OBJECTIVE: We have previously demonstrated that inhalation of the dust produced by dual frontal airbag deployment can result in significant bronchospasm in approximately 40% of mild to moderate asthmatics. This study was performed to determine the cause of the asthmatic response. DESIGN: Controlled laboratory study. MATERIALS AND METHODS: Asthmatics who were previously tested for their response to airbag effluents were exposed for twenty minutes to either 1) airbag effluents from airbag systems in which the airbag was insulated from the hot deployment module; 2) non-sulfur containing airbag effluents; 3) sodium chloride aerosol; or 4) sodium carbonate-bicarbonate aerosol (pH 10). Pre-exposure, post-exposure, and 2 hour post exposure pulmonary spirometry and mechanics were measured. Subject's filled out symptoms questionnaires before exposure, 2, 4, 8, 12, and 19 minutes into the exposure, immediately post-exposure, and 2 hours post-exposure. MEASUREMENTS AND MAIN RESULTS: Prevention of the pyrolysis of the passenger-side bag as it rested on the hot module after deployment did not diminish the asthmatic response. Removal of sulfur-containing oxidants from the airbag pyrotechnic chemistry, which may have led to sulfite production, similarly did not alleviate the asthmatic response to the airbag effluents. Lastly, when asthmatics were exposed to sodium chloride and sodium carbonate-bicarbonate aerosols at approximately the same concentration (approximately 220 mg/m3) as the airbag aerosol concentration that occurred in the in-car tests, they had responses similar to those produced by the airbag exposures. CONCLUSIONS: We conclude that the amount of soluble particulate contained in the aerosol discharged into the passenger compartment by dual frontal airbag deployment is largely the cause of the observed evoked asthmatic attacks. The alkaline pH of the airbag and carbonate aerosols may have added an additional degree of provocation.
OBJECTIVE: We have previously demonstrated that inhalation of the dust produced by dual frontal airbag deployment can result in significant bronchospasm in approximately 40% of mild to moderate asthmatics. This study was performed to determine the cause of the asthmatic response. DESIGN: Controlled laboratory study. MATERIALS AND METHODS: Asthmatics who were previously tested for their response to airbag effluents were exposed for twenty minutes to either 1) airbag effluents from airbag systems in which the airbag was insulated from the hot deployment module; 2) non-sulfur containing airbag effluents; 3) sodium chloride aerosol; or 4) sodium carbonate-bicarbonate aerosol (pH 10). Pre-exposure, post-exposure, and 2 hour post exposure pulmonary spirometry and mechanics were measured. Subject's filled out symptoms questionnaires before exposure, 2, 4, 8, 12, and 19 minutes into the exposure, immediately post-exposure, and 2 hours post-exposure. MEASUREMENTS AND MAIN RESULTS: Prevention of the pyrolysis of the passenger-side bag as it rested on the hot module after deployment did not diminish the asthmatic response. Removal of sulfur-containing oxidants from the airbag pyrotechnic chemistry, which may have led to sulfite production, similarly did not alleviate the asthmatic response to the airbag effluents. Lastly, when asthmatics were exposed to sodium chloride and sodium carbonate-bicarbonate aerosols at approximately the same concentration (approximately 220 mg/m3) as the airbag aerosol concentration that occurred in the in-car tests, they had responses similar to those produced by the airbag exposures. CONCLUSIONS: We conclude that the amount of soluble particulate contained in the aerosol discharged into the passenger compartment by dual frontal airbag deployment is largely the cause of the observed evoked asthmatic attacks. The alkaline pH of the airbag and carbonate aerosols may have added an additional degree of provocation.