Inflammation, Edema, and Peripheral Blood Changes in Lung-Compromised Rats After Instillation With Combustion-Derived and Manufactured Nanoparticles

Abstract

Increased exposure to pollution has been implicated in cardiovascular malfunction, and although studies show a relationship between PM10 and mortality, the exact biological causes are unclear. This study investigated how compromised lungs respond to instillation of nanoparticles, and the links between exposure to nanoparticles and the subsequent effects on the blood. Instillation of diesel exhaust particles and Cabosil caused significant permeability and inflammatory changes in both bleomycin-treated and control lungs, as shown by increased lung surface protein and lung:body weight ratio. This was true in edematous and maximally repairing lungs, but without significant hematological alterations. Plasma viscosity, a renowned marker for cardiovascular disease, correlated strongly statistically with free cell numbers, type I cell marker rT140, and lung acellular protein. These correlations are a new and novel insight into the mechanisms linking air pollution to cardiovascular mortality.

Potential Health Impact of Nanoparticles

“…However, when 14-nm carbon black NPs were coadministered with a bacterial endotoxin, these particles intensively aggravated lipopolysaccharide (LPS) -induced pulmonary inflammation (17,27). Intratracheal instillation of Cabosil, a commercially available NP of amorphous SiO 2 , caused significantly increased inflammatory changes in rat lungs compromised by bleomycin (17). These data suggest that engineered NPs could potentiate the effects of other inhaled stimuli (27).…”

“…In addition to the proinflammatory effects, NPs may also exacerbate existing lung diseases (17,27). Inoue et al (27) have demonstrated that intratracheal administration of 14 nm and 56 nm carbon black NPs induced slight lung inflammation and significant pulmonary edema compared with the phosphate buffered saline (PBS)-treated mice.…”

“…Inoue et al (27) have demonstrated that intratracheal administration of 14 nm and 56 nm carbon black NPs induced slight lung inflammation and significant pulmonary edema compared with the phosphate buffered saline (PBS)-treated mice. However, when 14-nm carbon black NPs were coadministered with a bacterial endotoxin, these particles intensively aggravated lipopolysaccharide (LPS) -induced pulmonary inflammation (17,27). Intratracheal instillation of Cabosil, a commercially available NP of amorphous SiO 2 , caused significantly increased inflammatory changes in rat lungs compromised by bleomycin (17).…”

Nanoparticle effects on rat alveolar epithelial cell monolayer barrier properties

“…Instillation of ultrafine carbon black particles (~14 nm) intratracheally into rat lungs led to a marked increase in lactate dehydrogenase (LDH) levels in bronchoalveolar lavage (BAL) fluid (Li et al 1999). Intratracheal instillation of diesel exhaust particles (~30 nm) and an amorphous silicon dioxide (commercially available as Carbosil, ~7 nm) into lungs of male Sprague-Dawley rats increased air-blood barrier permeability, inflammation and edema formation, leading to a strong correlation of plasma viscosity with an index of type I cell injury (reflected as rat type I cell marker found in lung lavage fluid) (Evans et al 2006). By contrast, healthy mice did not appear to respond to ultrafine carbon and platinum particles (15 and 25 nm, respectively) when inhaled for up to 6 hours at 110 μg/mL (Oberdorster 2001).…”

Role of Chemical Composition in Determining the Cardiovascular Effects of Particles

“…Intratracheal instillation of ultrafi ne DEPs into rat lungs increased both pulmonary infl ammation and air -blood barrier permeability (Miyabara et al, 1998 ;Tsurudome et al, 1999 ;Evans et al, 2006 ). Diesel exhaust UFPs also induced a neutrophilic infl ux in the lungs of mice and had DNA -damaging effects (Saber et al, 2005 ).…”