Epidemiological studies demonstrate associations between increasing levels of ambient particles and morbidity in the elderly with @entity66 . Such findings have been challenged partly because particles may not act alone to cause these effects. We hypothesized that carbonaceous ambient ultrafine particles and @entity1787 can act together to induce greater oxidative stress and @entity32 in the lung than when administered alone and that these effects would be amplified in the compromised, aging lung. Two models of a compromised lung were used: endotoxin priming and old-age @entity2415 ( @entity70487 @entity19 ). Young (10 wk) and old (22 mo) male F344 @entity35 and male @entity70487 @entity19 (14-17 mo) were exposed to ultrafine @entity505 particles (count median diameter 25 nm, 110 micrograms/m3) and to @entity1787 (1 ppm) alone and in combination for 6 h. Inhalation of low-dose endotoxin (70 and 7.5 units estimated alveolar deposited dose in @entity35 and @entity19 , respectively) was used to model @entity1729 . Cellular and biochemical lavage parameters and oxidant release from lung lavage cells were assessed 24 h after exposure. Inflammatory cell influx into the alveolar space was observed for both species and age groups: The combination of inhaled ultrafine @entity505 and @entity1787 after endotoxin priming resulted in the greatest increase in lavage-fluid neutrophils. In general, the unstimulated and stimulated release of reactive @entity26 species (ROS) from lavage inflammatory cells correlated well with the neutrophil response. There were significant effects of @entity505 particles as well as a consistent interaction between @entity505 and @entity1787 as determined by analysis of variance (ANOVA). However, this interaction was in the opposite direction in young @entity35 versus old @entity35 and old @entity70487 @entity19 : @entity505 and @entity1787 interacted such that ROS activity was depressed in young @entity35 , whereas it was enhanced in old @entity35 and old @entity70487 @entity19 , indicating age-dependent functional differences in elicited pulmonary inflammatory cells. These results demonstrate that ultrafine carbonaceous particles inhaled for short periods of time can induce significant @entity55 and oxidative stress that are modified by age, copollutants, and a compromised respiratory tract.

Pulmonary inflammatory response to inhaled ultrafine particles is modified by age, XXXX exposure, and bacterial toxin.

@entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation'] @entity66 :: ('MESH:D004194', 'Disease') :: ['cardiopulmonary disease'] @entity55 :: ('MESH:D011014', 'Disease') :: ['pulmonary inflammation'] @entity19 :: ('10090', 'Species') :: ['mice'] @entity26 :: ('MESH:D010100', 'Chemical') :: ['oxygen'] @entity2415 :: ('MESH:D004646', 'Disease') :: ['emphysema'] @entity505 :: ('MESH:D002244', 'Chemical') :: ['Carbon', 'carbon'] @entity70487 :: ('244152(Tax:10090)', 'Gene') :: ['TSK'] @entity1729 :: ('MESH:D012141', 'Disease') :: ['respiratory-tract infection'] @entity35 :: ('10116', 'Species') :: ['rats'] @entity1787 :: ('MESH:D010126', 'Chemical') :: ['ozone']
@entity1787 :: (MESH:D010126,Chemical) :: ['ozone']
