Morphological changes in rat lung after long-term exposure to diesel emissions.
Wistar rats were exposed for 24 mo to diesel emissions containing a low (0.2 ppm, 0.21 mg/m(3)), medium (1.04 ppm, 1.18 mg/m(3)), or high (2.96 ppm, 3.05 mg/m(3)) concentration of NO(2) and particles, or diesel emissions containing a medium (1.12 ppm, 0.01 mg/m(3)) concentration of NO(2) without particles. At 6-mo intervals during the exposure period, rats were autopsied, and their lungs were prepared for light- and electron-microscopic examination. Morphological evaluations included examination for hyperplasia of airway goblet cells, shift in the types of glycoprotein of intracellular mucus granules in goblet cells, infiltration of inflammatory cells in the airways, enlargement of the cross-sectional area of an alveolus as a parameter of air space enlargement, and development of alveolar holes, which is considered to be an early hallmark of alveolar destruction. The number of goblet cells with acid-form mucus granules increased with the exposure concentration and time; however, goblet cells did not show any hyperplastic changes. Furthermore, inflammatory cells such as alveolar macrophages, mast cells, plasma cells, neutrophils, and lymphocytes infiltrated the airways and the alveoli, and showed some cell-to-cell contact. Although no significant enlargement of the air space of the lungs was seen in any exposure group, the number of alveolar holes was significantly higher in the high-concentration group in comparison with the control group at each exposure time, and also increased in other exposure groups, even in the low-concentration group at certain exposure times. Morphological changes in the lungs were mild even in the animals exposed to the highest levels of diesel emissions for 24 mo. Elimination of particles from diesel emissions led to reduced morphological changes such as a decreased shift in the types of glycoprotein of mucus granules in goblet cells, decreased infiltration of inflammatory cells in the lungs, and reduced anthracosis.
Kato
A
A
Health Effects Research Division, Japan Automobile Research Institute, 2530, Karima, Tsukuba-shi, Ibaraki, 305-0822, Japan. akato@jari.or.jp.
Nagai
A
A
Kagawa
J
J
D000818:Animals; D001835:Body Weight / Q000187:drug effects; D001980:Bronchi / Q000187:drug effects / Q000473:pathology; D004305:Dose-Response Relationship, Drug; D020397:Goblet Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D008168:Lung / Q000187:drug effects / Q000473:pathology*; D008297:Male; D008855:Microscopy, Electron, Scanning; D009093:Mucus / Q000378:metabolism; D011009:Pneumoconiosis / Q000209:etiology / Q000473:pathology*; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D020545:Respiratory Mucosa / Q000187:drug effects / Q000473:pathology; D013047:Specific Pathogen-Free Organisms; D001335:Vehicle Emissions / Q000032:analysis / Q000633:toxicity*
D001335:Vehicle Emissions