Council for Tobacco Research
the Effect of Lifetime Exposure to Whole Cigarette Smoke in Bc3f1 Cum Mice [St Study Involving Nose Only Exposure with Mice]
Fields
- Type
- ABSTRACT
- PREPRINTED FORM
- Depository Date
- 31 Jan 1996
- Named Person
- Ctr
- Henry, C.J.
- Mai
- Cancer Res
- Henry, C.J.
- Master ID
- 300200234-0239
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- HT0119235-9235 Cigarette Smoke Increases Dna Replication in Lung and Sister Chromatid Exchange (Sce) in Bone Marrow of Mice [St Mice Studied After Nose Only Inhalation]
- HT0119236-9236 the Effect of Exposure to Whole Cigarette Smoke on Short-Term Endpoints in Bc3f1 Cum Mice. [St Test Involving Mice Who Inhaled Nose Only Smoke]
- Request
- 132
- Box
- 098
- Author
- Henry, C.J., Mai
- Billups, L.H., Mai
- Hall, W.C., Mai
- Avery, M.D., Mai
- Mullinax, H.D., Mai
- Kouri, R.E., Mai
- Dansie, D.R.,
- Billups, L.H., Mai
- Site
- Hoyt
- Brand
- 2r1
- Z00000, Reference Brands
- UCSF Legacy ID
- mpd1aa00
Document Images
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THE EFFECT OF LIFETIME EXPOSURE TO WHOLE CIGARETTE SMOKE IN
BC3F1/CUM MICE. C.J. Henry, L.B. Billups, W.C. Hall, M.D.
Avery, D.R. Dansie, H.D. Mullinax, and R.E. Kouri,
Microbiological Associates, Bethesda, PID 20816.
Using the SEM IIB cigarette smoke exposure system, "nose-
only" exposure of BC3F1/Cum mice to 2R1 cigarette smoke (high
tar, high nicotine) resulted in deposition of 100-200 ug smoke
particulates/mouse/day with '%,40z of the deposition in the
respiratory tract. These exposures resulted in increased:
lung microsomal monooxygenases and ornithine decarboxylase,
lung DNA synthesis, lung protein, lung/body weight ratios, and
numbers of sister chromatid exchanges in bone marrow. BC3F1/
Cum mice were free of 11 adventitious agents and were shown to
be a sensitive model for the chemical induction of lung car-
cinomas (Cancer Rcs. 41, in press, 1981). Mice were exposed to
smoke or slmm 5 days%week for 27 months. Over 1500 mice were
evaluated. The only smoke induced lesion was an accumulation
of pigmented alveolar macrophages. Incidence of spontaneous
lung cancer (i.e., alveolar adenocarcinomas) was '-5%. Ex-
posure to srnoke failed to alter this tumor incidence. Sur-
vivors post 27 months (ti500) were allowed to live out their
natural lifespan. No differences in probability of death from
lung cancer were observed in smoke or sham exposed mice up to
36 months of age. Expojure to smoke in this model system re-
sulted in significant changes in short-term endpoints, but no
carcinogenic effects were noted. Whether these results are re-
lated to the absence of particular viral pathogens or M co-
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Supported by The CouncLl for Tobacco Research-USA, Inc.
PRESENTAr10N PREFERENfA (i'gl ia Mone box only):
[] Shde ®Porter C]SdentifieFO.n a&iend6e Exh3it
Due to Ihe aire and eomplealty of the proyram. lirul deddona reprding elide or postez.ariona 1YDL BE
MADE AT r11E DISCRETION OF THE NATIONAL PROGRAM COMMITI'EE.
AUTHOR IP7FORMATiON: Paper to be prescnted by
Dr. Carol J. 11enrY
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of the author to whom all conerpondenx relating to rhe abatrad should Ee wrt
PreaentingAuthor: Dr. Carol J. Henry
- Microbiological Associates
OatrespondingAuthor: Dr. Carol J. Henry
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