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Philip Morris

Pathological Alterations in Syrian Golden Hamsters Lungs After Passive Exposure to Cigarette Smoke

Date: 1977
Length: 1 page
2063594132
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Author
Ketkar, M.B.
Mohr, U.
Reznik, G.
Characteristic
EXTR, EXTRA
Master ID
2063594010/4240
Related Documents:
Site
R530
Area
CARCHMAN,RICHARD/OFFICE
Litigation
Iwoh/Produced
Type
SCRT, REPORT, SCIENTIFIC
Named Organization
Toxicology
Date Loaded
07 Jun 1999

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! I I I I I I I I I I I I I I I I I ~'~ AUTHOR: KETKAR, M.B., G. REZNIK AND U. MOHR ~AT~: 1977 TIT~; PATHOLOGICAL ALTERATIONS IN SYRIAN GOLDEN HAMSTERS LUNGS AFTER PASSIVE EXPOSURE TO CIGARETTE SMOKE CITATION= Toxicology, 7, 265-273 (1977) 120 8-week old Syrian Golden hamsters were divided into 3 groups (2 treatment, 1 control) with 10 males and 10 females ,~rving as untreated controls. The animals from the 2 treatment groups were exlx~d to one of two types of experimental cigarettes: C1 (100% Virginia tobacco, 2.96 mg nic, 37.2 mg DPM, 3,5 vol ,q:- CO (20 males and 20 females) and C2 - 100% reconstituted tobacco, 0.5 mg nic, 12,3 mg DPM, 5.32 vol ~ CO (30 males and 30 females), All the experimental animals were expo~d to cigarette smoke once a day, 5 dayfweek for 52 weeks. Controls were sham expo~d for the same length of time. One day after termination of exposure, all the animals were killed. Tissue were fixed and examined for pathological changes. RNDING,S/RESULT$= F~','al I~ype~plasi,a was obsep,'ed in tile larynx of 7 smoke-exwsed animals in tile trachea of about 40%. Almost 50% of ihe smoke expensed hamsters (both cig. Types) demonstrated small, round-cell infiltration of the laryngeal and tr:v,'heal submuc~n. ,as well as tl~e lungs. Histological examination of lung tissue showed chronic pathological alterations. All of fl'te C2 smoke-exposed animals exhibited bronchial hype~plasia, but this was exhibited in only 50~ of the animals exposed to C1 smoke.One papilloma of the lobar bronchus and two pulmonaff adenomas were found in the CI animals, and 5 adenomas of the tung in the C2 group. Dark brown patches (2-3nm~ in diameter, were appavt'nt over tile tGal surface area of the lungs. It was shown that such tissue was composed of clumps of cells containing pale to dark.brown pigment -rims they ~fem, d to them ,~s "Brmvn Ceils". Qualitative as well as quantitative differences existed between the two treatment groups with respect to the occurrence of "Brown Cell" clumps. In animals expo~d to C1 smoke, the cells were numerous, large and compactly packed, however in t~ C2 exposed hamsters, the,.~ cells were few, small and loo~ly packed. These cells were usually situated in periva~ular and peribronchiat areas, however large clumps were also ob~rved in tl~e avelolar region, Ultrastructural examination of these cell clumps, revealed that they were alveolar macrophages, the cytoplasm of which was crowded with phagocytosed material of hi gh electron density. Nearly all of the smoke expo~d animals demonstrated perivascular inflammatory cells in the liver. Varying degrees of amyloidosis of liver and kidney tissues were ob~rved, but tiffs is normally typical of old animals, Hamsters exl~)~d to smoke of C1 cigarettes showed more "Brown Cells" in the lung than C2 expo~d animals. The authors state that this study demonstrated that the smoke of two different types of cigarettes produced varying effects on the marcophages of pulmonary alveolar tissue. From this they concluded that the respon~ of lung tissue to smoke exposure is dependent upon the amount of mainstream TPM, the amount of condensate, the time exlyo~d and the number of cigarettes. However, they state that the development of "Brown Cells" should be considered as a non-specific reaction of the lung to cigarette smoke exposure, The larger number of tumors found in the C2 ~oups could be accounted for by the lower amount of total condensate in this cigarette smoke, however significantly fewer macrophages were ob~rved in animals of this group. This led the authors to suggest that the low amount of condensate resulted in an insufficient activation of the defen~ mechanism of the macmphages, with the results that a larger number of some particles were left to cause tumor induction.

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