Research Program Area: Health & Exposure
Topic Areas: Health Effects of Air Pollution
Controlled laboratory studies were conducted utilizing two experimental animal models (Fischer-344 SPF male rats), one healthy and one impaired with elastase-induced emphysematous lung disease, to evaluate the nature and severity of responses to inhaled respirable aerosols (0.55 mg/m3 to 3.0 mg/m3) that were especially synthesized with selected realistic inorganic constituents to be typical of air pollution episodes in California, alone and in combination with ozone (0.4 ppm). Parallel comparative inhalation studies were performed with a respirable London-type aerosol (0.8 to 5.0 mg/m3) typical of the famous London smog episodes, alone and in combination with sulfur dioxide (1 to 21 ppm). Exposures were acute (3 days) or subchronic (30 days). The deleterious effects of the exposures were evaluated with selected lung biochemical measurements, measurements of lung particle clearance and permeability (using radiolabeled test aerosols), clinical signs of illness, and histological evaluation of lung inflammatory responses and structural alterations.
Neither aerosol was effective by itself in causing significant responses in healthy rats, but some significant aerosol effects were observed in association with ozone exposure or lung impairment. In the 3-day studies, there were some significant increases in total lung DNA and protein content in rats exposed to the synthetic California-type aerosol compared to rats not exposed to this aerosol. In addition, small airway inflammation was observed in animals exposed to ozone, and this effect was significantly exacerbated by the inhalation of either aerosol and in impaired animals. There was no observed aerosol concentration dependence. In the 3D-day studies, biochemical analyses showed increases in the lung content of hydroxyproline (indicative of collagen synthesis and potential lung fibrosis) in rats exposed to the California-type aerosol, and to London-type aerosol with 8°2 in impaired rats. Both aerosols tended to decrease the rate of tracheobronchial clearance of deposited test particles. There was no change in alveolar permeability. Exposure to ozone caused small airway lesions in the lungs and this was significantly exacerbated in impaired animals and by the inhalation of aerosols by impaired animals. Small airway fibrosis was caused by ozone, and this was significantly exacerbated by exposure to California-type aerosols. This study is apparently the first to demonstrate that aerosol / ozone interactions occur with atmospheres of composition and concentration similar to those found in the environment.
For questions regarding this research project, including available data and progress status, contact: Research Division staff at (916) 445-0753
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