Smoking and Tobacco Control Monograph No. 7 
Respiratory morbidity also has been investigated. Follovymp of outpatient 
visits by enrollees in a Kaiser-Permanente group over 1 year showed that there 
was a reduced risk for pneumonia and influenza but not other respiratory 
conditions, associated with use of low-tar and -nicotine products (Petitti and 
Friedman, 1985a). However, in comparison with nonsmokers, smokers using 
low-tar and -nicotine cigarettes had an increased risk for pneumonia, 
influenza, and COPD. 
Not all studies show less disease associated with lower yield cigarettes. 
One recent study from Finland found that symptom levels in young smokers 
who were just initiating smoking did not depend greatly on tar yield (Rimpela 
and Teperi, 1989). In this 6-year followup study, the youths were surveyed 
on several occasions, and the relationship between tar yield and symptom 
onset was determined. There was little evidence of less symptom occurrence 
in the new smokers using low-tar cigarettes in comparison with those 
smoking higher tar cigarettes. Moreover, symptoms were far more frequent 
in the smokers of low-tar cigarettes in comparison with nonsmokers. In a 
randomized trial in the United Kingdom, lower tar cigarettes were not 
associated with either lower symptom frequency or higher level of ventilatory 
function, as assessed by measuring the peak expiratory flow rate (Withey et 
al., 1992a and 1992b). The investigators monitored urinary nicotine 
metabolites and concluded that compensation led to comparable levels 
across the trial period. 
The evidence does not suggest a relationship between tar yield and lung 
function level. For example, in the Whitehall study (Higenbottam et al., 
1980), there was no cross-sectional relationship between tar yield and level 
of the forced expiratory volume in 1 second. In the Normative Aging Study 
(Sparrow et al., 1983), a longitudinal study of U.S. veterans, tar yield of the 
usual brand of cigarettes smoked was not associated with decline of forced 
expiratory volume in 1 second. 
C:ardiuva.vcular Harris (this volume) discusses mechanisms by which cigarette 
Disea.se smoking causes CVD. Through some of these mechanisms, cigarette 
smoking is anticipated to increase the incidence of new cases (i.e., to cause 
more disease), whereas other mechanisms are anticipated to exacerbate the 
status of those who already had disease (U.S. Department of Health and 
Human Services, 1990). Thus, factors promoting atherogenesis would 
increase incidence, whereas factors such as sympathomimetic stimulation 
by nicotine or impairment of oxygen delivery by carbon monoxide might 
be expected to have more immediate effects and contribute to morbidity 
and mortality among those with coronary artery disease. 
Strong evidence does not exist for either lower incidence or less morbidity 
from coronary heart disease (CUD) among smokers of lower yield cigarettes. 
In the American Cancer Society's Cd’S-1 study (Hammond et al., 1976), 
smokers (A lower tar |)roducts did have lower mortality from heart disease 
('fable 1 ). On the other hand, two case-control studies carried out during 
84 
