Acute Respiratory Toxicitiy of Advanced Composite Material (ACM) Combustion Atmospheres: B2-ACM
NAVAL HEALTH RESEARCH CENTER WRIGHT-PATTERSON AFB OH TOXICOLOGY DETACHMENT
Pagination or Media Count:
Exposure for 2 hr to smoke generated from pyrolysis of 100 g of B2-ACM was lethal to experimental animals. Surviving animals showed elevated carboxyhemogobin levels, severe respiratory acidosis, and diminished oxygen transport in the blood, the combination of which was deemed the cause of death. These animals also showed signs of pulmonary inflammatory response. Two days post exposure, animals exhibited pulmonary pathophysiology indicative of restrictive lung disease. The pattern of pulmonary dysfunction at 14 days post exposure was similar, with some measures of lung function returning to normal while others remained significantly different from normal values. Although no deaths occurred, similar patterns of pulmonary dysfunction were evident in animals exposed for 1 hr to smoke from pyrolysis of 55 or 100 g of 132-ACM. These animals also had elevated carboxyhemogobin levels, decreased blood pH, and diminished oxygen capacity immediately post exposure however these symptoms were not as severe as those in animals exposed for 2 hr to smoke generated from pyrolysis of 100 g of B2-ACM. Quantitative analysis of a few selected smoke gases CO, CO2, NOx, SO2 and aerosol particulate consistently accounted for over 80 of the amount of B2-ACM that actually burned. Calculation of the nominal concentration of the smoke correlated well with the chemical analysis, the bulk amount of B2-ACM used to generate the smoke, and the pyrolysis rate. Consequently these estimates of smoke concentration could be used for dose-response determinations which, in turn, provide a suitable basis for risk assessment.
- Anatomy and Physiology