# CARCINOGEN METABOLISM IN THE CIGARETTE SMOKING

> **NIH NIH R01** · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · 1988 · $206,787

## Abstract

Epidemiological studies have found a positive correlation between
cigarette smoking and emphysema, cardiovascular disease, and
cancer.  However, specific components in cigarette smoke that
are responsible for such activity, and the affected cells within the
respiratory tract have not been identified.  In this proposal, we
will use a nonhuman model that has shown changes in
intermediate variables related to these diseases after smoking
cigarettes in a human-liker manner.  The hypothesis to be tested
in this proposal is that exposure to different types of cigarettes
smoked under controlled conditions will cause biochemical and
morphological alterations in specific types of lung cells.  We will
compare the toxic and genotoxic effects of smoking different
types of cigarettes on cells of the bronchial epithelium (BECs),
the principal target tissue for development of bronchogenic
carcinoma in humans, and on pulmonary alveolar macrophages
(PAMs), cells that might contribute to the development of
smoking-related disease.  Cigarettes containing oil of cloves are
suspected of causing pulmonary edema and acute hemorrhage in
otherwise healthy junvenile cigarette smokers.  Eugenol, the
major consitutent of clove oil, producees acute pulmonary edema
in rodents similar to that observed in humans.  We will determine
if toxic responses in BECs and PAMs following exposure to clove
cigarette smoke are greater than those observed with other
cigarette types.  Pulmonary function will be evaluated following
exposure to known amounts of combustion products from four
types of cigarettes that vary in delivery of tar, nicotine, and
carbon monoxide.  Both histological and biochemical endpoints
will be evaluated in lung cells.  To evaluate the genotoxic
potential of the different types of cigarettes for BECs,
similarities in DNA adduct profiles and persistence of specific
DNA adducts will be correlated with extent of exposure.  The
ability of BECs to transport mutagens to adjacent cells will be
evaluated in a V79 cocultivation assay.  This approach, where
exposure can be controlled and quantitated, will provide
information for further studies to identify components in the
combustion of tobacco that have specific effects (toxic or
genotoxic) on various cell types in the lung.

## Key facts

- **NIH application ID:** 3171008
- **Project number:** 5R01CA033069-06
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCIENCE CENTER
- **SAM.gov UEI:** C3KXNLTAAY98
- **Principal Investigator:** MILTON V MARSHALL
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $206,787
- **Award type:** 5
- **Project period:** 1987-07-01 → 1990-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3171008

## Citation

> US National Institutes of Health, RePORTER application 3171008, CARCINOGEN METABOLISM IN THE CIGARETTE SMOKING (5R01CA033069-06). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3171008. Licensed CC0.

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