Effects of Diesel Exhaust Enriched Concentrated PM2.5 in Ozone Preexposed or Monocrotaline-Treated Rats

Abstract

Epidemiological studies have observed statistical associations between short-term exposure to increased ambient particulate air pollution and increased hospital admissions, medication use, pulmonary morbidity, and mortality. To examine the effects of particle air pollution in animals, rats with a preexisting pulmonary inflammation (induced by 1600 microg/m(3) ozone) or hypertension (induced by monocrotaline, MCT) were nose-only exposed to concentrated freshly generated diesel exhaust particles (DEP) mixed with ambient air (CDP). It was hypothesized that a single 6-h exposure to PM exacerbates respiratory inflammatory processes, which affects health parameters in the blood. Histopathology of lung and nose, bronchiolar lavage (BAL), and blood analyses were performed at 1, 2, and 4 days after of the CDP exposure. Morphometry of BrdU-labeled cells in lung and nose was performed at 4 days postexposure. One day after ozone exposure, a mild inflammatory reaction in the centriacinar area was present, consisting of an increase in cellularity of septa and in the number of alveolar macrophages, decreasing in time. Additional CDP exposure did not influence this pattern, except for alveolar macrophages that were loaded with CDP. The only effect seen in the nose after ozone exposure was a slight hypertrophy of the septal mucous cells. Additional exposure to CDP did not change this appearance. MCT-treated rats showed hypertrophy of the media of the pulmonary muscular arteries that was not effected by CDP. BrdU labeling of predominantly Clara cells in the terminal bronchioles was significantly increased after ozone exposure as well as after MCT treatment, whereas this labeling index was markedly enhanced after an additional exposure to CDP. However, no increases in Clara cell protein (CC16) levels were measured of Clara cell protein (CC16) in either BAL or blood. BrdU labeling in the nasal epithelium was not influenced by exposure to ozone or ozone + CDP. CDP exposures did not induce significant toxic effects in the lungs. CDP exposures clearly induced an oxidative stress that was indicated by increasing glutathione levels in BAL with time. In addition, blood fibrinogen levels were enhanced in pulmonary hypertensive rats exposed to CDP. The present study demonstrates that very high CDP concentrations are needed to result in pulmonary changes in animal models with a preexisting pulmonary inflammation or hypertension that continue for days after a single exposure. In addition, CDP has the potential to induce changes in blood. It has not yet been determined how the effects seen with CDP would compare to similar levels of ambient particles.

Spatial and seasonal distribution of aerosol chemical components in New York City: (2) Road dust and other tracers of traffic-generated air pollution

“…To date, Cassee et al (2002) and Gerlofs-Nijland et al (2007) provide the most comprehensive laboratory-based comparison of the effects of PM 2.5 on rodents in ambient air and in diesel engine exhaust particles (DEP). In both studies, they were able to produce acute pulmonary changes and increases in blood fibrinogen with both concentrated ambient particles (CAPs) and concentrated DEP, but it took far higher concentrations of DEP than CAPs to do so.…”

From Ambient Ultrafine Particles to Nanotechnology and Nanotoxicology

“…In a number of different studies using concentrated ambient particles (CAPs) (Ghio and Huang, 2004 ), PM (Li et al, 1997 ;Cassee et al, 2002 ), and model NPs (Warheit, 2004 ;Warheit et al, 2007a ;Lu et al, 2009 ), there is evidence that NPs can cause infl ammation in the lungs following pulmonary deposition. Pulmonary infl ammation could adversely affect the cardiovascular system and increased exposure to ambient PM results in systemic infl ammation as shown by elevated C -reactive protein, blood leukocyte, platelet fi brinogen, and increased plasma viscosity across a number of different studies (Donaldson et al, 2005a ).…”

Helseeffekter av byluftpartikler

“…Det er uklart hvordan svevestøv kan føre til skade på hjerte-karsystemet, men følgende mekanismer er aktuelle: 1) Svevestøvet kan øke koaguleringsprosessene i blodet og dermed føre til hjerteinfarkt (21,30,31). 2) Svevestøvet kan påvirke det autonome nervesystemet og dermed disponere for hjertearytmier (21,32).…”

“…Det er også etablert sensitive dyremodeller. I dyremodeller med kronisk bronkitt, hjertekarforstyrrelser eller lungeskader er det observert økt følsomhet for svevestøv (21,29,30,41).…”