Influence of Community Air Pollution on the Lungs of Mice. Part Ii: Image Analysis Quantitation of Lung Elastin

Abstract

Two groups of 330 male Swiss-Webster mice were equally divided, with each exposed continuously to the outdoor air in central Los Angeles (LA) and Santa Barbara (SB). Nearby monitoring stations provided data on nitrogen dioxide (Nod, ozone (O₃, sulfur dioxide, carbon monoxide, hydrocarbons, and particulates. The left lungs of all mice were perfusion inflated with 70% buffered formalin at 25 cm water pressure, and 6–μm paraffin-embedded lung sections were stained with aldehyde fuchsin for elastic fibers. Quantitative image analysis of the elastin and alveolar walls was carried out. Over the 43-day test period in Los Angeles, there were 21 exceedings of the state O₃ standard, but only 2 for Santa Barbara. The mean value for the 1-h average O₃ level in LA during the 43 days was 0.11 ppm, versus 0.03 ppm for Santa Barbara. The mean NO₂ level in LA was four times higher than that for Santa Barbara, 0.12 versus 0.03 ppm. The levels recorded for other pollutants (carbon monoxide, NO₂, sulfur dioxide, particulates, and hydrocarbons) were also consistently greater for LA. The main finding is a greater amount of lung elastin for the LA animals compared to those in Santa Barbara (p - .03). Mean elastic fiber area was also increased, but fell short of statistical significance (p <.09), and this was also true for mean elastic fiber linear intercepts and perimeters (p <.07 and p < .06, respectively). Lung volumes did not differ. While the data require confirmation, they are in accord with the majority of experimental animal studies where lung injury leads to an increase in elastin due to an apparently faulty elastogenesis, such as amiodarone- and cadmium chloride-induced fibrosis and elastase- or papain-induced emphysema. In Part I of this study, statistically significant increases in alveolar wall area and alveolar wall perimeters were detected using frozen sections of lung. In the present studv, neither alveolar wall area nor perimeter alterations were observed. The disparity may reflect on the basic nature of the alveolar wall alteration, that is, a loss of proteinaceous edema fluid secondary to the paraffin processing. An altered lung elastin implies an abnormality in lung elasticity and damage to the lung scaffolding, the latter further suggesting an incomplete regeneration of the overlying epithelium.