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Toxicological Sciences 61, 342-355 (2001)
Copyright © 2001 by the Society of Toxicology


RESPIRATORY TOXICOLOGY

Canines as Sentinel Species for Assessing Chronic Exposures to Air Pollutants: Part 1. Respiratory Pathology

L. Calderón-Garcidueñas*,{dagger},1, A. Mora-Tiscareño{dagger}, L. A. Fordham{ddagger}, C. J. Chung{ddagger}, R. García{dagger}, N. Osnaya{dagger}, J. Hernández{dagger}, H. Acuña{dagger}, T. M. Gambling§, A. Villarreal-Calderón{dagger}, J. Carson§, H. S. Koren and R. B. Devlin

* Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina; {dagger} Instituto Nacional de Pediatría, Mexico City 14410; {ddagger} Department of Radiology and § Center for Environmental Medicine and Lung Biology, University of North Carolina, Chapel Hill, North Carolina 27599–7310; and National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711

A complex mixture of air pollutants is present in the ambient air in urban areas. People, animals, and vegetation are chronically and sequentially exposed to outdoor pollutants. The objective of this first of 2 studies is to evaluate by light and electron microscopy the lungs of Mexico City dogs and compare the results to those of 3 less polluted cities in Mexico. One hundred fifty-two clinically healthy stray mongrel dogs (91 males/61 females), including 43 dogs from 3 less polluted cities, and 109 from southwest and northeast metropolitian Mexico City (SWMMC, NEMMC) were studied. Lungs of dogs living in Mexico City and Cuernavaca exhibited patchy chronic mononuclear cell infiltrates along with macrophages loaded with particulate matter (PM) surrounding the bronchiolar walls and extending into adjacent vascular structures; bronchiolar epithelial and smooth muscle hyperplasia, peribronchiolar fibrosis, microthrombi, and capillary and venule polymorphonuclear leukocytes (PMN) margination. Ultrafine PM was seen in alveolar type I and II cells, endothelial cells, interstitial macrophages (M{theta}), and intravascular M{theta}-like cells. Bronchoalveolar lavage showed significant numbers of alveolar macrophages undergoing proliferation. Exposure to complex mixtures of pollutants—predominantly particulate matter and ozone—is causing lung structural changes induced by the sustained inflammatory process and resulting in airway and vascular remodeling and altered repair. Cytokines released from both, circulating inflammatory and resident lung cells in response to endothelial and epithelial injury may be playing a role in the pathology described here. Deep concern exists for the potential of an increasing rise in lung diseases in child populations exposed to Mexico City's environment.

Key Words: dogs; air pollution; lungs; particulate matter; ultrafine particulate matter; ozone; endothelial and epithelial lung dysfunction; chronic lung inflammation; lung remodeling.


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