Chapter 5 
CANCER 
Other health effects of cigarette smoke, such as retardation of healing of 
peptic ulcers and interaction with certain therapeutic drugs, are not 
considered in detail here. 
The epidemiologic evidence on the degree (if any) to which filter-tipped 
and low-tar cigarettes have reduced the risks of smoking-related diseases are 
reviewed by Samet (this volume). 
The psychoactive drug in cigarette smoke is nicotine. Cigarette smoking 
is a highly controlled form of self-administration of this drug. Nicotine use 
is self-reinforcing. Attempts to stop smoking lead to craving, withdrawal 
symptoms, and high rates of relapse (U.S. Department of Health and Human 
Services, 1988; Harris, 1993). The psychoactive effects of nicotine are 
discussed in detail in chapters by Benowitz (this volume) and Henningfield 
and Schuh (this volume). 
Cigarette smoking causes cancers of the lung, esophagus, larynx, oral 
cavity, bladder, and pancreas in male and female smokers. In fact, cigarette 
smoking is the major cause of lung cancer in the United States, accounting 
for 90 percent of cases in men and 79 percent in women (U.S. Department 
of Health and Human Services, 1989). Smoking is also reported to increase 
the risks of cancers of the kidney, liver, anus, penis, and uterine cervix as 
well as several forms of acute leukemia (Garfinkel and Bofetta, 1990; 
U.S. Department of Health and Human Services, 1982, 1989, and 1990). 
Numerous epidemiological studies covering the experience of millions 
of men and women over many years show that smokers' risks of developing 
cancer increase with the number of cigarettes smoked daily, the lifetime 
duration of smoking, and early age of starting smoking. Smoking cessation 
gradually reduces cancer risk, although a persistent excess risk has been 
observed even two decades after cessation (U.S. Department of Health and 
Human Services, 1989 and 1990). Cigarette smoke interacts with other 
causative agents, including alcohol, asbestos, radon daughters, certain viruses, 
and certain workplace exposures, in the development of human cancers 
(U.S. Department of Health and Human Services, 1982, 1989, and 1990). 
Condensates collected from cigarette smoke cause mutations and damage 
to DNA (deoxyribonucleic acid) in laboratory assays of mutagenesis (Cairola, 
1982) as well as malignant transformation (in laboratory tests) of a chemical's 
ability to induce malignant changes in mammalian cells. The most widely 
used experimental system is the mouse skin bioassay, in which cancers are 
induced by the repeated application of condensates of cigarette smoke to 
the shaved skins of mice. 
Humans naturally puff on cigarettes. The puffed smoke, in a volume 
of about 30 to 70 mL, is temporarily retained in the smoker's mouth, after 
which it may be inhaled deeply into the lungs. By contrast, some laboratory 
animals breath by panting, and others are obligate nose breathers. Even with 
installation of smoke through artificial airways, it can be quite difficult to 
get the animals to inhale deeply, as human smokers do. Accordingly, the 
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