Our study of cohorts from three time periods provides a 50-year perspective on the evolution of smoking-related risks in the United States. We highlight five important findings.
First, the relative and absolute risks of death from smoking continue to increase among female smokers; the relative risks of death from lung cancer, COPD, ischemic heart disease, any type of stroke, and all causes are now nearly identical for female and male smokers. This finding is new and confirms the prediction that, in relative terms, “women who smoke like men die like men.”27
Convergence of the relative risks for men and women results from the convergence of smoking patterns among men and women since the 1960s28,29
and the aging of birth cohorts with the heaviest lifetime history of smoking. The risk of death from lung cancer among male smokers appears to have stabilized since the 1980s, whereas it continues to increase among female smokers.
Second, we found that for men 55 to 74 years of age and for women 60 to 74 years of age, the rate of death from all causes combined is now at least three times as high among current smokers as among those who have never smoked. This finding parallels and extends the findings in the British Doctors’ Study,30
the Million Women Study,31
and the U.S. National Health Interview Survey.32
These studies show that more than two thirds of all deaths among current smokers in these age groups are associated with smoking.
Third, the rate of death from COPD continues to increase among both male and female smokers in contrast to a significant decrease in risk among men who never smoked. This increase is not simply a function of aging, since it affects male smokers 55 years of age or older and female smokers 60 years of age or older. Nor can it be explained by differences in the average duration of smoking or the number of cigarettes smoked per day, since daily consumption was actually lower in the contemporary cohorts than in the CPS II cohort, and the average duration of smoking did not change significantly at any age. The ability to diagnose COPD has improved over time,33
but this would probably affect the number of prevalent cases more than the number of deaths for which COPD is considered to be the underlying cause of death. A plausible explanation for the continuing increase in deaths from COPD among male smokers is that cigarettes marketed since the late 1950s have undergone design changes that promote deeper inhalation of smoke.34
For example, the introduction of blended tobacco and genetic selection of tobacco plants lowered the pH of smoke; as a result, inhalation was easier and deeper inhalation was needed for the absorption of protonated nicotine. 35
Other design changes, such as the use of more porous wrapping paper and perforated filters, also diluted the smoke. Deeper inhalation of more dilute smoke increases exposure of the lung parenchyma. These and other design changes in cigarettes may also have contributed to the shift, beginning in the 1970s, in the histologic and topographic features of lung cancers in male smokers,36
with an increase in the incidence of peripheral adenocarcinomas that largely offset the decrease in squamous-cell and small-cell cancers of the central airways. The likely net effect of deeper inhalation on COPD could be wholly detrimental, since COPD results from injury to the lung parenchyma.
Fourth, our analyses of data from former smokers confirm that quitting smoking at any age dramatically lowers mortality from all major smoking-related diseases. As reported previously, nearly all the excess risk can be avoided if a person quits smoking before 40 years of age.17,31,32
Quitting smoking is much more effective than reducing the number of cigarettes smoked.
Finally, our analyses according to educational level show that the relative-risk estimates associated with current and former smoking among smokers with only a high-school education are generally similar to or larger than those among smokers who are college graduates. Only among male current smokers were the relative-risk estimates for ischemic and other heart disease significantly lower in the least-educated group. Hence, the relative-risk estimates presented here will in general correspond to those in a less-educated population. Similarly, differences in the time when information on smoking was obtained in the contemporary cohorts will not appreciably affect the results.
The strengths of our study include its size, prospective design, national scope, and 50-year time span. Our results provide estimates of temporal changes in cause-specific mortality and the contemporary risks from smoking in the United States. Its limitations are that it principally represents whites, 50 years of age or older, who were born between 1870 and 1954. We could not assess risks among younger contemporary smokers. Most current smokers in the contemporary cohorts had smoked for at least 30 years, limiting the range over which we could examine the influence of the duration of smoking.
In conclusion, there have been large, persistent increases in the risks of smoking-related deaths among female cigarette smokers over the past half century; in relative terms, the risks for women now equal those for men. The risks among male smokers have plateaued at the high levels of the 1980s, except for a continuing, unexplained increase in deaths from COPD.