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.