人哮喘的发病率更高。目前缺乏急性和慢性氯气暴露的特定生物标记物。氯气吸入的动物模型已经证明了氧化损伤和炎症的证据。早期的上皮损伤、气道高反应性和气道重塑可能会随着时间的推移而减弱。与人类一样，ALI/ARDS也可能发生，当绕过上呼吸道时，ALI/ARDS变得更有可能。氯毒性的吸入模型为测试潜在的药物救援剂提供了独特的机会。
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 beta-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.