© 1998 by Oxford University Press
Journal Of The National Cancer Institute, Vol 90, 1198-1205, Copyright © 1998 by Oxford University Press
SH Barsky, MD Roth, EC Kleerup, M Simmons and DP Tashkin
BACKGROUND: Tobacco smoking has been observed to cause molecular
alterations in bronchial epithelium that antedate the development of lung
carcinoma. The rising prevalence of marijuana and cocaine use among young
adults in the United States prompted us to investigate whether similar
molecular and histopathologic alterations occur in habitual smokers of
marijuana and/or cocaine who may or may not also smoke tobacco. METHODS:
Bronchoscopy was performed in 104 healthy volunteer subjects, including 28
nonsmokers and 76 smokers of one or more of the following substances:
marijuana, tobacco, and/or cocaine. Bronchial mucosa biopsy specimens and
brushings were analyzed for histopathologic changes, for
immunohistopathologic expression of intermediate or surrogate end-point
markers that are linked to an increased risk of cancer (Ki-67 [a marker of
cell proliferation], epidermal growth factor receptor, p53, Her-2/neu [also
known as erbB-2 and ERBB2], globular actin, and abnormal DNA ploidy).
Reported P values are two-sided. RESULTS: Smokers of any one substance or
of two or more substances exhibited more alterations than nonsmokers in
five to nine of the 10 histopathologic parameters investigated (all P <
.05), and they exhibited more molecular abnormalities than nonsmokers.
Differences between smokers and nonsmokers were statistically significant
(all P < or = .01) for Ki-67, epidermal growth factor receptor, globular
actin, and DNA ploidy. There was general agreement between the presence of
molecular abnormalities and histopathologic alterations; however, when
disagreement occurred, the molecular abnormalities (e.g., Ki-67 and
epidermal growth factor receptor) were more frequently altered (all P <
or = .01). CONCLUSIONS: These findings suggest that smoking marijuana
and/or cocaine, like tobacco smoking, exerts field cancerization effects on
bronchial epithelium, which may place smokers of these substances at
increased risk for the subsequent development of lung cancer.
ARTICLES
Histopathologic and molecular alterations in bronchial epithelium in habitual smokers of marijuana, cocaine, and/or tobacco
Department of Pathology, University of California, Los Angeles, USA. sbarsky@ucla.edu
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