Pulmonary alveolar proteinosis induced by hydrofluoric acid exposure during fire extinguisher testing
© Kim et al.; licensee BioMed Central. 2015
Received: 13 April 2014
Accepted: 3 February 2015
Published: 25 February 2015
Automatic fire suppression systems use hydrofluorocarbons (HF) to extinguish fires chemically. At high temperatures, HF can release hydrofluoric acid (HFA), a toxic, potentially lethal gas.
A 52-year-old male visited our Pulmonary Division with dyspnea of 8-months duration. He had been working at a facility that manufactured fire extinguishers. Bronchoscopy was performed and a transbronchial lung biopsy was taken from the right lower lobe. After the patient was diagnosed with pulmonary alveolar proteinosis (PAP), whole-lung lavage was performed. In this case, fire extinguisher gas induced pulmonary alveolar proteinosis. This material should be used with care and investigated further.
HFA is corrosive and penetrates organic materials, including body tissues. Depending on the mode of exposure, skin ulceration, pulmonary injury, or even systemic shock can result. This report describes PAP that developed after chronic, repeated exposure to fire extinguisher spray. Hydrofluoric acid can induce pulmonary disorders such as PAP.
Hydrofluorocarbons (HF) are used as extinguishing agents . The most frequently used HF is 1,1,1,2,3,3,3-hepatofluoropropane, which is generally non-toxic and stable . However, it can decompose over time, when exposed to high temperature or under certain environmental conditions . Hydrofluoric acid (HFA), an aqueous form of HF, is highly water-soluble and a weak acid . Exposure to HFA might not cause symptoms initially. Over time, however, fluoride ions bind to intracellular calcium or magnesium, causing liquefactive tissue necrosis or systemic electrolyte disturbance [3,4]. Tracheobronchitis, pulmonary edema, pneumonia, bronchospasm, and acute respiratory failure syndrome have been reported after HFA exposure [1,4-6]. However, there are no reports of pulmonary alveolar proteinosis (PAP) secondary to HF extinguishing agents. We report the diagnosis and successful treatment of PAP that developed after fire extinguisher testing. PAP has been reported in workers exposed to aluminum dust, paint, sawdust, silica, synthetic plastic fumes, and indium-tin oxide. However, there are no reports of PAP after repeated fire extinguisher use.
Pulmonary alveolar proteinosis is a rare pulmonary disorder in which surfactant proteins and lipids accumulate within the intra-alveolar spaces [7,8]. PAP is classified into primary and secondary forms: secondary PAP is caused by hematological agents, infection, or the inhalation of dust or fumes [7-9]. PAP has been reported in workers exposed to aluminum dust, paint, sawdust, silica, synthetic plastic fumes, and indium-tin oxide . However, there are no reports on PAP after fire extinguisher use, as occurred in our patient. The hydrocarbon used in fire extinguishers is 1,1,1,2,3,3,3-hepatofluoropropane, which is non-toxic under stable conditions, but can decompose into HF at high temperatures, particularly in combination with extended exposure to humidity, contaminants, certain metals, metal surfaces, or contact with certain liquids or vapors . HFA is corrosive and penetrates organic materials, including body tissues. Depending on the mode of exposure, skin ulceration, pulmonary injury, or even systemic shock can result [2-5]. Wu et al. investigated HFA exposures occurring from 1991 to 2010: dermal exposure was the most frequent (83.6%), but inhalation only (7.1%), combined dermal and inhalation (1.9%), and combined ocular and inhalation (0.3%) exposure were also reported . Kono et al. and Kawaura et al. also reported pulmonary injury accompanied by acute respiratory distress syndrome after HFA inhalation [5-7]. Zierold et al. reported that three US military personnel died of acute respiratory failure after using a fire extinguisher in their vehicle following a rocket-propelled grenade attack. They presumably inhaled the HFA generated from HF by the high temperature within the vehicle .
In our case, a high-temperature garbage incinerator was located in the same room where the patient performed the fire extinguisher spray test. Most likely, the HF was converted to HFA, which was then inhaled. Notably, we did not measure the concentration of autoantibodies to granulocyte–macrophage colony-stimulating factor (GM-CSF) in this patient. However, Cummings et al. asserted that inhalational exposure cannot be excluded when primary PAP is suspected [10,11]. In addition, Inoue et al. reported a dust inhalation history in 23% of primary PAP cases [11,12]. In our case, we surmise that the GM-CSF autoantibody status is less important. The limitation of this paper is a single case. Therefore we needed further studies to determine if there is an association with HFA.
In conclusion, this report describing PAP that developed after chronic, repeated fire extinguisher spray exposure reveals that hydrofluoric acid can induce pulmonary disorders such as PAP in addition to pneumonitis and acute respiratory failure. These findings highlight the need for caution and greater attention to this risk.
Written informed consent was obtained from the patient for publication of this case report. A copy of the written consent is available for review by the Editor–in–chief of this journal.
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