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Tobacco smoke induced lung lesions persist post exposure in spontaneously hypertensive rats
Author(s) -
Wilson Dennis W.,
TeeSy Christel,
Witschi HansPeter,
Pinkerton Kent
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.565.14
Subject(s) - medicine , squamous metaplasia , lung , metaplasia , airway , pathology , physiology , dysplasia , lung cancer , parenchyma , bronchopulmonary dysplasia , epithelium , anesthesia , biology , pregnancy , genetics , gestational age
To access tobacco smoke (TS) effects on lung cancer, reversibility of airway and parenchymal lesions, and cardiac disease, we performed a lifetime study of spontaneously hypertensive (SH) rats. Male SH rats were exposed to filtered air or TS (average of 60 mg/m3) for 6 hr./day, 3 days/week for 39 weeks after which all animals were allowed to live out their lifespan. We developed survival curves, quantitated airway mucous substance, estimated cell division rates (BrdU) and subjectively evaluated lung lesions. Rats previously exposed to TS had a four‐fold increase in airway mucous substances, modest but not significant increases in BrdU incorporation, and persistent mucous and squamous metaplasia in large airways. TS exposed rats had accumulations of large pigmented alveolar macrophages, some of which progressed to fibrosing granulomas. Lung lesions consistent with congestive heart failure developed with equal incidence in both control and TS exposed rats. While we found no evidence of dysplasia or neoplasia, we conclude that both metaplastic airway lesions and alveolar inflammation elicited by TS persist long after cessation of exposure. Supported by Philip Morris and NIEHS ES011634.