Kb. Gross et al., MECHANISM OF INDUCTION OF ASTHMATIC ATTACKS INITIATED BY THE INHALATION OF PARTICLES GENERATED BY AIRBAG SYSTEM DEPLOYMENT, The journal of trauma, injury, infection, and critical care, 38(4), 1995, pp. 521-527
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: Asthmatic
s who were previously tested for their response to airbag effluents we
re exposed for twenty minutes to either 1) airbag effluents from airba
g systems in which the airbag was insulated from the hot deployment mo
dule; 2) non-sulfur containing airbag effluents; 3) sodium chloride ae
rosol; or 4) sodium carbonate-bicarbonate aerosol (pH 10). Pre-exposur
e, post-exposure, and 2 hour post exposure pulmonary spirometry and me
chanics were measured. Subject's filled out symptoms questionnaires be
fore exposure, 2, 4, 8, 12, and 19 minutes into the exposure, immediat
ely post-exposure, and 2 hours post-exposure. Measurements and Main Re
sults: Prevention of the pyrolysis of the passenger-side bag as it res
ted on the hot module after deployment did not diminish the asthmatic
response. Removal of sulfur-containing oxidants from the airbag pyrote
chnic chemistry, which may have led to sulfite production, similarly d
id not alleviate the asthmatic response to the airbag effluents. Lastl
y, when asthmatics were exposed to sodium chloride and sodium carbonat
e-bicarbonate aerosols at approximately the same concentration (approx
imate to 220 mg/m(3)) as the airbag aerosol concentration that occurre
d in the in-car tests, they had responses similar to those produced by
the airbag exposures. Conclusions: We conclude that the amount of sol
uble particulate contained in the aerosol discharged into the passenge
r compartment by dual frontal airbag deployment is largely the cause o
f the observed evoked asthmatic attacks. The alkaline pH of the airbag
and carbonate aerosols may have added an additional degree of provoca
tion.