Smoking and Tobacco Control Monograph No. 7 
distribution and retention of smoke components in the respiratory systems 
of laboratory animals may not mimic natural human smoking. Nevertheless, 
long-term smoke inhalation regularly induces tumors of the larynx in Syrian 
golden hamsters. Direct installation of cigarette tar into the airways of 
laboratory animals causes lung cancers (Hoffmann and Hecht, 1990; 
U.S. Department of Health and Human Services, 1982). 
MS cigarette smoke contains more than three dozen distinct chemical 
species considered to be tumorigenic in humans or animals (Hoffmann and 
Hecht, 1990; U.S. Department of Health and Human Services, 1982 and 
1989). Among the most prominent are PAHs such as benzo(fl)pyrene (BaP); 
aza-arenes such as dibenzo-acridine; N-nitrosamines such as NDMA; aromatic 
amines such as 4-aminobiphenyl; aldehydes such as formaldehyde; other 
organics such as benzene; and certain inorganic compounds such as arsenic, 
nickel, and chromium. Some of these chemicals alone are capable of 
initiating tumors in laboratory animals; others can promote the development 
of previously initiated cancers. Still others indicate direct human 
epidemiological evidence of carcinogenicity. 
Certain chemical components of smoke may contribute to specific 
cancers. For example, TSNAs may contribute to cancers of the lung, larynx, 
esophagus, and pancreas, whereas 4-aminobiphenyl and certain aryl amines 
may contribute to cancer of the bladder (Vineis, 1991). Benzene in cigarette 
smoke may play a role in smoking-induced leukemia (Melikian et al., 1993). 
NONCANCEROUS Cigarette smoking is the main cause of chronic obstructive lung 
LUNG DISEASES disease (COLD), also called chronic obstructive pulmonary disease 
(U.S. Department of Health and Human Services, 1984a). Smoking accounts 
for 84 percent of COLD deaths in men and 79 percent in women (U.S. 
Department of Health and Human Services, 1989). 
COLD is a slowly progressive illness that develops after repeated insults 
to the lung over many years. In the early years after starting to smoke, an 
individual may report no symptoms. However, even at this early stage 
breathing tests can often detect abnormalities in the small terminal airways 
of the lung (Beck et al., 1981; Seely et al., 1971; U.S. Department of Health 
and Human Services, 1984a), and these abnormalities have been directly 
observed in autopsy studies of young smokers who died suddenly 
(Niewoehner et al., 1974). For smokers in their twenties, there is already a 
dose-response relationship between the extent of abnormal lung tests and 
the number of cigarettes smoked daily. In random population surveys, from 
17 to 60 percent of adult smokers younger than age 55 have detectable small 
airway dysfunction (U.S. Department of Health and Human Services, 1984a). 
Over the course of an individual's two decades or more of smoking, a 
constellation of chronic respiratory changes develops. I'hese chronic lung 
injuries include (1 ) mucus hypersecretion with chronic cough and phlegm; , 
(2) airway thickening and narrowing, resulting in obstruction to airflow I 
during expiration; and (3) emphysema, that is, abnormal dilation of the air i 
spaces at the end of the res[)iratory tree, with destruction of the walls lining 
62 
