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Toxicologic Pathology
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Articles

Comparative Pathology of Environmental Lung Disease: An Overview

Francis H. Y. Green1, Val Vallyathan2 and Fletcher F. Hahn3

1 Respiratory Research Group, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada
2 National Institute for Occupational Safety and Health, Center for Disease Control, Morgantown, WV 26505-2888, USA
3 Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA

Correspondence: Address correspondence to: Francis H. Y. Green, Professor, Pathology and Laboratory Medicine, Faculty of Medicine, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alberta T2N 4N1, Canada; e-mail:fgreen{at}ucalgary.ca

Environmental factors play a major role in a majority of lung diseases. Asthma, chronic obstructive pulmonary disease (COPD), lung cancer, and many interstitial lung diseases are influenced or caused by environmental factors. Animals and humans may respond differently to the same agent, and a study of the comparative pathology between the two is useful for optimizing animal models of environmental lung disease and for evaluating their predictive value in carcinogenicity studies. This overview describes the most common nonneoplastic pathologic pulmonary responses to inhaled environmental agents in the human and contrasts them with the responses observed in rats exposed to the same agents. We show both similarities and difference in response to the same agents; furthermore, both species have unique responses to some agents (for example, progressive massive fibrosis in the human and proliferative squamous lesions in the rat). Quantitative analysis of the grades of response to three environmental particulate dusts revealed differences between the 2 species at the cellular level. Specifically, acute intra-alveolar inflammation, alveolar epithelial hyperplasia, and alveolar lipoproteinosis were all greater in rats than in humans exposed to the same agents. These differences may account for differences between the 2 species in carcinogenic response to nonfibrous particulates.

Key Words: Pneumoconiosis • occupational • environmental lung disease • comparative pathology • rat • human

Toxicologic Pathology, Vol. 35, No. 1, 136-147 (2007)
DOI: 10.1080/01926230601132055


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