Smoking and Tobacco Control Monograph No. 7 
dose-response relationship between lung cancer risk and the extent of filter 
cigarette smoking was not observed (Pathak et al., 1986). Other recent case- 
control studies have provided comparable results (Wilcox et al., 1988; 
Kaufman et al., 1989). 
Temporal patterns of lung cancer rates also have been interpreted as 
indicating lower lung cancer risks among smokers of lower tar and nicotine 
cigarettes. It has been suggested that the recent decline in lung cancer 
mortality rates among younger males may reflect changes in the cigarette 
(World Health Organization, 1986). This downturn has been observed in 
the United States and other countries (Gilliland and Samet, 1994). 
Nonmalignant Cigarette smoking has diverse effects on the structure and function of 
Respiratory the lung and is a cause of chronic bronchitis and chronic obstructive 
Diseases pulmonary disease (COPD) (U.S. Department of Health and Human 
Services, 1984). The persistent obstruction to airflow in the lung that is the 
hallmark of COPD reflects underlying changes in the small airways of the 
lung and emphysema, which is the permanent destruction of the air spaces 
of the lung. Chronic bronchitis, a condition of chronic sputum production, 
reflects hyperplasia of the lining of the airways of the lung and mucous gland 
proliferation. Compared with nonsmokers, smokers have a greater frequency 
of cough and production of phlegm, manifestations of the inflammation of 
the lung and increased mucus production secondary to smoking, and 
wheezing; smokers also have lower lung function. 
A significant number of adults in the United States have COPD, which 
now causes more than 60,000 deaths annually (U.S. Department of Health 
and Human Services, 1984). The natural history of this disorder has been 
described through longitudinal investigations that have monitored lung 
function over time in smokers and nonsmokers (U.S. Department of Health 
and Human Services, 1984; Sherman et al., 1993). In nonsmokers, lung 
function increases through late adolescence and early adulthood, maintains 
a plateau across the third and fourth decades, and then begins to decline. 
In smokers, the decline begins at a younger age and tends to be steeper. 
The rate of decline increases with the number of cigarettes smoked per day 
but varies widely among smokers. With continued smoking, those with 
more rapid rates of decline eventually deteriorate to a level of lung function 
associated with impairment, and COPD is diagnosed. Although cessation 
earlier in the evolution of the disease is followed by return of the rate of 
decline to that of nonsmokers (U.S. Dej)artment of Health and Human 
Services, 1990), smoking cessation at this point in the natural history of 
the disease is not followed by im[)rovement in lung function. 
l indings have been reported that provide insights concerning tar and 
nicotine yields and res[)iratory sym[)toms and lung function level. Auerbach 
and c(41eagues (1979) quantitated smoking-related changes in the lungs of 
men having autopsies at a Veterans Administration hospital in New Jersey. In 
a rigorously investigated series of autopsied lungs, these investigators showed 
that smokers from a period during which cigarettes had com{)aratively high 
yields (A tar and nicotine (1955 to 1960) had more changes in the airways at 
82 
