Yamei Wang1
Chuihua Sun
Xiaojuan Sun- 1Department of Occupational Diseases, Weifang People’s Hospital, Weifang, Shandong, China
- 2Department of Critical Care Medicine, Weifang People’s Hospital, Weifang, Shandong, China
Background: Trichloroisocyanuric acid (TCCA) is a potent disinfectant and bleaching agent widely used in industrial applications. When TCCA comes into contact with water, chlorine gas and hypochlorous acid are produced. Although acute respiratory distress syndrome (ARDS) induced by chlorine gas inhalation is rare, if untreated, it can progress to severe respiratory failure. Currently, no standardized glucocorticoid dosing protocol exists for ARDS management in such cases.
Case presentation: This report details the case of a 49-year-old male who developed ARDS following chlorine gas inhalation during an occupational TCCA incident. Upon admission, the patient exhibited shortness of breath, coughing, and dyspnea. Initial laboratory tests revealed leukocytosis and elevated inflammatory markers. Imaging showed bilateral patchy ground-glass opacities, and arterial blood gas analysis indicated severe hypoxia. The patient was treated with non-invasive mechanical ventilation and a graded corticosteroid regimen, leading to gradual improvement in his clinical condition. During this course, the patient developed fever, frequent dry cough, and occasional sputum production. Sputum cultures identified Candida albicans as the pathogen, prompting a shift in treatment to include fluconazole for antifungal therapy, cefoperazone-sulbactam for antibacterial coverage, and continued corticosteroid therapy. The patient recovered progressively and was discharged on the 51st day without complications.
Conclusion: Chlorine gas inhalation can result in severe ARDS, underscoring the need for early diagnosis and prompt intervention. This case underscores the importance of a graded corticosteroid regimen in combination with non-invasive mechanical ventilation in ARDS management. Additionally, fluconazole and cefoperazone effectively address secondary pulmonary fungal infections caused by Candida albicans.
1 Introduction
Trichloroisocyanuric acid (TCCA) is a potent chlorine-based disinfectant renowned for its strong bactericidal and bleaching properties. It is widely applied in industries such as swimming pool and drinking water sanitation, aquaculture, and consumer chemicals (1–3). In damp or high-temperature environments, TCCA decomposes, generating heat, releasing chlorine gas, and potentially leading to violent explosions (4, 5). The toxicity primarily stems from chlorine poisoning and the damage caused by the chemical products released (6, 7). Chlorine gas, with its highly oxidizing and corrosive properties, can cause acute poisoning and tissue damage, especially to the eyes, skin, and mucous membranes (8–10). The respiratory system is particularly vulnerable to chlorine inhalation, with the severity of lung injury depending on the gas concentration, exposure duration, and ventilation conditions (11, 12).
The toxic effects of TCCA are mainly attributed to the high concentration of chlorine gas released during its decomposition (11). Chlorine reacts with moisture in bronchial cells to form hydrochloric acid and hypochlorous acid, causing bronchospasm and lung damage (13, 14). The core mechanism of chlorine gas toxicity lies in its potent oxidative nature. Chlorine induces oxidative damage to mitochondrial DNA (mtDNA), leading to the excessive generation of reactive oxygen species (ROS) that disrupt mitochondrial function (15, 16). This damage affects the expression of lung DNA glycosylase OGG1 and nitric oxide synthase, further exacerbating mtDNA oxidative damage, altering the mitochondrial proteome, and promoting the formation of mitochondrial permeability transition pores, which facilitate cell death (17, 18). Hypochlorous acid, a byproduct of oxidation, inhibits antioxidant enzymes like catalase and glutathione peroxidase, intensifying cellular damage (19, 20). Injury to alveolar epithelial cells and the endothelial cells of capillaries triggers the release of inflammatory mediators (e.g., TNF-α, IL-1, IL-6, IL-8), which activate neutrophils and macrophages to release additional proteases and ROS such as superoxide, hydrogen peroxide, and hydroxyl radicals (14, 21, 22). This inflammatory cascade damages the alveolar epithelium, disrupts the basement membrane, impedes fluid resorption, and promotes the accumulation of proteins and blood cells in the alveolar spaces. Prolonged inflammation and oxidative stress lead to abnormal lung tissue repair, resulting in fibrotic hyperplasia, which manifests as irreversible restrictive ventilatory dysfunction and impaired gas exchange (16, 17).
Clinically, low-level exposure to chlorine gas may be asymptomatic, while higher concentrations can induce symptoms such as cough, chest tightness, mediastinal oscillation, acute respiratory distress syndrome (ARDS), respiratory failure, and even cardiopulmonary arrest (23, 24). Severe chlorine gas poisoning may also lead to the rare complication of mediastinal emphysema (25). For example, Li et al. reported 27 patients who experienced symptoms from chlorine gas inhalation due to TCCA, with 11 diagnosed with severe poisoning. Of these, two young patients developed mediastinal emphysema (12). A previous study also documented a 26-year-old woman who developed mediastinal emphysema after inhaling chlorine gas from a household cleaning product. Other complications of chlorine gas poisoning include chemical pneumonitis and ARDS (26–28). As no specific antidote exists for inhalation-induced lung injury, management is generally supportive, with targeted therapies such as lung-protective ventilation, prone positioning, nebulized bronchodilators, and systemic corticosteroids playing beneficial roles (29–31).
Corticosteroids, potent anti-inflammatory agents, inhibit the synthesis of proinflammatory mediators and modulate systemic immune responses (30). They are commonly used in the treatment of conditions such as COVID-19, viral pneumonia, community-acquired pneumonia, and ARDS (32–35). Recent clinical guidelines recommend the conditional use of corticosteroids in patients with ARDS, based on moderate evidence (36). A meta-analysis indicated that corticosteroids, including methylprednisolone and dexamethasone, are associated with reduced mortality in patients with ARDS (37). However, no randomized controlled trials have compared the efficacy of different corticosteroid doses in treating lung injury, and initial steroid dosing varies among physicians (38). This study presents a case of chlorine gas poisoning from TCCA exposure. Although chlorine gas inhalation can be fatal, timely intervention can lead to recovery. Given that corticosteroids reduce proinflammatory mediators and prevent diffuse alveolar damage, the patient was treated with high-dose methylprednisolone in a tapering regimen, alongside non-invasive ventilatory support. As the glucocorticoid dosage was gradually reduced, the patient developed new symptoms, including fever and purulent sputum, suggesting a secondary infection. Sputum cultures confirmed Candida albicans infection. Clinicians should remain vigilant for emerging symptoms, such as fever, purulent sputum, or new and worsening radiographic findings.
2 Case presentation
A 49-year-old male, engaged in poultry greenhouse disinfection, was resting in a sealed 10-square-meter room containing TCCA powder. Due to excessively high temperatures, the powder exploded violently, releasing a substantial volume of smoke. The patient was awakened by the explosion’s sound and the pungent odor, prompting him to immediately flee the room. His condition deteriorated rapidly, with symptoms including headache, dizziness, tearing, shortness of breath, coughing, pink frothy sputum, and dyspnea. Two hours later, he was transferred to a local hospital for treatment. Due to breathing difficulties, the patient was unable to lie flat and assumed a sitting position. On day 1, computed tomography (CT) scan revealed interlobular septal thickening and patchy ground-glass opacities in both lungs, indicating acute lung injury (Figures 1A1, A2). The patient was treated with moxifloxacin and cefuroxime for infection, methylprednisolone for inflammation, and alternating eye treatments with deproteinized bovine blood extract gel, levofloxacin eye drops, and bromofenac sodium eye drops. Despite slight improvement in symptoms, the patient remained unable to lie flat. He was subsequently admitted to our department with a diagnosis of chlorine poisoning, chemical pneumonia, and ARDS. Since the onset of symptoms, the patient had exhibited poor mental status, loss of appetite, and sleep disturbances. He had a 3-year history of hypertension but had not been on any antihypertensive medications.
Figure 1. (A1–C1) Chest X-ray on Day 1, Day 3, and Day 5. (A2–C2) Images of chest computed tomography (CT) on Day 1, Day 3, and Day 5. (A1,A2) By Day 1, the Chest X-ray and CT images show diffuse consolidation in both lungs, predominantly in the lower regions, indicative of acute lung injury. (B1,B2) By Day 3, the lesions show rapid absorption, suggesting a positive response to treatment. (C1,C2) By Day 5, the lesions have almost completely resolved, reflecting significant recovery and resolution of lung injury.
Upon arrival at the emergency department, the patient’s vital signs were as follows: heart rate 90 beats per minute, temperature 37.3 °C, respiratory rate 19 breaths per minute, and blood pressure 138/81 mmHg. Eye examination revealed secretions on both eyelids, conjunctival congestion, and corneal opacity, with no yellow staining of the sclera. A small area of skin damage was noted on the right anterior chest, but no abnormalities were observed in the mucosa. Chest expansion was restricted due to pain, and respiratory auscultation revealed extensive diffuse dry and wet rales in both lungs, with no other notable physical findings. Initial blood tests showed the following: white blood cells (WBC) 24.98 × 109/L, neutrophil granulocytes (GRAN) 23.78 × 109/L, total protein (TP) 56.4 g/L, serum albumin (ALB) 31.1 g/L, C-reactive protein (CRP) 122.0 mg/L, D-dimer 2.97 μg/mL, prothrombin time (PT) 14.9 s, prothrombin activity (PT%) 69.4%, fibrinogen (FIB) 5.12 g/L, activated partial thromboplastin time (APTT) 30.4 s, and thrombin time (TT) 14.1 s. Biochemical results showed AST 47 U/L, ALB 36.0 g/L, glucose (GLU) 8.0 mmol/L, urea (UREA) 8.7 mmol/L, LDL-C 1.83 mmol/L, Apo-A 0.71 g/L, LDH 377 U/L, CK 597 U/L, and CK-MB 8.26 ng/mL. Urinalysis indicated proteinuria (1+), but other tests, including hepatitis B markers, troponin, BNP, and procalcitonin, were unremarkable. After receiving high-flow oxygen via a nasal cannula (6 L/min), arterial blood gas analysis revealed a pH of 7.43, PaCO2 of 38.8 mmHg, and PaO2 of 71.1 mmHg (Table 1). The PaO2/FiO2 ratio was 158, confirming severe ARDS. The patient was promptly placed on non-invasive ventilatory support with the following settings: positive end-expiratory pressure (PEEP) 12 cmH2O, FiO2 1.0, tidal volume 430 mL, and respiratory rate 15 breaths per minute. The treatment regimen included intravenous moxifloxacin and cefuroxime for infection, glutathione for antioxidant therapy, Ginkgo biloba extract to improve circulation, and nebulized treatments with budesonide, formoterol fumarate, and ambroxol for sputum clearance and asthma relief. For ocular management, the patient received bromfenac sodium eye drops, levofloxacin eye drops, deproteinized bovine blood extract eye drops, and recombinant bovine matrix cell growth factor eye gel to address conjunctival congestion, corneal epithelial defects, and mild edema.
Table 1. Summary of patient’s laboratory test results.
On day 3, a repeat CT scan revealed patchy ground-glass opacities in both lungs (Figures 1B1, B2), with the SpO2/FiO2 ratio measuring 207. The patient received intravenous methylprednisolone sodium succinate (200 mg daily), cefuroxime (1.5 g every 8 h), and oral coenzyme Q (10 mg three times daily). By the fourth day, re-examination showed WBC 19.53 × 109/L, GRAN 17.64 × 109/L, LDH 373 U/L, CK 597 U/L, CK-MB 8.26 ng/mL, CRP 38.1 mg/L, D-dimer 1.52 μg/mL, PT 15.0 s, PT% 69.01%, FIB 4.09 g/L, APTT 27.7 s, and TT 14.0 s. On day 5, a CT scan revealed reduced ground-glass opacity and minimal pleural effusion (Figures 1C1, C2), with the SpO2/FiO2 ratio improving from 207 to 229. Given the patient’s improvement, the glucocorticoid dosage was reduced from 200 mg daily to 160 mg daily. By day 6, laboratory results showed WBC 13.56 × 109/L, GRAN 10.69 × 109/L, TP 56.4 g/L, and ALB 31.1 g/L. On day 8, the SpO2/FiO2 ratio increased to 257, reflecting further stabilization. The glucocorticoid dosage was reduced to 80 mg daily. Follow-up results indicated WBC 15.66 × 109/L, GRAN 11.73 × 109/L, TP 54.1 g/L, and ALB 29.3 g/L. By day 12, a chest CT showed small bilateral pleural effusions and partial improvement in bilateral pneumonia, confirming the treatment’s effectiveness (Figures 2A1, A2). On day 12, laboratory results indicated WBC 14.87 × 109/L, GRAN 10.34 × 109/L, TP 54.1 g/L, and ALB 29.3 g/L, with the SpO2/FiO2 ratio rising to 334, indicating marked improvement in oxygenation. The methylprednisolone sodium succinate dosage was further reduced to 40 mg daily. Due to decreased albumin levels, a high-protein, nutrient-dense diet was recommended. A consultation with the nutrition department led to the prescription of 40 g of whole protein nutritional supplements and 10 g of whey protein per serving.
Figure 2. (A1–D1) Chest X-ray on Day 12, Day 19, Day 25, and Day 51. (A2–D2) Images of chest computed tomography (CT) on Day 12, Day 19, Day 25, and Day 51. (A1,A2) On Day 12, the Chest X-ray and CT images show diffuse consolidation in both lungs, primarily in the lower regions. (B1,B2) By Day 19, the lesions show rapid absorption, indicating a favorable response to treatment. (C1,C2) By Day 25, the lesions are nearly resolved, suggesting substantial recovery and resolution of lung injury. (D1,D2) By Day 51, the lesions have almost completely resolved, indicating further recovery and complete resolution of lung injury.
Given the patient’s stable condition and improvement in various parameters, including WBC 11.88 × 109/L, GRAN 7.54 × 109/L, and SpO2/FiO2 ratio of 334 on day 17, the medication regimen was adjusted from intravenous methylprednisolone 40 mg to oral administration of 20 mg. The following day, the patient began experiencing frequent dry cough with occasional small amounts of sputum. A bacterial sputum test identified a fungal infection, confirming a secondary Candida albicans infection. On day 19, a CT scan revealed solid micronodules in both lungs, primarily consisting of proliferative lesions (Figures 2B1, B2). Fluconazole was initiated for antifungal treatment, while corticosteroid therapy was continued, and cefoperazone-sulbactam was added for antibacterial coverage. By day 25, the CT scan showed multiple solid micronodules in both lungs, most of which were hyperplastic (Figures 2C1, C2). No significant abnormalities were observed in arterial blood gas analysis, myocardial enzyme spectrum, or BNP. Due to the patient’s bronchial asthma (reactive airway dysfunction syndrome) following poisoning, treatment with budesonide-formoterol, tiotropium bromide, and acetylcysteine was administered for cough relief, asthma control, and sputum clearance. On day 46, laboratory results showed K 3.97 mmol/L, TP 58.2 g/L, ALB 36.5 g/L, HDL-C 0.69 mmol/L, LDL-C 2.72 mmol/L, LDH 240 U/L, CK 29 U/L, WBC 12.56 × 109/L, LYMF 4.17 × 109/L, GRAN 7.78 × 109/L, RBC 4.60 × 1012/L, and CRP 1.6 mg/L (Table 1). Pulmonary function testing revealed extremely severe mixed ventilatory dysfunction with normal diffusion capacity. On day 51, the CT scan showed new localized patellar ground-glass opacities in the middle lobe of the right lung, along with solid micronodules in both lungs, primarily consisting of proliferative foci (Figures 2D1, D2). With active treatment, the patient’s condition continued to improve. The patient was advised to rest adequately, avoid exposure to toxic substances, and continue taking methylprednisolone, coenzyme Q10, and betamethasone sustained-release glycyrrhizin tablets, in addition to inhaling tiotropium bromide and budesonide-formoterol powder.
3 Discussion
Trichloroisocyanuric acid (TCCA) is a harmful gas commonly produced in chlorine disinfection environments, with chlorine gas released during its decomposition being the primary cause of inhalation-induced lung injury (4, 5). This gas can irritate the eyes, skin, and respiratory system, resulting in symptoms that range from mild to severe. The severity of lung injury is determined by the concentration of chlorine gas, exposure duration, and the minute ventilation of the exposed individual (11). Low exposure levels (below 15 ppm) typically cause mucosal irritation without symptoms, while higher concentrations (above 30 ppm) may result in chemical pneumonitis and bronchiolitis obliterans. Exposure to concentrations exceeding 400 ppm can cause immediate respiratory arrest (39, 40). Although no specific antidote exists for inhalation-induced lung injury, supportive treatments have advanced significantly (41). Recent innovations, such as high-volume hemofiltration and extracorporeal membrane oxygenation, have shown promising results (28, 42). Studies also suggest that nebulized sodium bicarbonate may aid in treating inhalation lung injury by neutralizing acid production in the pulmonary epithelium (43). Current treatment strategies mainly focus on supplemental oxygen, protective ventilation, nebulized bronchodilators, and intravenous corticosteroids (28, 44).
Acute respiratory distress syndrome is a severe clinical syndrome characterized by progressive respiratory difficulty and persistent hypoxemia (45). It can arise from various causes, including inhalation of toxic gases, pneumonia, bacterial, viral, or fungal infections, sepsis, severe trauma, and burns (46, 47). The disease involves injury to both the alveolar epithelium and capillary endothelium, resulting in inflammatory exudation from the alveolar capillaries, activation of macrophages and neutrophils, and the development of pulmonary edema and atelectasis (48). The clinical manifestations of ARDS vary depending on the underlying cause, exhibiting distinct physiological features that influence the patient’s response to treatment (49). Systemic corticosteroids have been considered a potential therapy to control inflammation and improve survival in ARDS (33, 50). Recent clinical guidelines recommend corticosteroid use for ARDS management, based on moderate evidence. However, no multicenter randomized controlled trials have evaluated glucocorticoid treatment specifically for ARDS caused by chlorine gas (36). While various treatment regimens for ARDS from other causes have been tested, the results remain controversial. Meduri et al. demonstrated that a low-dose, prolonged methylprednisolone regimen alleviated systemic inflammation in patients with severe early ARDS (within 72 h of symptom onset), improving lung and extrapulmonary organ function, and reducing the duration of mechanical ventilation and ICU stay. In contrast, methylprednisolone administration between 7 and 14 days after ARDS diagnosis was associated with significantly increased 60- and 180-day mortality rate (51). Several studies have employed a high-dose protocol (1,000 mg/day for the first 3 days) followed by a moderate taper (2 mg/kg/day over 2 months) (52). Zeiner et al. found that high-dose methylprednisolone improved respiratory function and survival in 65% of patients with refractory COVID-19-related ARDS (53). However, other studies indicate that initial high-dose methylprednisolone therapy followed by tapering may have adverse effects on patients with ARDS (54). Therefore, corticosteroid treatment should be individualized, based on the underlying pathogenesis and severity of ARDS.
In this study, the patient exhibited acute symptoms commonly reported in other cases, including chest tightness, tachycardia, shortness of breath, and the need for oxygen, all indicative of chlorine inhalation-related complications such as chemical pneumonitis, pulmonary edema, and ARDS. The management of chlorine gas inhalation injury is predominantly conservative. Currently, no universally accepted guidelines exist regarding the dosage, duration, or course of glucocorticoid therapy for patients with ARDS (55). The available data on systemic steroid use are limited to a small number of case reports. Table 2 summarizes various case reports involving chlorine exposure, steroid use, and subsequent outcomes. One case, reported by Bleifuss et al., was managed with standard ARDS care, including inhaled epoprostenol, bronchodilators, intravenous dexamethasone, and prone positioning (56). Chian et al. described a case with a prolonged 176-day hospital stay due to ARDS, where the patient’s condition improved with high-dose corticosteroid treatment, a tapering regimen, and extracorporeal life support during ICU care, followed by rehabilitation (57). Similarly, Babu et al. reported a case with a 28-day hospital stay and a favorable prognosis, managed with a 2 mg/kg methylprednisolone bolus on day 10 of intubation, followed by 2 mg/kg in divided doses (44). Conversely, Petilla et al. reported a case initially treated with intravenous ceftriaxone and methylprednisolone (250 mg/day) without adjunctive oxygen or antidote treatment, which resulted in prolonged ICU stay and recurrent bilateral pneumothorax, requiring bilateral excision of emphysematous bullae and pleurodesis (58). In our patient, high-dose methylprednisolone with a tapering regimen and non-invasive ventilatory support were employed. Due to a secondary Candida albicans infection, the patient received the fluconazole for antifungal treatment, cefoperazone sulbactam for antibacterial treatment, and continued with corticosteroid therapy. With active treatment, the patient’s prognosis remained relatively favorable.
Table 2. Published cases in chloride inhalational injury.
According to the latest Berlin criteria, the diagnosis of ARDS requires a comprehensive clinical evaluation, including the acute onset of respiratory distress within 1 week, bilateral patchy infiltrates on chest X-ray and CT scans, and a PaO2/FiO2 ≤ 300 mmHg or SpO2/FiO2 ≤ 315 (45). The SpO2/FiO2 ratio can serve as an alternative indicator of hypoxemia when arterial blood gas sampling is not feasible (59, 60). Studies have confirmed that the SpO2/FiO2 ratio closely correlates with PaO2/FiO2, aiding in earlier ARDS diagnosis and enabling timely implementation of lung-protective ventilation and fluid management strategies (61, 62). Since the patient could not tolerate arterial blood gas sampling, blood gas analysis was performed during two emergency treatment sessions. Dosage adjustments were made based on a comprehensive assessment of the patient’s clinical symptoms, SpO2/FiO2 ratio, CT imaging, and laboratory results (50, 59). After receiving low-dose steroids, the patient developed a Candida infection and was treated with fluconazole for antifungal therapy and cefoperazone sulbactam for antibacterial treatment. In patients receiving reduced glucocorticoid dosages, caution is necessary to prevent secondary infections, and the temporary use of antibiotics and antifungal agents may be required.
Glucocorticoids exert potent anti-inflammatory and immunosuppressive effects by binding to intracellular glucocorticoid receptors (GR), playing a pivotal role in modulating immune responses (63–66). These effects include a strong inhibition of neutrophil and macrophage chemotaxis, phagocytosis, and bactericidal activity, achieved through decreased expression of ROS, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) (67, 68). The glucocorticoid-GR complex directly prevents the activation of toll-like receptor-2 (TLR-2), NF-κB, and activator protein-1, thereby inhibiting the expression of downstream proinflammatory genes (69, 70). Additionally, glucocorticoids suppress the expression of co-stimulatory molecules, cytokines, and chemokines in T cells, leading to potent T cell inhibition (71). Furthermore, by reducing IL-12 and IFN-γ production in macrophages and dendritic cells, glucocorticoids diminish Th1 cell activation while promoting Th17 differentiation. This shift enhances the expression of the anti-inflammatory mediator TGF-β and triggers a transition from Th1 to Th2 immunity [(65), (71, 72)]. Since fungal infections primarily rely on cellular immunity for prevention, the suppression of this immunity by glucocorticoids heightens the risk of latent infections (35, 73). As glucocorticoid dosage is tapered, the immune system gradually recovers, but this process is slow and insufficient to effectively combat fungal antigens accumulated during the period of immunosuppression, leading to the reactivation of latent infections (73, 74).
This case provides valuable insights into the rationale for glucocorticoid dosage adjustments and underscores the potential benefit of early systemic corticosteroid use in patients with chlorine-induced lung injury. However, as a single case report, the findings cannot be generalized, and further investigation through large-scale, multicenter studies is necessary to determine the effectiveness of systemic corticosteroids for chlorine-induced lung injury.
4 Conclusion
The early application of a high-dose corticosteroid tapering regimen combined with non-invasive mechanical ventilation can effectively manage ARDS caused by chlorine gas inhalation. When arterial blood gas sampling is not feasible, the corticosteroid dosage adjustments are based on a comprehensive assessment of the clinical symptoms, SpO2/FiO2 ratio, CT imaging, and laboratory results. Additionally, vigilance for secondary infections during treatment is crucial, requiring prompt intervention for symptoms such as fever, purulent sputum, or new and progressing lung abnormalities on imaging. More importantly, large-scale randomized controlled studies are needed to explore the application of systemic corticosteroids in chlorine-induced lung injury.
Data availability statement
The original contributions presented in the study are included in the article/supplementary material, further inquiries can be directed to the corresponding author.
Ethics statement
The studies involving humans were approved by Weifang People’s Hospital Medical Research Ethics Committee. The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article. Written informed consent was obtained from the participant/patient(s) for the publication of this case report.
Author contributions
YW: Formal analysis, Writing – original draft, Data curation, Investigation. JM: Formal analysis, Writing – original draft, Data curation, Investigation. XT: Investigation, Formal analysis, Writing – original draft. CS: Writing – original draft, Data curation. LL: Writing – original draft, Visualization, Conceptualization. XS: Supervision, Project administration, Conceptualization, Writing – review & editing, Methodology.
Funding
The author(s) declare that no financial support was received for the research and/or publication of this article.
Acknowledgments
We thank Bullet Edits Limited for the linguistic editing and proofreading of the manuscript.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Keywords: trichloroisocyanuric acid, respiratory failure, case report, corticosteroid therapy, management
Citation: Wang Y, Meng J, Tian X, Sun C, Liu L and Sun X (2025) Chlorine gas poisoning by trichloroisocyanuric acid and respiratory failure: a case report of a 49-year-old patient. Front. Med. 12:1676596. doi: 10.3389/fmed.2025.1676596
Received: 30 July 2025; Revised: 09 November 2025; Accepted: 12 November 2025;
Published: 10 December 2025.
Edited by:
Narasaiah Kolliputi, University of South Florida, United StatesReviewed by:
Eren Ogut, Istanbul Medeniyet University, TürkiyeDianlong Ge, Chinese Academy of Sciences (CAS), China
Copyright © 2025 Wang, Meng, Tian, Sun, Liu and Sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Xiaojuan Sun, c3VueGlhb2p1YW4xMjNAMTYzLmNvbQ==