A fatal case following exposure to zinc chloride and hexachloroethane from a smoke bomb in a fire simulation at a school

Abstract

Introduction. The common mixture for smoke bombs contains zinc oxide and a chlorine donor, which allows for the formation of fine particles of zinc chloride. We report a fatal case of exposure to a smoke bomb used for a fire training exercise at a school. Case report. A 21-year-old student inhaled zinc oxide/hexachloroethane from a smoke bomb during a fire simulation at a school. Fever and tachypnea began six hours after exposure. Radiological evaluation showed a mixed interstitial-alveolar bilateral infiltrates. Despite supportive care, the patient died of multi-organ failure nine days after inhalation. Discussion. ZnCl inhalation is characterized by a lag period between exposure and evidence of respiratory toxicity, ranging from ten to 32 days, depending on the inhaled dose of ZnCl. Subjects inhaling even a small amount of aerosols from a smoke bomb should be carefully managed in a hospital setting where their respiratory function can be closely monitored. Conclusion. This case highlights the risk of serious injury and even death from smoke bombs containing zinc chloride aerosol in schools and suggests that these smoke bombs should not be used for fire simulation or activities where human exposure is suspected, particularly in schools.

Keywords :

• Zinc oxide
• Hexachloroethane
• Smoke bombs
• Irritant smoke

Introduction

White smoke has a variety of uses as an obscurant and is widely used for military as well as civilian purposes including fire-fighting training (1–3). Several methods of smoke production have been developed. Chemical smoke includes small particles (solid or liquid), which become hydrated in contact with air; certain environmental conditions play a major role, especially relative humidity. Usually, the common mixture for white smoke contains zinc oxide and a chlorine donor, such as hexachloroethane (HCE), as major components. This mixture allows for the formation of fine particles of zinc chloride (ZnCl). In general, zinc salts are not harmful to the lungs but zinc chloride smoke is an important exception (4). Additional substances may be included (aluminium, calcium silicide) for precise combustion together with related major components (5). Phosgene, tetrachloroethylene, carbon tetrachloride, carbon dioxide and carbon monoxide may also be produced, although the concentration in the smoke cloud is likely to be low. Furthermore, zinc chloride aerosols are extremely hygroscopic and form solution droplets that will increase in size in the high humidity of the respiratory tract. Due to the corrosivity of the combustion products this type of smoke bomb is potentially harmful upon inhalation by unprotected people and if encountered in confined spaces can be lethal. Case reports of non-fatal lung damage produced by this type of smoke bombs have been reported by several authors (5) with fatal cases being rarely reported (6,7).

The aim of this report is to describe a fatal case following exposure to zinc chloride and hexachloroethane (ZnCl-HCE) from a smoke bomb during a fire simulation at a school.

Case report

A smoke bomb was detonated during a training and simulation exercise at a school. The designated place for the exercise was a small bathroom with toilet cubicles (sharing the same ceiling) and wash basin area. The bathroom had a small elevated window looking onto the school yard. The smoke bomb exploded in the cubicle closest to the window. The smoke came out rapidly through the window into the open air. Nevertheless, the official in charge of the exercise heard someone coughing in the bathroom; he immediately gained access to the restroom and found a student inside the second cubicle. The 21-year-old student with Down syndrome was quickly taken to the Casualty Department and was diagnosed with smoke inhalation. The symptoms initially reported were marked agitation, nausea, strong irritation of the eyes, tachypnea, cyanosis, wheezing, and normal heart sounds. The level of conscious status was normal. No changes in hemodynamic status, chest roentgenogram, and pulmonary function were found. The patient was administered the following drugs at the Casualty Department: antiemetics, gastric protectives, steroids, bronchodilators, oxygen at 24% and sedatives. Six hours later his temperature was 37.7°C, heart rate was 120 beats/minute, respiratory rate was 36 breaths/minute, and the sputum was blood-tinged. A chest radiograph revealed a mixed interstitial-alveolar infiltrate in bases of both lung fields suggesting adult respiratory distress syndrome (ARDS) and the patient was admitted to the Intensive Care Unit. One day later the tachypnea and temperature (38.5°C) increased; the sputum had turned purulent and the patient presented low oxygen saturation episodes (sO₂ = 82.3% to 80.3%), with pO₂ in blood ranging 73.8 to 47.3 mm Hg, and epigastric pain so that a higher concentration of oxygen (40%) and antibiotic therapy with levofloxacine were started. The clinical course during the next three days was characterized by long periods of low sO₂ and an irritative cough. The heart and respiratory rates increased further. Treatment included physiotherapy to help clear the abundant secretions and antipyretic drugs to control fever peaks. Oxygen with mask to 50% led to desaturation. Five days later muscular respiratory fatigue appeared with temperature above 39°C, severe hypoxemia with hypercapnia, hypotension, oliguria and the patient developed an important general impairment with typical interstitial-alveolar bilateral condensation in chest X-ray requiring orotracheal intubation with mechanical breathing support as the oxygenation index that indicates the arterial oxygen pressure over the fractional concentration of oxygen in the inspired gas (PaO₂/FIO₂) decreased to a value lower than 150. During the next three days vasoactive amines were needed for the management of the haemodynamic instability. Also high concentrations of oxygen and control of fever (ranged 38.5 to 39°C) with antipyretic drugs and physical support were administered. Nine days after smoke exposure the patient developed shock, hypotension, right pneumothorax with bronchopulmonary shunt, and severe respiratory and renal failure with oliguria and increased levels of blood urea nitrogen, creatinine and potassium leading to death from multi-organ failure.

Autopsy findings

Post-mortem examination confirmed severe damage to the mucous membranes of tracheobronchial and upper respiratory tracts. Lungs, liver, kidneys and spleen showed congestion and edema. Additionally, an excess of fluid in pleural and peritoneal spaces was observed. Severe pulmonary congestion, pneumonitis and edema were the main respiratory findings. Large thrombus occupied the right heart cavities expanding into the right atrium.

Microscopic findings

Microscopic findings of lungs included blood vessel congestion, haemorrhagic areas, intraalveolar and interstitial oedema and intraalveolar fibrosis. Alveolar walls were covered with hyaline membranes and inflammatory signs revealing severe chemical alveolitis (inflammatory cells and aggregates of macrophages). Diffuse alveolar damage and obliteration and widespread occlusion of microvessels by endothelial cell proliferation and clots were detected. The main heart findings were intracavitary thrombosis areas and thrombi in epicardic blood vessels.

Discussion

The main finding of the present report was that exposure to a smoke bomb based on ZnCl-HCE in a fire simulation led to the death of a 21-year-old man due to ARDS followed by multi-organ failure. In 1945 Evans described for the first time the deaths of 10 people out of 70 in the Corradino tunnel (Malta) who were exposed to ZnCl aerosol during World War II (1). Other investigators have also reported cases of deaths caused by accidental inhalation of ZnCl (6,8–11).

One of the typical features of ZnCl inhalation is the lag period between exposure and severe respiratory failure. In the present study the patient died nine days after exposure. This is in agreement with previous reports in which patients died 10 days after inhalation (10). However, modest exposure to ZnCl smoke leads to a remarkable delay in the appearance of quantifiable damage to lung parenchyma and induction of ARDS (12); thus other reports have shown a longer lag time of 25–32 days (9). The lag period appears to be directly related to the inhaled dose of ZnCl. Within this context, subjects inhaling even a small amount of aerosols from a smoke bomb should be carefully managed in a hospital setting where their respiratory function can be closely monitored.

The pattern of clinical symptoms and pathological findings in the present study is similar to with those described previously in subjects who inhaled acute high doses of ZnCl (10,13–16). Likewise, in experimental animals histological changes derived from ZnCl exposure are also consistent with those described in humans (17).

Both the ratio of the two main components of the smoke bomb and exposure in a confined space may have played an important role in the clinical evolution of our patient. Moreover, the fire simulation occurred in a Spanish coastal region with relatively high humidity, probably leading to a more effective hydration of ZnCl aerosol particles.

In the present study, the mental capability of the subject could have negatively influenced the decision to abandon the room quickly, which in turn would have had an impact on inhaling a higher dose of the toxic compounds.

In conclusion, there is a strong potential risk of ZnCl-HCE smoke bombs, particularly when used in confined spaces, causing serious injury or death and they should not be used for fire simulation or activities where human exposure is suspected. Particularly, we emphasise that the use of this toxic for fire simulation at schools should be strictly forbidden.

Acknowledgments

The authors would like to acknowledge the permission of the family for publishing this article, and wish to thank Isabel J. Macdonald for her assistance in the language reviewing.