Project at a Glance
Title: Nitric acid toxicity: potential for particle and ozone interactions.
Principal Investigator / Author(s): Keinman, Michael
Contractor: UC Irvine
Contract Number: 92-334
Research Program Area: Health & Exposure
Topic Areas: Acid Deposition, Health Effects of Air Pollution
The objective of this project was to determine whether or not airborne particles increased the potential for adverse health effects due to exposure to nitric acid (HNO3), under conditions relevant to exposure of people to urban air pollution in California. This project examined air pollutant atmospheres containing HNO3 in combination with ozone (O3) and fine carbon (C) particles. Fischer 344/N rats were exposed, nose-only, to 5 different atmospheres at 60 percent relative humidity: (1) purified air [PA]; (2) 0.15 ppm O3 [O3]; (3) 50 mg/m3 HNO3 + 0.15 ppm O3. [Ac + O3]; (4) 50 mg/m3 HNO3 + 50 mg/m3 C [Ac + C]; and (5) 50 mg/m3 HNO3 + 0.15 ppm O3 + 50 mg/m3 C [Ac + O3 + C]. Exposures were for 4 hours / day, three consecutive days / week, for up to four weeks, with animals evaluated at six different time points. The study, in addition to determining whether or not exposure to ambient concentrations of HNO3, O3 and C, alone and in mixtures would cause acute responses, examined whether or not responses would be attenuated (as reported for O3, alone), persist, or intensify during repeated exposures. Rats were killed after 1, 2, 3, 6, 9 and 12 exposure days. The 3, 6, 9 and 12 days of exposure occurred over 1, 2, 3 and 4 weeks, respectively. The regimen represented periodic, elevated concentration human exposures, and the components and concentrations selected for study were based on air monitoring data in a heavily polluted region in South Coast Air Basin of California.
Endpoints were evaluated that were related to human respiratory diseases such as bronchitis, emphysema and respiratory infections. The endpoints included quantification of morphological alterations of respiratory tract tissue compartments; determination of changes in respiratory tract cell populations and mucus secretion, and evaluation of impairment of lung defenses (epithelial permeability and macrophage functions).
The concentrations used were in the range of peak ambient exposures for each of the components. The exposure durations were short, relative to human lifetime ambient exposures. We did not expect, nor did we see, large perturbations in respiratory tissues or pulmonary defenses. The changes we observed were small and most did not achieve statistical significance. There were, however, patterns in the observed responses which suggest potential health consequences of ambient exposures to HNO3, O3 and C.
Alveolar chord length and alveolar wall thickness were increased in the lungs of rats exposed to the HNO3 + C atmosphere. Ozone alone and in combination with HNO3-containing atmospheres tended to decrease septal wall thickness. The volume of trapped gas in the collapsed lungs from the Ac + O3 rats was increased.
For questions regarding this research project, including available data and progress status, contact: Heather Choi at (916) 322-3893
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