Management of Chlorine Gas-Related Injuries From the Graniteville, South Carolina, Train Derailment

Mackie, Emily; Svendsen, Erik; Grant, Stephen R.; Michels, Jill E; Richardson, William H.

doi:10.1017/dmp.2014.81

Cited by 37 publications

(28 citation statements)

References 27 publications

(153 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This resulted in the largest U.S. civilian population ever exposed to chlorine . Following the accident, nine people died immediately, 72 were hospitalized, several hundred people immediately became sick and received medical care, and thousands were exposed . An exposure registry was developed, and community health screenings were provided in 2005–2007 .…”

Section: Persistent Effects Of Chlorine Exposure In Humansmentioning

confidence: 99%

Persistent effects of chlorine inhalation on respiratory health

Hoyle

Svendsen

2016

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

Chlorine gas is a toxic respiratory irritant that is considered a chemical threat agent because of the potential for release in industrial accidents or terrorist attacks. Chlorine inhalation damages the respiratory tract, including the airways and distal lung, and can result in acute lung injury. Some individuals exposed to chlorine experience a full recovery from acute injury, whereas others develop persistent adverse effects, such as respiratory symptoms, inflammation, and lung-function decrements. In animal models, chlorine can produce persistent inflammation, remodeling, and obstruction in large or small airways, depending on species. Airways with pseudostratified epithelium are repaired efficiently, with surviving basal epithelial cells serving as progenitor cells that repopulate the complement of differentiated cell types. Distal airways lacking basal cells are repaired less efficiently, leading to chronic inflammation and fibrosis at these sites. Persistent chlorine-induced airway disease in humans is treated with asthma medication to relieve symptoms. However, such treatment does not ameliorate the underlying disease pathogenesis, so treatments that are more effective at preventing initial development of airway disease after irritant gas exposure and at reversing established disease are needed.

show abstract

Section: Persistent Effects Of Chlorine Exposure In Humansmentioning

confidence: 99%

Persistent effects of chlorine inhalation on respiratory health

Hoyle

Svendsen

2016

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

show abstract

“…The accidental release of large amounts of Cl 2 in 30 large cities worldwide during the last 20 years (49) and the deliberate release of Cl 2 during acts of terrorism (37) caused significant mortality and morbidity to humans and animals (3,10,49,64). Cl 2 generated from the mixing of household products (bleach with acidic solutions) as well as swimming pool accidents results in bronchoconstriction especially in people with preexisting lung diseases (70,74).…”

mentioning

confidence: 99%

Hyaluronan mediates airway hyperresponsiveness in oxidative lung injury

Lazrak

Creighton

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

Chlorine (Cl2) inhalation induces severe oxidative lung injury and airway hyperresponsiveness (AHR) that lead to asthmalike symptoms. When inhaled, Cl2 reacts with epithelial lining fluid, forming by-products that damage hyaluronan, a constituent of the extracellular matrix, causing the release of low-molecular-weight fragments (L-HA, <300 kDa), which initiate a series of proinflammatory events. Cl2 (400 ppm, 30 min) exposure to mice caused an increase of L-HA and its binding partner, inter-α-trypsin-inhibitor (IαI), in the bronchoalveolar lavage fluid. Airway resistance following methacholine challenge was increased 24 h post-Cl2 exposure. Intratracheal administration of high-molecular-weight hyaluronan (H-HA) or an antibody against IαI post-Cl2 exposure decreased AHR. Exposure of human airway smooth muscle (HASM) cells to Cl2 (100 ppm, 10 min) or incubation with Cl2-exposed H-HA (which fragments it to L-HA) increased membrane potential depolarization, intracellular Ca2+, and RhoA activation. Inhibition of RhoA, chelation of intracellular Ca2+, blockade of cation channels, as well as postexposure addition of H-HA, reversed membrane depolarization in HASM cells. We propose a paradigm in which oxidative lung injury generates reactive species and L-HA that activates RhoA and Ca2+ channels of airway smooth muscle cells, increasing their contractility and thus causing AHR.

show abstract

“…Concentrations of Cl 2 upon the initial release of the gas reached up to 500 ppm, a dose above the lethal concentration of Cl 2 in many animal studies . In addition, adverse environmental damages from the accident were extensive, as animal deaths and bleaching of vegetation occurred up to 1 km from the site of the accident …”

Section: Chlorine As An Occupational and Public Health Hazardmentioning

confidence: 99%

Chlorine‐induced cardiopulmonary injury

Carlisle

Lam

Svendsen

et al. 2016

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

Chlorine (Cl2) is utilized worldwide for a diverse range of industrial applications, including pulp bleaching, sanitation, and pharmaceutical development. Though Cl2 has widespread use, little is known regarding the mechanisms of toxicity associated with Cl2 exposure, which occurs during industrial accidents or acts of terrorism. Previous instances of Cl2 exposure have led to reported episodes of respiratory distress that result in high morbidity and mortality. Furthermore, studies suggest that acute Cl2 exposure also results in systemic vascular injury and subsequent myocardial contractile dysfunction. Here we review both lung and cardiac pathology associated with acute Cl2 inhalation and discuss recently published data that suggests that mitochondrial dysfunction underlies the pathogenesis of Cl2-induced toxicity. Lastly, we discuss our findings that suggest that upregulation of autophagy protects against Cl2-induced lung inflammation and can be a potential therapeutic target for ameliorating the toxic effects of Cl2 exposure.

show abstract

Management of Chlorine Gas-Related Injuries From the Graniteville, South Carolina, Train Derailment

Cited by 37 publications

References 27 publications

Persistent effects of chlorine inhalation on respiratory health

Persistent effects of chlorine inhalation on respiratory health

Hyaluronan mediates airway hyperresponsiveness in oxidative lung injury

Chlorine‐induced cardiopulmonary injury

Contact Info

Product

Resources

About