The United States has one of the world's largest per capita fire death rate
s. House fires alone kill >9,000 Americans annually, and smoke inhalation i
s the leading cause of mortality from structural fires. Animal models are n
eeded to develop therapies to combat this problem. We have developed a muri
ne model of smoke inhalation through the design, construction, and use of a
controlled-environment smoke chamber. There is a direct relationship betwe
en the quantity of wood combusted and mortality in mice. As with human vict
ims, the primary cause of death from smoke inhalation is an elevated blood
carboxyhemoglobin level. Lethal (78%) and sublethal (50%) carboxyhemoglobin
levels were obtained in mice subjected to varying amounts of smoke. Mice e
xposed to wood smoke demonstrated more dramatic pathology than mice exposed
to cotton or polyurethane smoke. A CD-1 model of wood smoke exposure was d
eveloped, demonstrating type II cell hypertrophy, cytoplasmic blebbing, cyt
oplasmic vacuolization, sloughing, hemorrhage, edema, macrophage infiltrati
on, and lymphocyte infiltration. The bronchoalveolar lavage fluid of smoke-
exposed mice demonstrated a significant increase in total cell counts compa
red with those in control mice. These findings are comparable to the lung t
issue response observed in human victims of smoke inhalation.