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.

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.

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.

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.

Should cities invest in sheltering-in-place measures against chlorine truck attacks by terrorists?

After an intentional release of chlorine in an office district, public responses such as sheltering-in-place could save many lives if rapid enough. However, previous work does not estimate how fast and effective such responses would be for several possible investments in attack detection, public alert, and building ventilation, nor whether such measures would be cost effective. We estimate public response times with investment options in place, and resulting changes in fatalities as well as system costs, including false alarm costs, and cost effectiveness in terms of cost per net death avoided. The measures do have life-saving potential, especially if all response times are at or near the lower limits of the ranges assumed in this article. However, due to uncertainties, it is not clear that responses would be rapid enough to save many people. In some cases total fatalities would increase, since sheltering after chlorine vapor has already entered buildings can increase occupants' chlorine exposure. None of the options considered have median cost per statistical life saved meeting a cost-effectiveness threshold of $6.5 million across all of the chlorine exposure dose-response and ingress-delay models considered here, even if there were one attack per year in the area covered by the system. Given these and other issues discussed in this article, at this point investments to improve sheltering-in-place capability appear not to be robust strategies for reducing fatalities from chlorine attack in an office district.

[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.

Chlorine gas exposure at a metal recycling facility--California, 2010.

On June 8, 2010, chlorine gas was released from a ruptured, 1-ton, low-pressure tank being recycled at a California metal recycling facility. A total of 23 persons, including employees, customers, and workers at nearby businesses, were treated for the effects of the fumes at seven area hospitals. Chlorine is a corrosive, greenish-yellow gas that is heavier than air and can cause severe respiratory damage; it is used widely in water purification, sewage treatment, and disinfectant washes for foods. Following the incident, the Agency for Toxic Substances and Disease Registry (ATSDR) and CDC collaborated with the California Department of Public Health (CDPH) on an Assessment of Chemical Exposures (ACE) to determine 1) the circumstances surrounding those exposed during the chlorine gas release, 2) health effects associated with exposures, and 3) recommendations for preventing recurrences. This report describes the chlorine gas release in California and summarizes the results of the ACE investigation. Of 29 persons potentially exposed to chlorine gas, 27 were interviewed to collect information regarding their exposures. In addition, information regarding acute health effects and symptoms was abstracted from medical records. At the time of the chlorine gas release, 15 persons were outdoors, and 13 were exposed for >30 minutes before they were decontaminated. Twenty-three persons reported experiencing one or more upper or lower respiratory tract symptoms within 24 hours of exposure; six persons were hospitalized for 1-11 days. Based on these findings, CDPH issued a statewide alert to all recycling facilities on how to handle containers with potential hazardous waste.

Pneumomediastinum from acute inhalation of chlorine gas in 2 young patients.

Trichloroisocyanuric acid is a high-efficiency and-low toxicity fungicide and bleach. It is commonly used as disinfectant for industrial circulating water, swimming pools, restaurants, and other public places in China. When trichloroisocyanuric acid is put into water, chlorine gas is produced. Chlorine gas is a potent pulmonary irritant that causes acute damage in both the upper and lower respiratory tracts (J Toxicol Clin Toxicol. 1998;36(1-2):87-93). Pneumomediastinum is a rare complication in patients with acute chlorine gas poisoning. A small amount of gas can be asymptomatic, but a large amount of gas entering the mediastinum suddenly will lead to respiratory and circulatory disorder, mediastinal swing, or even cardiopulmonary arrest. Severe chlorine gas poisoning patients usually need mechanical ventilation; if the pneumomediastinum is not found on time, threat to life would be greatly increased. It requires a high index of suspicion for diagnosis and rapid treatment. The proper use of ventilator, timely and effective treatment of original disease, and multiple system organ support had significant impact on the prognosis. The pneumomediastinum case secondary to inhalation of chlorine gas that we report here should remind all emergency department physicians to maintain a high index of suspicion for this disease and seek immediate and proper intervention when treating patients with acute chlorine gas poisoning, once diagnosed, especially in younger patients.

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.

Long-term outcomes of acute irritant-induced asthma.

RATIONALE: The long-term outcomes of acute irritant-induced asthma (IIA) are mostly unknown. OBJECTIVES: To study the long-term outcomes of IIA. METHODS: We reassessed 35 subjects who experienced IIA at a mean interval of 13.6 +/- 5.2 years. MEASUREMENTS AND MAIN RESULTS: The causal agent was chlorine in 20 cases (57%). At diagnosis, the mean +/- SD FEV(1) was 74.5 +/- 19.5% predicted, and all subjects showed bronchial hyperresponsiveness. At reassessment, all subjects reported respiratory symptoms, and 24 (68%) were on inhaled steroids. There were no significant improvements in FEV(1) and FEV(1)/FVC values. Twenty-three subjects had a methacholine test, and only six subjects had normal levels of responsiveness. Of the remaining 12 subjects, six had improvement in FEV(1) after bronchodilator >or=10%. In samples of induced sputum obtained from 27 subjects, six had eosinophils >or=2%. Levels of inflammatory and remodeling mediators were higher than in control subjects but were no different from subjects with occupational asthma due to sensitization. Quality of life score was 4.4 +/- 1.5 on a 0 (worst) to 7 (best) scale. Twelve subjects had an abnormal depression score. CONCLUSIONS: This study provides the first evidence of significant long-term impact of acute IIA on various outcomes.

Acute accidental exposure to chlorine gas: clinical presentation, pulmonary functions and outcomes.

BACKGROUND: To study the clinical presentation, pulmonary functions and outcomes in subjects who were accidentally exposed to chlorine gas. METHODS: Prospective observational study of 64 patients who sustained acute accidental exposure to chlorine gas during a leak in the chlorination system of the public bathing pool of a temple. RESULTS: The major presenting symptoms and signs included acute dyspnoea (100%), chest discomfort (100%), cough (97%), eye irritation (88%), giddiness (72%), vomiting (46%), and heaviness in the head (44%); tachycardia (100%), tachypnoea (96%) and polyphonic wheezing (28%). All patients were managed in the emergency room with humidified oxygen inhalation and beta-2 agonist nebulisation and 52 were discharged within six hours. Twelve patients were severely affected and required hospitalisation; three of them were admitted into the intensive care unit. Three patients developed pulmonary oedema six to eight hours following admission. Pulmonary function testing (n = 12) at presentation revealed obstructive defect in eight and mixed obstructive-cum-restrictive defect in four patients. The mean duration of hospital stay was 5.1 +/- 2.1 days. None of the patients died. Reactive airway dysfunction syndrome (RADS) was observed in three of the 12 hospitalised patients, who complained of manifested persistent cough that lasted for three months period following discharge. Serial pulmonary functions recovered to normal range by the end of the six months in all patients and remained so at one-year follow-up. CONCLUSION: Acute exposure to chlorine gas is an uncommon, but important public health hazard and can cause RADS, acute lung injury and pulmonary function abnormalities, which are reversible on prompt and appropriate management.

[Radiographic and computed tomographic manifestations of chest in patients with acute chlorine gas poisoning].

OBJECTIVE: To investigate the radiographic and computerized tomographic features of chest in patients with acute chlorine poisoning and its diagnostic value. METHODS: Twenty-eight cases of chlorine poisoning were reviewed. And their radiographic and computerized tomographic features were compared and analyzed. RESULTS: Radiographic findings: among 28 patients, 9 cases were normal and 2 cases had no abnormalities on the first chest X-ray and became abnormal one or two days later. And there were abnormal findings in first chest X-ray in 17 patients:acute tracheal inflammation of peribronchitis (n = 3), acute chemical bronchopneumonia (n = 6) and diffuse interstitial and central pulmonary edema (n = 8). CT manifestations: At Days 1-3, the patients of mild poisoning had scattered patchy dense shadow; those of moderate to severe poisoning showed multiple patchy or diffuse infiltration (ground-glass opacity). And partial consolidation, air bronchogram and pleural effusion could be observed. At Days 4-10, the manifestations of mild poisoning were largely absorbed; those of moderate to severe poisoning manifested the absorption of diffuse or multiple patchy effusion and a fading of shadow. And the size of lung consolidation became smaller than before. At Day 10 after onset, 4 patients completely recovered. At Days 30-40, 6 cases showed traces of fibrous shadow and one case showed small punctiform opacities in both lungs. And at Day 42, there was slight ground-glass change. CONCLUSION: Acute chlorine gas poisoning in varying degrees may manifest acute bronchial pneumonia and acute pulmonary edema. During treatment, a series of chest X-ray examinations will help to follow the changes of disease. And CT examination can offer a more accurate evaluation of lung lesions.

Toxicology and military anaesthesia.

The combination of trauma and poisoning is a situation likely to be faced by a deployed force at some point. This article provides practical advice on how to deal with poisoned patients without deviating from the concept of damage control resuscitation. The constraints of limited diagnostics, both at the scene and clinically, and lack of antidotal therapy are fundamental to the practice of clinical toxicology. Some of the specific therapies such as atropine and oximes were not evaluated prior to their introduction and there are few randomised controlled trials of poisoned patients. Most of the diagnoses will be made on clinical grounds and most of the therapy will be supportive; this article aims to reassure military anaesthetists in the process of dealing with the poisoned trauma patient.

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.

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.

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.

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.