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Epidemiology and Prevention |
Department of Epidemiology and Surveillance, American Cancer Society, Atlanta, Georgia 30329 [W. D. F., C. A. L., S. J. H., M. J. T.]; Office of Epidemiology, Missouri Department of Health and Senior Services, Jefferson City, Missouri 65102 [B-P. Z.]; and Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia 30322 [W. D. F., C. A. L.]
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ABSTRACT |
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We studied participants in the Cancer Prevention Study II, followed from 1982 through 1988. After restricting to people 40–79 years old who smoked 
40 cigarettes per day at enrollment, we fit Poisson models for four age groups and evaluated lung cancer mortality (M) in relation to smoking duration (D) and intensity (I) on a double-log scale, as suggested by the Armitage-Doll multistage carcinogenesis model.
The age-specific mortality estimates for men (Mm) and for women (Mw), when transformed to the original scale, were:
ages 40–49: ^Mm = e-17.9 x D1.9 x I0.95, ^Mw = e-20.2 x D2.8 x I0.96;
ages 50–59: ^Mm = e-17.4 x D2.6 x I0.52, ^Mm = e-17.2 x D2.2 x I0.75;
ages 60–69: ^Mm = e-15.7 x D2.4 x I0.37, ^Mm = e-14.1 x D1.5 x I0.78;
ages 70–79: ^Mm = e-13.0 x D1.8 x I0.39, ^Mm = e-13.2 x D1.3 x I0.95.
Our study confirms that years of cigarette smoking is far more important than the number of cigarettes smoked per day in predicting lung cancer risk in United States men, regardless of age, and provides new evidence that a qualitatively similar pattern holds for women. The results support measures to prevent the uptake of smoking by adolescents and increase cessation. We discuss reasons why the associations we observe are lower than those reported by R. Doll and R. Peto (J. Epidemiol. Commun. Health, 32: 303–313, 1978).
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INTRODUCTION |
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TopABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Doll and Peto (1) addressed this issue in their historic analysis of one of the few large cohort studies in which the effects of intensity and duration have been estimated separately. They modeled the relationship between incidence of lung cancer and cigarette smoking duration and intensity by using data from the 20-year follow-up of male British physicians, and they concluded that incidence was proportional to approximately the fourth or fifth power of smoking duration (as measured by age) and to the second power of smoking intensity (measured as cigarettes/day). The findings of their research have been widely interpreted to mean that smoking duration is much more important than smoking intensity in causing lung cancer and that the development of lung cancer may be a five- or six-step process.
Some have attempted to interpret these patterns of risk theoretically in terms of the stages of lung cancer development. According to the multistage theory of carcinogenesis (2, 3, 4, 5)
, an ordered sequence of discrete cellular changes that are heritable when somatic cells divide is needed to transform a normal epithelial cell into a progenitor of a carcinoma (1
, 5)
. If we denote the incidence of a specific carcinoma after t years of exposure to an environmental carcinogen as It, then a simple multistage theory predicts that
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For two decades, no data from other large, prospective studies have been evaluated to verify these findings. In our study, we used data from the first 6 years of follow-up of the American Cancer Society CPS-II4 to examine lung cancer mortality in relation to cigarette smoking duration and intensity, and especially to evaluate the double-log linear relationship suggested by the multistage theory of carcinogenesis of Armitage and Doll (2, 3, 4, 5) . We used the smoking duration reported by respondents rather than age (less some constant), as did Doll and Peto (1) . Our analyses also considered women as well as men. Additionally, to separate the effect of duration of exposure to cigarette smoke from that of age, we stratified the data by age and examined the relationship among the different age groups.
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MATERIALS AND METHODS |
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In this study, we defined current smokers as persons who reported having smoked at least one cigarette per day for at least 1 year, who were currently smoking cigarettes only, and who had never smoked pipes or cigars. Our analyses, like those of Doll and Peto (1)
, excluded former smokers. We also excluded persons who had smoked other tobacco products besides cigarettes and persons with incomplete or implausible data on amount or duration of smoking. We restricted our analysis to persons 40–79 years of age, to facilitate comparisons with the results of Doll and Peto (1)
and because relatively few lung cancer deaths had occurred before age 40 or after age 79. To allow for latency in lung cancer development, we restricted our analyses to follow-up of people who had smoked at least 10 years. We excluded those who smoked more than 40 cigarettes per day, reported lung cancer at enrollment, or started smoking before age 10. Our analyses included the 93,215 currently smoking men and the 24,159 currently smoking women in CPS-II who met eligibility criteria (Table 1)
. In sensitivity analyses, we also included the 127,162 nonsmoking men and 355,363 nonsmoking women who met eligibility criteria (Table 1)
. The intensity of smoking was defined as the self-reported average number of cigarettes smoked per day, and duration of smoking was defined as the self-reported total number of years of smoking (or, if those data were missing, the difference between age of initiation and age). We advanced age and duration of smoking as follow-up progressed, assuming that smokers continued to smoke. For example, during the first and second year of follow-up, a 59-year-old who had smoked for 20 years at enrollment was considered to be 60 and 61 years old in these years, respectively, and to have smoked for 21 and 22 years.
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50 years) and assigned a score corresponding to the observed mean for each category (15.6, 25.7, 35.3, 44.4, and 53.6 years, for men and 15.2, 25.6, 34.8, 44.0, and 53.4 years for women, respectively).
Similarly, we classified intensity of smoking into five categories of cigarettes per day (1–9, 10–19, 20–29, 30–39, and 40) and assigned a score corresponding to the observed mean for each category (4.5, 12.8, 20.8, 30.6, and 40 cigarettes per day for men and 5.0, 12.5, 20.6, 30.5, and 40 cigarettes per day per day for women, respectively). We used a log link function and log-transformed the duration and intensity, so that the modeled relationship between lung cancer mortality (
m) and cigarette smoking duration (Dk) and intensity (Ik) for the age group k could be expressed as
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0k is the intercept estimate for age group k and Dk and Ik are parameter estimates for duration and intensity of smoking, respectively. To examine graphically the association between lung cancer mortality and smoking behavior, we fit Poisson regression models separately for smoking duration and then for intensity for each age- and sex-specific group. We assumed that smoking duration advanced during the 6-year follow-up, because no information on smoking was collected after enrollment. We ignored the lag time between malignant transformation and clinical diagnosis of lung cancer, which other researchers have assumed to be 3.5 years (1 , 13) . Sensitivity analyses suggested the potential biases resulting from these simplifications to be small (data not shown). We also assessed why our results differed quantitatively, although not qualitatively, from those of Doll and Peto (1) by sequentially making changes, so that our method of analysis more closely approximated theirs. First, we reanalyzed our data (model 2) using age minus 22.5 as a surrogate for duration of smoking in the model, but otherwise ignored age and used the reported intensity +6, rather than intensity itself, changes that reflect how Doll and Peto (1) modeled duration and intensity. Finally, we further modified our analyses by including nonsmokers (model 3), an approach also used by Doll and Peto (1) . We used PROC GENMOD of SAS (14 , 15) to fit the Poisson models. We evaluated the goodness-of-fit of the models by using both the deviance statistic and residuals (14 , 16 , 17) . Final models fit well for all age groups. In sensitivity analyses, we reanalyzed data after dividing each age group at the midpoint. The model continued to fit well, although control for age was required for adequate fit among 60- to 69-year-old men (results not shown).
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RESULTS |
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TopABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, and was somewhat lower for women than men (11)
. Smokers age 70–79 at baseline smoked about three to five fewer cigarettes per day than those age 40–49 years. Older persons tended to have smoker longer but to have begun at older ages. As expected, lung cancer risk increased as age advanced, with the lung cancer death rate 30–40 times higher for smokers 70–79 years of age than for smokers 40–49 years of age.
Graphical Representation of Lung Cancer Mortality by Duration and by Intensity of Cigarette Smoking.
When we plotted lung cancer mortality by duration (Fig. 1
for men and Fig. 3
for women) and intensity of cigarette smoking (Fig. 2
for men and Fig. 4
for women) on a log-log scale, the straight-line model fit the data well for all age groups and did not depart substantially from a linear relation, although the slopes and intercepts of the fitted lines differed between gender and age groups. Middle-aged men and women tended to have slightly greater proportionate increases in mortality with amount smoked demonstrated by slightly steeper slopes for both intensity and duration, and greater negative intercepts, whereas older men and women usually had more gradual increases. Consequently, the difference in lung cancer mortality between the younger and older age groups, as shown on a log-log scale, tended to diminish slightly with heavier and more prolonged smoking.
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. For both men and women 40–49 years of age, mortality increased roughly in proportion to the second power of smoking duration and to the first power of intensity. For men 70–79 years of age, mortality increased roughly in proportion to the second power of smoking duration and the square root of intensity. The increases for women depended somewhat more strongly on intensity than they did for men, and perhaps slightly less strongly on duration, although the overall patterns were similar. For equivalent duration and intensity of smoking, the estimated absolute risk of lung cancer was higher for older smokers than for younger smokers, reflecting a rapid increase with age in the baseline rates. These results are consistent with the graphical representation of lung cancer mortality and smoking described previously (Figs. 1
2
3
4)
. Results were similar when we excluded men who first started to smoke at age 40 or older, or when we included men who reported that they had started to smoke before age 10 (data not shown).
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, for both men and women. The ratios of the two exponents (Dk/Ik) for men, were 2.0, 4.6, 6.5, and 4.6 for persons 40–49, 50–59, 60–69, and 70–79 years of age, respectively. For women, the corresponding ratios were: 2.9, 2.9, 1.9, and 1.4, respectively.
Comparison with Results of Doll and Peto.
We repeated the analyses using alternative statistical models to determine why our results differed quantitatively from those of Doll and Peto (Ref. 1
; Table 3
). These analyses, like those of Doll and Peto (1)
, are restricted to men. Results of our main analysis (Table 3
, model 1) showed that lung cancer mortality among men increased in proportion to the square root of intensity (ß 
0.4), whereas Doll and Peto (1)
estimated that the increase (in incidence) was proportional to the intensity squared (ß 2). We found that the increase in lung cancer was proportional to duration raised to the 2.3 power, whereas Doll and Peto (1)
estimated the it as duration raised to the 4.5 power.
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DISCUSSION |
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TopABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The quantitative differences between our findings and those of Doll and Peto (1)
are largely attributable to three differences in the specification of age, duration, and intensity in the statistical model and to whether nonsmokers are included in the analysis. Our primary analyses directly considered age in estimating the association between lung cancer mortality and duration and intensity of smoking. Doll and Peto (1)
, in contrast, studied a much smaller cohort and used age as a surrogate for duration. Therefore, their approach effectively precluded the separation of years of smoking from attained age. When we repeated our analyses using age minus 22.5 as a proxy for duration and adding 6 to the reported number of cigarettes per day, paralleling the approach of Doll and Peto (1)
, the association between lung cancer mortality and duration increased to 4.4, the same as reported by Doll and Peto. Furthermore, after these modifications, the association between lung cancer mortality and intensity increased from 0.41 to 0.69. Doll and Peto (1)
found a stronger association with intensity (exponent 2.0) but noted that the estimated exponent for duration of smoking depended on the constant chosen to be subtracted from age. Finally, we included nonsmokers in our analyses to replicate even more closely the approach of Doll and Peto (1)
. With the inclusion of nonsmokers, our estimates are similar to those of Doll and Peto (1.6 versus 2 for intensity; 4.6 versus 4.5 for duration). Doll and Peto (1)
noted that had they used (cigarettes/day +1) instead, the estimated exponent for smoking intensity would also have been approximately one. The rationale for adding a constant to duration and intensity was presumably because the logarithm of duration and intensity would otherwise have been undefined in nonsmokers. The residual, relatively small differences between our results and those of Doll and Peto (1)
may be attributable to chance or to other differences in design between the studies. For example, the CPS-II cohort was larger, more heterogeneous, and were followed for a shorter time.
Our analyses considered only the first 6 years of follow-up to minimize misclassification of smoking during follow-up. This approach was necessary because smoking histories were obtained only at baseline, and many current smokers would have quit during more prolonged follow-up.
The observation that the duration of smoking is such a strong determinant of lung cancer risk has important implications for public health. It supports efforts to prevent or delay the uptake of smoking among adolescents. Such measures include excise taxes to increase the price of cigarettes and counter-advertising (19 , 20) . It reinforces the need for more effective smoking cessation programs that motivate smokers to quit at earlier ages (21) . Finally, it predicts a steep increase in lung cancer incidence and mortality over time in countries in which the tobacco epidemic has only recently begun, even though smokers in some of these countries smoke fewer cigarettes per day, on average, than in the United States or in the United Kingdom (22 , 23) .
Whether age plays an independent role in carcinogenesis, separate from its correlation with cumulative genetic damage, has been debated without clear resolution, partly because limited data from humans are available to examine this issue (24
, 25)
. In our study, we stratified the analysis on age and found that the estimated exponents for both duration and intensity of smoking decreased with increasing age (Table 2)
. Moreover, the close correlation of age at initiation, attained age, and the duration of smoking effectively prevents us from studying the effects of age at initiation in current smokers (26
, 27)
.
These findings should not be interpreted as implying that older smokers are at lower risk of dying from lung cancer. The opposite is true, in fact, because older smokers incur a greater absolute risk of lung cancer than younger smokers for the same duration and intensity of smoking. The reductions in the estimated exponents for relative risks signify only that the incidence rate ratios are smaller for older smokers than for younger smokers, given the same duration and intensity of smoking, as reported by Thun et al. (11) .
Another point that warrants special attention is that when relating lung cancer mortality with duration and intensity of smoking on a double-log scale, a small slope in older age groups does not imply that increases in the duration or intensity of smoking have little effect on lung cancer risk of older smokers. Because the slope is positive, lung cancer risk increases exponentially with duration and intensity of smoking.
One hypothesis to explain the decrease in the association between lung cancer and the duration and intensity of cigarette smoking at older ages relates to the multistage model of carcinogenesis (2 , 24 , 25) . For individuals who start smoking at a young age, cigarette smoke may be more essential to the accumulation of multiple genetic mutations than at older ages. At older ages, when smokers have already developed many partially altered cells and the absolute risk of developing lung cancer is higher, other factors may contribute to the progression of cells to invasive cancer.
A second factor that may explain the lower exponents associated with duration and intensity of cigarette smoking at older ages is that the declining exponents may reflect underreporting of exposure. For example, older persons may be more likely to misreport the number of years of cigarette smoking than are younger persons because of recall bias. Similarly, current daily cigarette consumption may be an inaccurate measure of lifetime smoking intensity (28) . For example, it is unlikely that a person who currently smokes two packs a day has been smoking this amount ever since he or she started. Smokers may have changed their lifetime smoking behavior to compensate for the changing nicotine yields in manufactured cigarettes (29 , 30) . In any case, the self-reported number of cigarettes smoked per day is only a crude measure of the "true" dose of cigarette smoke (1 , 5 , 30) . Whether the lower exponents for duration and intensity of cigarette smoking at older ages reflect biological factors, underreporting, or misclassification of exposure at older ages is unknown and cannot be answered with our data.
The data both from the British doctors’ study (1)
and the data from CPS-II demonstrate a power relationship between lung cancer mortality and smoking duration. This finding accords with the multistage carcinogenesis theory (2
, 3
, 5
, 32)
. Under the Armitage-Doll model (see Eq. A
), if there were no misreporting of smoking duration by men 40–49 years of age (see previous discussion), then the exponent of three among men 40–49 years of age estimated in this study might suggest at least four critical stages of lung cancer development (i.e., Dk in Eq. B
is equivalent to n - 1 in Eq. A ; because Dk is approximately 3, n 4). However, the problem is likely more complex than that is represented in Equation A
if one attempts to examine age, duration, and intensity simultaneously, even using a simplified multistage theory of carcinogenesis (32)
.
The underlying assumptions of the Armitage-Doll model have been criticized by some researchers. For example, the model does not take into account the selective growth advantage that early genetic mutations may confer over normal cells or factors that may complicate the kinetics of human epithelial cells (5 , 33, 34, 35) . Alternative multistage models, most with less restrictive assumptions, have been proposed (5 , 34 , 36, 37, 38, 39, 40, 41, 42, 43, 44, 45) . Most of these models predict a power relationship between the incidence rate of carcinoma and the duration of exposure to environmental carcinogens, although the interpretations of the exponents differ.
In summary, we found that cigarette smoking duration is a stronger predictor of lung cancer mortality than is cigarette smoking intensity, regardless of age in both men and women. Furthermore, we found that lung cancer risk was proportional to approximately the second or third power of cigarette smoking duration among men and women 40–49 years of age. This finding suggests, under the Armitage-Doll multistage model of carcinogenesis, that cigarette smoking affects at least four stages of lung cancer development. We also found that the estimated exponents for both the duration and intensity of cigarette smoking decrease with increasing age.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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1 Supported in part by the Centers for Disease Control and Prevention. 
2 To whom requests for reprints should be addressed, at Rollins School of Public Health, Emory University, 1527 Clifton Road, Atlanta, GA 30329. Phone: (404) 727-8716.
3 Present address: Office of Epidemiology, Missouri Department of Health and Senior Services, 920 Wildwood Drive, P.O. Box 570, Jefferson City, MO 65102.
4 The abbreviation used is: CPS-II, Cancer Prevention Study II.
Received 9/ 6/02. Revised 6/23/03. Accepted 7/23/03.
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REFERENCES |
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