Human chlorine gas exposition and its management - an umbrella review on human data.

Even though exposure to chlorine gas has been quite frequent in the past few decades, no specific antidotes exist. This umbrella review aimed to investigate possible recommendations for treatment after a chlorine gas exposure. A published systematic review protocol that adapted the existing Navigation Guide methodology was used for including studies without comparator. Using PubMed, Web of Science, Google scholar for all potentially relevant systematic reviews, two authors independently included papers and extracted data. The risk of bias and quality of evidence was assessed by two independent review teams blinded to each other. A qualitative summary of the study findings was conducted for this overview. There were a total of 31 studies, from 4 systematic reviews, that met the inclusion criteria, comprising 3567 reported cases, with only two studies with comparators. Six studies reported pre-hospital management of patients after exposure to chlorine gas. With respect to the treatment, the most used were oxygen therapy, endotracheal intubation, ß2-agonists, and corticosteroids. This review found a high quality of evidence for the effectiveness of pre-hospital management (i.e. exposure cessation) on survival at hospital discharge after exposure to chlorine gas. Oxygen administration was effective with moderate quality of evidence, as well as other types of treatment (e.g. ß2, corticosteroids), but with a low level of evidence. This umbrella review highlighted the low level of evidence for existing treatments of chlorine gas poisoning. This project was supported by the French Pays de la Loire region and Angers Loire Métropole (TEC-TOP project). There is no award/grant number. The review protocol was registered on PROSPERO under the registration number CRD42021231524.

Acute chlorine poisoning caused by an accident at a swimming pool.

Chlorine is an irritant gas that is widely used in water purification. Several previous reports had reported accidents of inhalation injuries at swimming pools. However, there have been limited data on the detection of on-site chlorine concentration. This study aims to report a chlorine leakage accident at a swimming pool caused by improper disinfection operations. Calculation using the gas diffusion simulation software showed that the on-site chlorine concentration was 221.45 ppm. When the accident occurred, there were 92 individuals at the swimming pool and the gym, among which 61 were referred to the emergency department of five different hospitals for feeling ill. Among them, 22 patients underwent chest high-resolution computed tomography scans in our hospital. According to the findings, 4 (18.2%) patients had peribronchitis, 3 (13.6%) had tracheobronchitis, 4 (18.2%) had pneumonia, 4 (18.2%) had interstitial pulmonary edema, and 3 (13.6%) had alveolar pulmonary edema. The symptoms of 22 patients who visited our hospital significantly improved after comprehensive treatment. Three months after the accident, 8 of 17 patients presented obstructive ventilation defects or small airway dysfunction. The accidental exposure to chlorine may induce acute poisoning with various respiratory injuries and prolonged lung dysfunction.

Forensic issues arising in the assessment of chlorine-related deaths in a domestic setting.

A retrospective review of autopsy files at the Forensic Science South Australia, Australia, was undertaken over a 20-year period from January 2000 to December 2019 for all cases where chlorine had caused or contributed to death. Two cases were identified out of a total of 25,121 autopsies (0.008%): a 53-year-old man who committed suicide in a cellar with granulated chlorine, and a 49-year-old woman with asthma who died of acute bronchospasm due to exposure to chlorine gas while mixing swimming pool chemicals in her kitchen. Chlorine-related deaths are uncommon in domestic situations. However, the absence of biomarkers and non-specific findings at autopsy complicate the diagnosis, particularly as environmental levels are not stable. While accidents with cleaning agents or swimming pool reagents are the most common event in the literature in domestic settings (exclusive of industrial or transportation accidents), suicide may also very rarely occur. Individuals with asthma and chronic respiratory diseases are at higher risk of an adverse outcome upon exposure to chlorine gas, with inattention to proper storage conditions and handling protocols being additional risk factors.

Determination of 3-chloro-l-tyrosine as a novel indicator of chlorine poisoning utilizing gas chromatography-mass spectrometric analysis.

Chlorine gas exposure occurs in chemical warfare, industrial and household accidents. In forensic science, the generation of chlorine gas by mixing sodium hypochlorite detergent and strong acid detergent cannot be overlooked because of the possibility of suicide method (NaClO + 2HCl â†’ NaCl + H2O + Cl2). Though typical autopsy findings are obtained in chlorine exposure, such as pulmonary edema, useful biomarkers don't exist. In this research, we developed an analytical method of 3-chloro-l-tyrosine (Cl-Tyr) in blood as a novel marker of chlorine poisoning utilizing gas chromatography-mass spectrometry (GC-MS). Cl-Tyr was purified using protein precipitation and cation-exchange solid phase extraction, derivatized by the silylation agent and subjected to GC-MS. The quantification range was 10-200 ng/mL and good reproducibility was obtained. We applied the developed method to analyze Cl-Tyr in autopsy sample, which is suspected of chlorine poisoning, and detected 59.7 ng/mL Cl-Tyr in left heart blood. To our knowledge, this is the first report of determination of the chlorinated biomolecule in the human autopsy sample from chlorine poisoning.

Halogen exposure injury in the developing lung.

Owing to a high-volume industrial usage of the halogens chlorine (Cl2 ) and bromine (Br2 ), they are stored and transported in abundance, creating a risk for accidental or malicious release to human populations. Despite extensive efforts to understand the mechanisms of toxicity upon halogen exposure and to develop specific treatments that could be used to treat exposed individuals or large populations, until recently, there has been little to no effort to determine whether there are specific features and or the mechanisms of halogen exposure injury in newborns or children. We established a model of neonatal halogen exposure and published our initial findings. In this review, we aim to contrast and compare the findings in neonatal mice exposed to Br2 with the findings published on adult mice exposed to Br2 and the neonatal murine models of bronchopulmonary dysplasia. Despite remarkable similarities across these models in overall alveolar architecture, there are distinct functional and apparent mechanistic differences that are characteristic of each model. Understanding the mechanistic and functional features that are characteristic of the injury process in neonatal mice exposed to halogens will allow us to develop countermeasures that are appropriate for, and effective in, this unique population.

The introduction of gas warfare and its medical response in world war one.

The introduction of gas warfare in World War One was impactful, as it both expanded the breadth of warfare and fueled the invention of techniques required to treat these new injuries. Gas injuries were responsible for 91,000 of 1.3 million deaths in World War One. Gassed soldiers had wounds which the world had never seen. They presented in large scale to medical tents and base hospitals across Europe. As gas casualties poured in, doctors and nurses had to treat these conditions in the best way they knew. Gas warfare changed how war was performed and how casualties of this attack were treated. The techniques learned from treating the multitudes of men with gas burns led to advances in the field of burn care, which have helped to improve mortality and reduce morbidity in hospitals across the world.

Choking agents and chlorine gas - History, pathophysiology, clinical effects and treatment.

INTRODUCTION: Choking agent exposure, among them chlorine gas, occurs in household or industrial accidents, chemical warfare and terrorist attacks. AIMS: Review of published animal and human data regarding the history, pathophysiology, clinical effects and management of chlorine exposure. PATHOPHYSIOLOGY: Highly soluble agents cause quick upper respiratory tract symptoms. Chlorine gas has a medium solubility, also causing delayed lower airway symptoms, mainly due to its oxidizing potential by releasing hypochlorous and hydrochloric acid, but also by interacting with Transient Receptor Potential channels. SYMPTOMS: Eyes may show conjunctival injection, abrasions and corrosions. Burns of the oronasal mucosa and trachea can occur. Dyspnea, bronchospasm and possible retrosternal pain occur frequently. Glottis edema or laryngospasm are acute life-threatening emergencies. Chlorine gas can cause toxic pneumonitis, lung edema and acute respiratory distress syndrome (ARDS). MANAGEMENT: General management includes physical examination, pulse oximetry and arterial blood gases. Eyes should be irrigated, humidified oxygen and inhalative bronchodilators administered. An EKG, cardiac enzymes and complete-blood-count should be obtained if there is retrosternal pain. Routine chest x-ray is not recommended - except if pulmonary edema is suspected. Laryngoscopy should be performed if glottis edema is suspected. Sodium bicarbonate inhalation after chlorine gas inhalation is discussed controversially. Mechanical ventilation with continuous-positive-airway-pressure or intubation/tracheotomy with high positive-end-expiratory-pressure may be necessary. Glucocorticoids for prevention of pulmonary edema should be applied restrictively. Prophylactic antibiotics are not recommended. In severe ARDS, extracorporeal membrane oxygenation (ECMO) can be considered. CONCLUSION: Treatment is mainly symptom oriented. New and promising therapies are in development.

Fatal chlorine gas exposure at a metal recycling facility: Case report.

At least four workers at a metal recycling facility were hospitalized and one died after exposure to chlorine gas when it was accidentally released from an intact, closed-valved cylinder being processed for scrap metal. This unintentional chlorine gas release marks at least the third such incident at a metal recycling facility in the United States since 2010. We describe the fatal case of the worker whose clinical course was consistent with acute respiratory distress syndrome (ARDS) following exposure to high concentrations of chlorine gas. This case report emphasizes the potential risk of chlorine gas exposure to metal recycling workers by accepting and processing intact, closed-valved containers. The metal recycling industry should take steps to increase awareness of this established risk to prevent future chlorine gas releases. Additionally, public health practitioners and clinicians should be aware that metal recycling workers are at risk for chlorine gas exposure.

Civilian exposure to chlorine gas: A systematic review.

INTRODUCTION: Halogen pulmonary irritants (HPIs) are volatile liquids that directly damage the respiratory mucosa. Chlorine is readily available in large volumes as an industrial chemical and has a significant potential for accidental or deliberate release. We conducted a systematic review to determine the clinical features; treatment and long-term sequelae of civilian chlorine gas exposure. METHODS: A systematic review was conducted using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methodology. Medline; Ovid and Google Scholar databases were searched from 1966 to January 2017. A database of relevant papers was compiled and descriptive statistics used to summarise the data. RESULTS: Thirty-six papers describing 37 incidents involving 1566 individual acute exposers to chlorine gas were identified. The most common reported features were cough (29%), dyspnoea (22%), sore throat (16%), eye features (12%) and excessive sputum or haemoptysis (7%). Acute management included high-flow oxygen (32.8%); steroids (28.4%); bronchodilators (28.2%) and ventilation (2.3%). Nine deaths (0.6%) were reported. Follow-up data available in 60% of cases; full recovery was reported in 90% of cases where data was available. DISCUSSION: Acute chlorine gas exposure in civilian incidents presented with acute respiratory features and irritation of the eyes and throat. The development of pulmonary oedema or ARDS was relatively rare when compared to military experience in the First World War.

Use of noninvasive ventilation in severe acute respiratory distress syndrome due to accidental chlorine inhalation: a case report. / Uso da ventilação não invasiva em síndrome do desconforto respiratório agudo grave por inalação acidental de cloro: um relato de caso.

Acute respiratory distress syndrome is characterized by diffuse inflammatory lung injury and is classified as mild, moderate, and severe. Clinically, hypoxemia, bilateral opacities in lung images, and decreased pulmonary compliance are observed. Sepsis is one of the most prevalent causes of this condition (30 - 50%). Among the direct causes of acute respiratory distress syndrome, chlorine inhalation is an uncommon cause, generating mucosal and airway irritation in most cases. We present a case of severe acute respiratory distress syndrome after accidental inhalation of chlorine in a swimming pool, with noninvasive ventilation used as a treatment with good response in this case. We classified severe acute respiratory distress syndrome based on an oxygen partial pressure/oxygen inspired fraction ratio <100, although the Berlin classification is limited in considering patients with severe hypoxemia managed exclusively with noninvasive ventilation. The failure rate of noninvasive ventilation in cases of acute respiratory distress syndrome is approximately 52% and is associated with higher mortality. The possible complications of using noninvasive positive-pressure mechanical ventilation in cases of acute respiratory distress syndrome include delays in orotracheal intubation, which is performed in cases of poor clinical condition and with high support pressure levels, and deep inspiratory efforts, generating high tidal volumes and excessive transpulmonary pressures, which contribute to ventilation-related lung injury. Despite these complications, some studies have shown a decrease in the rates of orotracheal intubation in patients with acute respiratory distress syndrome with low severity scores, hemodynamic stability, and the absence of other organ dysfunctions.

Uso da ventilação não invasiva em síndrome do desconforto respiratório agudo grave por inalação acidental de cloro: um relato de caso / Use of noninvasive ventilation in severe acute respiratory distress syndrome due to accidental chlorine inhalation: a case report

RESUMO A síndrome do desconforto respiratório agudo é caracterizada por lesão pulmonar inflamatória difusa, classificada em leve, moderada e grave. Clinicamente observam-se hipoxemia, opacidades bilaterais na imagem pulmonar e diminuição da complacência pulmonar. A sepse está entre as causas mais prevalentes (30 - 50%). Dentre as causas diretas de síndrome do desconforto respiratório agudo, a inalação de cloro é uma causa incomum, gerando, na maior parte dos casos, irritação de mucosas e vias aéreas. Apresentamos um caso de síndrome do desconforto respiratório agudo grave após inalação acidental de cloro em piscina, sendo utilizada ventilação não invasiva como tratamento com boa resposta neste caso. Classificamos como síndrome do desconforto respiratório agudo grave baseado na relação pressão parcial de oxigênio/fração inspirada de oxigênio < 100, embora a classificação de Berlin seja limitada em considerar pacientes com hipoxemia grave manejados exclusivamente com ventilação não invasiva. A taxa de falha da ventilação não invasiva nos casos de síndrome do desconforto respiratório agudo está em torno de 52%, estando associada à maior mortalidade. As possíveis complicações do uso da ventilação mecânica não invasiva com pressão positiva na síndrome do desconforto respiratório agudo seriam o atraso para a intubação orotraqueal sendo a mesma realizada em uma condição clínica pior e um alto nível de pressões de suporte, somados a esforços inspiratórios profundos, gerando elevados volumes correntes e pressões transpulmonares excessivas, que contribuem para injúria pulmonar associada à ventilação. Apesar disto, alguns estudos mostraram diminuição nas taxas de intubação orotraqueal em pacientes com síndrome do desconforto respiratório Agudo com baixos escores de gravidade, estabilidade hemodinâmica e ausência de outras disfunções orgânicas.

ABSTRACT Acute respiratory distress syndrome is characterized by diffuse inflammatory lung injury and is classified as mild, moderate, and severe. Clinically, hypoxemia, bilateral opacities in lung images, and decreased pulmonary compliance are observed. Sepsis is one of the most prevalent causes of this condition (30 - 50%). Among the direct causes of acute respiratory distress syndrome, chlorine inhalation is an uncommon cause, generating mucosal and airway irritation in most cases. We present a case of severe acute respiratory distress syndrome after accidental inhalation of chlorine in a swimming pool, with noninvasive ventilation used as a treatment with good response in this case. We classified severe acute respiratory distress syndrome based on an oxygen partial pressure/oxygen inspired fraction ratio <100, although the Berlin classification is limited in considering patients with severe hypoxemia managed exclusively with noninvasive ventilation. The failure rate of noninvasive ventilation in cases of acute respiratory distress syndrome is approximately 52% and is associated with higher mortality. The possible complications of using noninvasive positive-pressure mechanical ventilation in cases of acute respiratory distress syndrome include delays in orotracheal intubation, which is performed in cases of poor clinical condition and with high support pressure levels, and deep inspiratory efforts, generating high tidal volumes and excessive transpulmonary pressures, which contribute to ventilation-related lung injury. Despite these complications, some studies have shown a decrease in the rates of orotracheal intubation in patients with acute respiratory distress syndrome with low severity scores, hemodynamic stability, and the absence of other organ dysfunctions.

Gas: the greatest terror of the Great War.

The Great War began just over a century ago and this monumental event changed the world forever. 1915 saw the emergence of gas warfare-the first weapon of mass terror. It is relevant to anaesthetists to reflect on these gases for a number of reasons. Firstly and most importantly we should acknowledge and be aware of the suffering and sacrifice of those soldiers who were injured or killed so that we could enjoy the freedoms we have today. Secondly, it is interesting to consider the overlap between poison gases and anaesthetic gases and vapors, for example that phosgene can be formed by the interaction of chloroform and sunlight. Thirdly the shadow of gas warfare is very long and covers us still. The very agents used in the Great War are still causing death and injury through deployment in conflict areas such as Iraq and Syria. Industrial accidents, train derailments and dumped or buried gas shells are other sources of poison gas hazards. In this age of terrorism, anaesthetists, as front-line resuscitation specialists, may be directly involved in the management of gas casualties or become victims ourselves.

Challenges During a Chlorine Gas Emergency Response.

OBJECTIVE: A chlorine gas release occurred at a poultry processing plant as a result of an accidental mixing of sodium hypochlorite and an acidic antimicrobial treatment. We evaluated the public health and emergency medical services response and developed and disseminated public health recommendations to limit the impact of future incidents. METHODS: We conducted key informant interviews with the state health department; local fire, emergency medical services, and police departments; county emergency management; and representatives from area hospitals to understand the response mechanisms employed for this incident. RESULTS: After being exposed to an estimated 40-pound chlorine gas release, 170 workers were triaged on the scene and sent to 5 area hospitals. Each hospital redistributed staff or called in extra staff (eg, physicians, nurses, and respiratory therapists) in response to the event. Interviews with hospital staff emphasized the need for improved communication with responders at the scene of a chemical incident. CONCLUSIONS: While responding, hospitals handled the patient surge without outside assistance because of effective planning, training, and drilling. The investigation highlighted that greater interagency communication can play an important role in ensuring that chemical incident patients are managed and treated in a timely manner. (Disaster Med Public Health Preparedness. 2016;10:553-556).

A case of a chlorine inhalation injury in an Ebola treatment unit.

We present a 26-year-old male British military nurse, deployed to Sierra Leone to treat patients with Ebola virus disease at the military-run Kerry Town Ebola Treatment Unit. Following exposure to chlorine gas during routine maintenance procedures, the patient had an episode of respiratory distress and briefly lost consciousness after exiting the facility. Diagnoses of reactive airways disease, secondary to the chlorine exposure and a hypocapnic syncopal episode were made. The patient was resuscitated with minimal intervention and complete recovery occurred in less than 1 week. This case highlights the issues of using high-strength chlorine solution to disinfect the red zone. Although this patient had a good outcome, this was fortunate. Ensuring Ebola treatment centres are optimally designed and that appropriate management systems are formulated with extraction scenarios rehearsed are important to mitigate the chlorine-associated risk.

Nitrite therapy improves survival postexposure to chlorine gas.

Exposure to relatively high levels of chlorine (Cl2) gas can occur in mass-casualty scenarios associated with accidental or intentional release. Recent studies have shown a significant postexposure injury phase to the airways, pulmonary, and systemic vasculatures mediated in part by oxidative stress, inflammation, and dysfunction in endogenous nitric oxide homeostasis pathways. However, there is a need for therapeutics that are amenable to rapid and easy administration in the field and that display efficacy toward toxicity after chlorine exposure. In this study, we tested whether nitric oxide repletion using nitrite, by intramuscular injection after Cl2 exposure, could prevent Cl2 gas toxicity. C57bl/6 male mice were exposed to 600 parts per million Cl2 gas for 45 min, and 24-h survival was determined with or without postexposure intramuscular nitrite injection. A single injection of nitrite (10 mg/kg) administered either 30 or 60 min postexposure significantly improved 24-h survival (from ∼20% to 50%). Survival was associated with decreased neutrophil accumulation in the airways. Rendering mice neutropenic before Cl2 exposure improved survival and resulted in loss of nitrite-dependent survival protection. Interestingly, female mice were more sensitive to Cl2-induced toxicity compared with males and were also less responsive to postexposure nitrite therapy. These data provide evidence for efficacy and define therapeutic parameters for a single intramuscular injection of nitrite as a therapeutic after Cl2 gas exposure that is amenable to administration in mass-casualty scenarios.

Management of chlorine gas-related injuries from the Graniteville, South Carolina, train derailment.

A widely produced chemical, chlorine is used in various industries including automotive, electronics, disinfectants, metal production, and many others. Chlorine is usually produced and transported as a pressurized liquid; however, as a gas it is a significant pulmonary irritant. Thousands of people are exposed to chlorine gas every year, and while large-scale exposures are uncommon, they are not rare. Symptoms are usually related to the concentration and length of exposure, and although treatment is largely supportive, certain specific therapies have yet to be validated with randomized controlled trials. The majority of those exposed completely recover with supportive care; however, studies have shown the potential for persistent inflammation and chronic hyperreactivity. This case report describes an incident that occurred in Graniteville, South Carolina, when a train derailment exposed hundreds of people to chlorine gas. This report reviews the events of January 6, 2005, and the current treatment options for chlorine gas exposure.(Disaster Med Public Health Preparedness. 2014;0:1-6).

The effect of exposure to chlorine on pulmonary function tests and respiratory and allergic symptoms in Iranian lifeguards.

Lifeguards are frequently exposed to various irritant chemicals including chlorine during work, which can induce respiratory and allergic disorders. In this study, pulmonary function tests (PFTs) and self-reported respiratory and allergic symptoms in lifeguards were compared with matched control subjects. The frequency of respiratory and allergic symptoms was evaluated in a sample of 38 Iranian male lifeguards and 38 control subjects with similar age, having other jobs from the general population, using a questionnaire including questions on work-related respiratory and allergic symptoms in the past year, smoking habits, and duration of working as a lifeguard. PFTs were also measured in lifeguard subjects before and 15 min after 200 µg inhaled salbutamol and baseline PFT in controls. A total of 22 (55%) participants reported work-related respiratory symptoms. Sputum (39.4%) and cough (18.4%) were the most common symptoms and only 7.9% and 15.8% of lifeguards reported wheezing and shortness of breath, respectively. Both sputum and breathlessness were significantly higher in lifeguards than control group (p < 0.05 and p < 0.005, respectively). Most allergic symptoms (sneezing and runny nose) in lifeguards were also significantly greater than control group (p < 0.05 for both cases). In addition, all respiratory (except sputum and wheezing) and allergic symptoms were significantly higher in lifeguards during work compared with rest period (p < 0.05 to p < 0.005). Most PFT values were also significantly lower in lifeguards than control subjects (p < 0.05 to p < 0.001). In addition, most (all) PFT values were significantly improved after 200 µg inhaled salbutamol (p < 0.05 to p < 0.001). These results showed that lifeguards have higher frequencies of work related respiratory symptoms and allergic symptoms particularly during the work period. PFT values were also significantly reduced among lifeguards.

[Observation on both Na(+)-K+ Atpase activity and expression of Na(+)-K+ AtPase alpha1 mRNA in lung tissues of rats acute poisoned with nickel carbonyl].

OBJECTIVE: To examine the change of Na(+)-K+ ATPase activity and the expressions of Na(+)-K+ ATPase alpha1 mRNA in lung tissues of rats poisoned by nickel carbonyl and to discuss the mechanism of lung injury. METHODS: One hundred seventy healthy rats (85 male and 85 female) were exposed by inhalation of 20,135 and 250 mg/m3 nickel carbonyl for 30 min. Rats poisoned by chlorine gas with a concentration 250 mg/m3 served as positive group and healthy SD rats served as no-treatment negative group. The rats were euthanized on 1, 2, 3 and 7 d after the administration of nickel carbonyl or chlorine gas. In various treatment groups, Na(+)-K+ ATPase activity was studied by colorimetric method and the expressions of Na(+)-K+ ATPase alpha1 mRNA were determined by RT-PCR. RESULTS: Na(+)-K+ ATPase activity and expressions of Na(+)-K+ ATPase alpha1 mRNA in lung tissues decreased in all treatment groups and chlorine gas-poisoned group, especially it was obvious decreased on the 2ed and 3rd day (P < 0.05). CONCLUSION: Nickel carbonyl could induce lung damage and decrease Na(+)-K+ ATPase activity and expressions of Na(+)-K+ ATPase alpha1 mRNA in lung.