CELLULAR AND IMMUNOLOGICAL INJURY WITH PM-10 INHALATION

Citation
Mt. Kleinman et al., CELLULAR AND IMMUNOLOGICAL INJURY WITH PM-10 INHALATION, Inhalation toxicology, 7(5), 1995, pp. 589-602
Citations number
34
Categorie Soggetti
Toxicology
Journal title
ISSN journal
08958378
Volume
7
Issue
5
Year of publication
1995
Pages
589 - 602
Database
ISI
SICI code
0895-8378(1995)7:5<589:CAIIWP>2.0.ZU;2-Y
Abstract
irborne particles less than 10 mu m (PM-10) in mass median aerodynamic diameter (MMAD) are associated with adverse effects on human health i ncluding chronic lung diseases and mortality, but the mechanisms by wh ich these particles might cause or aggravate diseases are not specific ally known. PM-10 represents a complex mixture, both in terms of size and chemical composition, and it contains both aqueous-media soluble a nd insoluble particles. Furthermore, the ambient aerosol composition v aries markedly in different locations and al different times in the sa me location. To test the effects of PM-10 on pulmonary defenses in rel ation to specific cell targets, barrier-reared Sprague-Dawley rats wer e exposed to purified air (control), to two important constituents of the fine-particle (<1 mu m MMAD) fraction of PM-10-ammonium sulfate [( NH4)(2)SO42-] (20 or 70 mu g SO42- m(-3), 0.2 mu m MMAD) and ammonium nitrate [NH4NO3] (90 or 350 NO3- mu g m(-3), 0.6 mu m MMAD). Rats were also exposed to resuspended road dust (300 and 900 mu g m(-3), 4.0 mu m MMAD), an important contributor to the coarse (>2.5 mu m MMAD) frac tion of PM-10. Exposures were 4 h/day, 4 days/wk for 8 wk. Macrophage- dependent lung defense functions (antigen binding to Fc receptors and respiratory burst activity) were significantly depressed by NO3-, SO42 -, and the high-concentration road dust exposures, compared to purifie d air controls. Lung permeability, as determined from measurements of albumin concentrations in bronchoalveolar lavage fluid, was significan tly greater in rats exposed to high concentrations of road dust and NO 3-, but not to SO42-, when compared to air-exposed controls. Quantitat ive histopathologic analyses, which included measurements of alveolar nuclear density, alveolar chord length, alveolar septal thickness, and alveolar cross sectional area, showed moderate to substantial changes . In general, the severity of the responses was in the order of SO42- > NO3- > road dust. The findings are consistent with those of epidemio logical studies. This study also supports the hypothesis that the fine fraction of PM-10 is more toxic than the coarse fraction.