Cellular and Immunologic Injury with PM-10 Inhalation
Open Access
- 1 January 1995
- journal article
- research article
- Published by Taylor & Francis in Inhalation Toxicology
- Vol. 7 (5), 589-602
- https://doi.org/10.3109/08958379509014467
Abstract
Airborne particles Jess than 10 μsm (PM-10) in mass median aerodynamic diameter (MMAD) are associated with adverse effects on human health including chronic lung diseases and mortality, but the mechanisms by which these particles might cause or aggravate diseases are not specifically known. PM-10 represents a complex mixture, both in terms of size and chemical composition, and it contains both aqueous-media soluble and insoluble particles. Furthermore, the ambient aerosol composition varies markedly in different locations and at different times in the same location. To test the effects of PM-10 on pulmonary defenses in relation to specific cell targets, barrier-reared Sprague-Dawley rats were exposed to purified air (control), to two important constituents of the fine-particle < 1 μm MMAD) fraction of PM-10–ammonium sulfate [(NH4)2SO42-] (20 or 70 μg SO42- m−3, 0.2 μm MMAD) and ammonium nitrate [NH4NO31 (90 or 350 NO3 μg m −3, 0.6 μm MMAD). Rats were also exposed to resuspended road dust (300 and 900 μg m−3, 4.0 μm MMAD), an important contributor to the coarse (> 2.5 μm MMAD) fraction of PM-10. Exposures were 4 h/day, 4 dayslwk for 8 wk. Macrophage-dependent lung defense functions (antigen binding to Fc receptors and respiratory burst activity) were significantly depressed by NOf, SO42-, and the high-concentration road dust exposures, compared to purified air controls. Lung permeability, as determined from measurements of albumin concentrations in bronchoalveolar lavage fluid, was significantly greater in rats exposed to high concentrations of road dust and NO3−, but not to SO42-, when compared to air-exposed controls. Quantitative 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 epidemiological studies. This study also supports the hypothesis that the fine fraction of PM-10 is more toxic than the coarse fraction.Keywords
This publication has 29 references indexed in Scilit:
- Inhalation of resuspended road dust, but not ammonium nitrate, decreases the expression of the pulmonary macrophage Fc receptorToxicology Letters, 1994
- Effects of Inhaled Fine Particles and Ozone on Pulmonary Macrophages and EpitheliaInhalation Toxicology, 1993
- A neighborhood-scale study of PM10 source contributions in Rubidoux, CaliforniaAtmospheric Environment. Part A. General Topics, 1992
- Modes in the size distributions of atmospheric inorganic aerosolAtmospheric Environment. Part A. General Topics, 1990
- Respiratory health effects associated with ambient sulfates and ozone in two rural Canadian communitiesEnvironmental Research, 1989
- Air Pollution Impact on Phagocytic Capacity of Peripheral Blood Macrophages and Antioxidant Activity of Plasma among School ChildrenArchives of environmental health, 1988
- Effects of pollutant atmospheres on surface receptors of pulmonary macrophagesJournal of Toxicology and Environmental Health, 1988
- Airway Permeability in Rats Exposed to Ozone or Treated with Cytoskeleton-Destabilizing DrugsExperimental Lung Research, 1988
- Relative permeability of nasal, tracheal, and bronchoalveolar mucosa to macromolecules in rats exposed to ozoneJournal of Toxicology and Environmental Health, 1986
- Analysis of health effects resulting from population exposures to acid precipitation precursors.Environmental Health Perspectives, 1985